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1
Hoffmann, Ruth. "Investigation of helenalin-induced cell death in Bcl-2 overexpressing Jurkat cells". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-122215.
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Fruasaha, Petronilla A. "Regulation of Calcium Entry Pathway in Jurkat T Cells". Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1231558093.
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Joensuu, Jenny. "Online Image Analysis of Jurkat T Cells using in situ Microscopy". Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-153313.
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Cell cultivation in bioreactors would benefit from developed monitoring systems with online real-time imaging to evaluate cell culture conditions and processes. This opportunity can be provided with the newly developed in situ Microscope also called ISM. The ISM probe is mounted into the wall of a bioreactor and consists of a measurement zone with an illuminating light source to obtain real-time images of moving cells in suspension. The instrument is linked to advanced imaging analysis software which can be specifically adapted for the objects in study. The aim of this project is to analyze the T lymphocyte cell line Jurkat T cells using the ISM equipment and identify specific features of the cells that can be obtained. The results show that the equipment and linked software are suitable for monitoring cell density, cell size distribution and cell surface analysis of the Jurkat cells during cultivation. The ISM could also detect induced changes in cell size caused by osmotic shifts and the course of an infection occurring in the cell suspension using a developed software for online real-time monitoring.
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Jabur, Soumya. "Design and optimisation of a microfluidic system for single cell encapsulation". Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/design-and-optimisation-of-a-microfluidic-system-for-single-cell-encapsulation(6c4b7877-1339-45a9-90e7-b23b7e622621).html.
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This thesis describes a novel approach for cell encapsulation in alginate gel microbeads. The main aim of the thesis was to optimise a microfluidic setup and chip to encapsulate cells in monodisperse alginate gel microbeads. A number of cytotoxicity tests were therefore carried out to determine the effect of formulations used for the production, degradation and gelation of calcium alginate gel beads. Results from these tests revealed that the formulations used had little or no significant effect on cell growth, and therefore, alginate was deemed to be a suitable cell encapsulating material for further investigations. Alginate gel microbeads were produced using hydrodynamic focusing techniques. For this purpose two different microfluidic setups were constructed. Fluids (oil, acidified oil and samples) were driven through the microfluidic setup by gravity. However, a number of drawbacks using this setup arose, such as polydispersity and reproducibility. Syringe pumps were introduced into the design of the second microfluidic setup as a means of driving fluids through the setup. In addition three different microfluidic chips were fabricated with the aim of producing the ideal alginate gel microbead. The first microfluidic chip (PMMA MC1) was fabricated from PMMA and involved producing alginate gel microbeads that were internally gelified. This chip suffered from a number of drawbacks such as continuous blockages within the microfluidic channels, which led to the development of the second microfluidic chip. This chip was also fabricated from PMMA (PMMA MC2) but in contrast to PMMA MC1, gelification occurred externally, i.e. gelation took place off chip, and in this case the alginate microdroplets were dropped into a well containing 1 mL of acidified oil. This encapsulating procedure caused immediate cell death, which indicated that the internal gelation of alginate gel microbeads was favoured. These results also indicated that the design of the microfluidic chip needed developing in order to produce the ideal microbeads that can be used for cell encapsulation. This led to the fabrication of a novel microfluidic chip (PC MC3) which was fabricated from polycarbonate (PC) and involved internal gelation of the calcium alginate gel microbeads. The combination of using the optimised microfluidic setup and PC MC3, in addition to alternations in some of the solutions used to make the alginate microbeads, resulted in the production of the desired ideal gel microbeads containing cells. Snap shots of the encapsulated cells obtained using fluorescence microscopy after 24 hours of encapsulation, revealed that the cells showed some characteristics of living cells, yet at the same time they also showed some characteristics of dead cells. These findings demonstrate the potential use of the optimised microfluidic setup and PC MC3 chip for many biological and medical applications.
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Al-Saffar, Nada M. Salman. "Investigations of Fas- and chemotherapy induced apoptosis in Jurkat T-cells using MRS". Thesis, Institute of Cancer Research (University Of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271613.
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Clay, Charles Michael. "Synthesis of Isatin Derivatives Used for the Inhibition of Pro-Apoptotic Jurkat T Cells". Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1315518391.
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Mellott, Alayna N. "Divalent Metal Cation Entry and Cytotoxicity in Jurkat T Cells: Role of TRPM7 Channels". Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1597319673881729.
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Bush, Jennifer E. "Synergistic interactions of chlorambucil, DHA, and TRAIL in Jurkat and H460 human cancer cells". Huntington, WV : [Marshall University Libraries], 2003. http://www.marshall.edu/etd/descript.asp?ref=348.
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Shaw, Jeremy Joseph Porter. "The Implications Of Gap Junction Inhibition In Jurkat Cell-CellCommunication And Proliferation". Kent State University Honors College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1398988837.
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Johnson, Victoria Louise. "Regulation of biochemical and morphological features of chemical- and receptor-mediated apoptosis in Jurkat T cells". Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29651.
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Evidence suggests that the signalling events which occur after apoptotic stimulation, define two basic mechanisms for the induction of apoptosis. The first is dependent on signalling via the mitochondria and the second is dependent upon signalling directly from the death receptors. After induction of apoptosis, there is a convergence in signalling at the level of caspase activation and subsequent biochemical and morphological changes. Therefore the efficacy of various inhibitors of apoptosis is dependent upon the initiating signal. In order to understand the apoptotic pathway, the mechanisms by which these inhibitors regulate chemical- and receptor-mediated apoptosis must be understood. The anti-apoptotic oncoprotein, Bcl-2, was shown to inhibit both staurosporine and Fas-mediated apoptosis in a manner which was partially dependent upon the level of Bcl-2 protein expressed. During both staurosporine and Fas-induced apoptosis Bcl-2 acted downstream of caspase-8 activation. High levels of Bcl-2 expression did not effectively inhibit apoptosis induced by anti-Fas but inhibited AICD by inhibiting the secretion of sFasL at a level above caspase-8 activation. The peptide based caspase inhibitor z-VAD-FMK resulted in a novel nuclear morphological change, characterized by partially condensed nuclear morphology and could be dissociated from the externalisation of PS, HMW DNA fragmentation and preceded the appearance of a condensed nuclear morphology during staurosporine-induced apoptosis. Furthermore, the appearance of the partially condensed nuclear morphology was independent of effector caspases. The nuclear morphological change occurred downstream of cytochrome c release, disruption of mitochondrial membrane potential and could be inhibited by Bcl-2. Finally the role of caspase-3 and DFF40/45 were examined in staurosporine- and Fas-mediated apoptosis. Using the MCF-7 cell line, it was found that caspase-3 and DFF40/45 were dispensable for the formation of HMW DNA fragments. Furthermore, the serine protease inhibitor, TPCK which has been previously shown to inhibit oligonucleosomal-length DNA fragmentation, was found to exert this effect by acting downstream of DFF40 activation.
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Pidde, Aleksandra. "Dynamics of the membrane potential: studies of the membrane potential of Jurkat cells using wavelet and wavelet bispectral analysis". Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670401.
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Fluctuations are fundamental for living organisms. They arguably result from interactions with the complex, and unpredictable environment, and can often be manifested as temporal variability. The cell must continually resist the external variations in the osmotic pressure by continuous adjustments in the intracellular concentrations. This happens through a highly specialised network of membrane transporters, and is manifested in the dynamics of the membrane potential. The aim of the work presented here is to provide understanding and insight into the dynamics of the free-running membrane potential in nonexcitable cells, based on experimental data. In order to achieve this, first the quantitative comparisons of the average values of the membrane potential and their standard deviations recorded in various conditions are made. The analysis is further extended through the use of the wavelet transform to investigate the time and frequency components of the signal. This work is the first to report an intermittent oscillations in the membrane potential around frequency of 8 mHz but also around frequencies of 0.03, 0.05 or 0.09 Hz. To further understand this dynamics from univariate time series, time-reversibility is investigated and a novel wavelet-bispectral density analysis is developed. The wavelet-bispectral density allows for a formal quantitative, not merely qualitative interpretation of the results of wavelet-bispectral analysis. Finally, the newly developed autowavelet-bispectral analysis is applied to the recordings of the membrane potential. These indicate possible nonlinear couplings between different oscillatory modes in the cellular membrane potential.Les fluctuacions són fonamentals pels éssers vius i probablement siguin el resultat d’interaccions amb un entorn complex i impredictible. Aquest tipus d’activitat es pot manifestar en forma de variabilitat temporal. Les cèl.lules han de resistir contínuament les variacions externes de la pressió osmòtica fent reajustaments continus de les concentracions intracel.lulars. Això és possible gràcies a una xarxa altament especialitzada de transportadors de membrana i dóna lloc a la dinàmica del potencial de membrana. L’objectiu d’aquest treball és proporcionar una millor comprensió de la dinàmica del potencial lliure de membrana en cèl.lules no excitables a partir de dades experimentals. Amb aquest objectiu i en primer lloc, comparem la mitjana i la desviació estàndard del potencial de membrana en diferents condicions de registre. Complementem aquesta anàlisi investigant les components temporo-freqüencials de la senyal mitjançant la transformada wavelet. Aquest és el primer treball on es reporten oscil.lacions intermitents del potencial de membrana amb una freqüència aproximada de 8 mHz, però també al voltant de 0.03, 0.05 i 0.09 Hz. Per entendre millor aquest comportament en el context d’una sèrie temporal univariada, utilitzem el biespectre-wavelet i l’anàlisi de reversibilitat del temps. A més, proposem una nova mesura, la densitat biespectral-wavelet, que permet fer una interpretació quantitativa -i no només qualitativa- dels resultats de l’ànalisi biespectralwavelet. L’aplicació del nou formalisme als registres del potencial de membrana posa de manifest l’existència de possibles acoblaments no lineals entre diferents modes oscil.latoris en el potencial de membrana.
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Kirschke, Stephanie Olivia. "Investigation of the apoptosis signal transduction mediated by the marine pyridoacridine alkaloid Ascididemin in human leukemic Jurkat T cells". Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-7287.
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Akdeniz, Deniz. "The roles of Def6a and Swap70b in zebrafish embryogenesis and haematopoiesis and DEF6 interactome analysis in Jurkat T cells". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/51837/.
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Medio-lateral narrowing (convergence) and anterior-posterior elongation (extension) are two of the most important cell movements of the gastrulation period leading to the formation of embryonic body axis. In vertebrates, convergence and extension (CE) cell movements are regulated by the non-canonical Wnt/Planar cell polarity (PCP) signalling pathway which requires the activation of its downstream effectors, Rho GTPases. DEF6 and SWAP70 are guanine nucleotide exchange factors (GEFs) catalysing the activation of Rho GTPases to regulate the re-arrangement of actin cytoskeleton, cell polarity and cell movements. Although it has been shown that the zebrafish orthologous, Def6a and Swap70b, act downstream of Wnt5b or Wnt11 signalling pathway, respectively, regulating the CE cell movements during gastrulation, little is known about the underlying molecular mechanisms and direct downstream targets of Def6a and Swap70b. To further elucidate the function of def6a and swap70b within the non-canonical Wnt/PCP signalling pathway, Transcription Activator-Like Effector Nucleases (TALENs)-induced mutagenesis was employed to establish knock-out mutant lines lacking either def6a (qmc811), swap70b (qmc809) or both (qmc813). Phenotypic and whole-mount in situ hybridisation analyses have revealed that the anterior movement and the convergence of the lateral mesendodermal and ectodermal cells were severely impaired in def6a and/or swap70b-deficient zebrafish embryos, indicating that def6a and swap70b are required for normal CE cell movements during gastrulation. Ectopic expression of Cdc42 GTPase robustly rescued the CE cell movement defects in both def6aqmc811/qmc811 and swap70bqmc809/qmc809 homozygous mutant lines whereas ectopic expression of RacI robustly rescued CE cell movement defects only in swap70bqmc809/qmc809 homozygous mutant line, suggesting that Def6a and Swap70b acts upstream of Cdc42 and Cdc42/RacI respectively. Elevated expression of wnt5b and wnt11 detected in the mutant lines indicated that abrogation of def6a and swap70b functions interfered with Cdc42/RacI-mediated Jnk activation that negatively regulates expression of wnt11 and perhaps wnt5b. In adult def6a and/or swap70b-deficient fish, a decreased number of myeloid population was observed, suggesting that both proteins are required for balanced cell differentiation during haematopoiesis. Generation of the double homozygous mutant line revealed that def6a and swap70b act in a partially redundant manner during zebrafish embryogenesis and in a non-redundant manner during haematopoiesis. DEF6 is highly expressed in T cells and plays an immunoregulatory role in cell polarity-induced immunological synapse (IS) formation, T cell receptor (TCR) signalling, T cell activation, differentiation and inflammatory responses. Recently, it has been shown that DEF6 may also be involved in the mRNA surveillance and translation. However, the molecular mechanisms that it may be involved in and its interactors in T cells are still unknown. Hence, a novel method, BioID, which enables the promiscuous biotinylation of proximal and interacting proteins of a target protein in mammalian cells, was adapted to identify DEF6 interactome in Jurkat T cells. Notably, in vivo BioID-DEF6 fusions yielded 127 clusters of interacting and vicinal proteins, including 2 known binding partners, Rac2 and PKC and 1 known close proximity partner, PABP. GO-term classification of the identified proteins showed that the proteins are enriched not only in actin cytoskeleton organisation and mRNA translation, but also in transcription, mRNA splicing/processing, protein folding/modification and metabolic processes. Co-localisation of DEF6 with Coronin1A (CORO1A), an actin cytoskeleton regulator during IS formation, in resting and activated cells provided proof of principle for the interactome analysis suggesting that DEF6 is a multifunctional protein involved in the regulation of cytoskeletal organisation, transcription, mRNA splicing, protein folding/processing and metabolic processes.
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Schneider, Olivia Dawn. "An Analysis of the Effects of Pertussis Toxin on T Cell Signaling". University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1258667926.
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Shrestha, Ramesh. "Micro-Pipette Thermal Sensor: A Unique Technique for Thermal Characterization of Microfluids, Microspheres, and Biological Cells". Thesis, University of North Texas, 2020. https://digital.library.unt.edu/ark:/67531/metadc1703406/.
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In this research work, an innovative method for measurement of thermal conductivity of a small volume of liquids, microsphere, and the single cancer cell is demonstrated using a micro-pipette thermal sensor (MPTS). The method is based on laser point heating thermometry (LPHT) and transient heat transfer. When a single pulse of a laser beam heats the sensor tip which is in contact with the surrounding liquids or microsphere/cells, the temperature change in the sensor is reliant on the thermal properties of the surrounding sample. We developed a model for numerical analysis of the temperature change using the finite element method (FEM) in COMSOL. Then we used MATLAB to fit the simulation result with experiment data by multi-parameter fitting technique to determine the thermal conductivity. To verify the accuracy in the measurement of the thermal conductivity by the MPTS method, a 10µl sample of de-ionized (DI) water, 50%, and 70% propylene glycol solution were measured with deviation less than 2% from reported data. Also, to demonstrate that the method can be employed to measure microparticles and a single spherical cell, we measured the thermal conductivity of poly-ethylene microspheres with a deviation of less than 1% from published data. We estimated the thermal conductivity of two types of cell culture growth media for the first time and determined the thermal conductivity of cancerous Jurkat Clone E6-1 to be 0.538 W/m.K ± 2%. Using the sensor of 1-2μm tip size, we demonstrated the MPTS technique as a highly accurate technique for determining the thermal conductivity of microfluidic samples, microparticles, biological fluids, and a non-invasive method for measuring the thermal conductivity of single cancer cell. This MPTS technique can be beneficial in developing a diagnosis method for the detection of cancer at an early stage. We also compared three effective thermal conductivity models for determining the weight percentage of Jurkat cell, considering water and protein as the major constituents. We discovered that a combination of Maxwell-Euken and effective medium theory model provides the closest approximation to published data and, therefore, recommend for the prediction of the cell composition.
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Khoo, Yi Vonn. "Apoptotic cell death via oxidative stress mediated caspase-dependent mechanism in Jurkat T cells by cardamonin and its transition metal Cu (II) and Fe (II) complexes". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/51601/.
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Cancer is a leading cause of death worldwide as cancer cells have the ability to develop resistance to chemotherapeutic agents due to their high expressions of resistance gene. More research on alternative strategies to eradicate this type of malignant cells is highly desired by using natural products with fewer side effects. This study initially investigates the cytotoxicity of 20 novel semi-synthetic cardamonin derivatives and complexes in A549 lung and HK1 nasopharyngeal cancer cell lines. Structure activity relationship analysis revealed the factors affecting cytotoxicity were modification of hydroxyl group, presence of alkene group, addition of chemical groups, with the greatest cytotoxicity advantage being complexing with metal ions. Cardamonin-Cu(II) and cardamonin-Fe(II) complexes were determined as the two most cytotoxic compounds and were selected for further cytotoxic analysis in normal MRC5 lung and normal Hs68 foreskin cell lines. Results showed toxicity in MRC5 lung cells but was less toxic in Hs68 foreskin cells, suggesting some level of selectivity from cardamonin, cardamonin-Cu(II) and cardamonin-Fe(II) depending on the type of cells exposed to. Subsequently, cardamonin and its two complexes were tested in Jurkat T leukaemic cells and results showed highest susceptibility in this leukaemic cell line prompting further investigation on differential susceptibility of adherent and suspension cells. THP-1 monocytic leukaemia cell line cultured in both suspension and adherent phase demonstrated increased resistance in THP-1-derived macrophages in adherent phase compared to THP-1 monocytes in suspension form. Herein, we investigated the effects of interference from inhibitors of p38α and p38β MAP kinase and found THP-1-derived macrophages’ increased resistant towards cardamonin, cardamonin-Cu(II) and cardamonin-Fe(II) complexes were independent of p38α and p38β MAP kinase pathway. As Jurkat T cells exhibited lowest IC50 values in cardamonin, cardamonin-Cu(II) and cardamonin-Fe(II)-treated cells, we next explored the underlying mechanism of action in this cell. All three compounds were found to induce apoptotic cell death via the intrinsic mitochondrial pathway in Jurkat T cells as evidenced by the morphological changes, phosphatidylserine externalisation, caspase-3, -9 and PARP-1 cleavage, and collapse of mitochondrial membrane potential. Caspase-8, an initiator caspase of the extrinsic pathway was not activated. The presence of a caspase inhibitor, Z-VAD-FMK, was able to inhibit caspase processing and block cell death, further confirming the induced apoptotic cell death was caspase-dependent. As previous studies have reported the ability of metals to induce apoptosis through oxidative stress, the effects of these three compounds on reactive oxygen species (ROS) generation and intracellular glutathione (GSH) levels were explored. Results revealed cardamonin and cardamonin-Fe(II)-induced depletion of intracellular GSH and production of ROS; whereas cardamonin-Cu(II) did not significantly affect intracellular GSH levels but generated ROS. The presence of low molecular weight thiols, N-acetylcysteine (NAC), L-cysteine and GSH as well as Trolox, a ROS scavenger, blocked cardamonin and cardamonin-Fe(II)-induced Jurkat T cell death, while D-cysteine, which cannot be metabolised to GSH had no effect. However, these low molecular weight thiols had no effect on cardamonin-Cu(II)- treated cells with the exception of Trolox, confirming the role of ROS in cardamonin- Cu(II)-induced Jurkat T cell death. Furthermore, intracellular ROS and GSH levels were recovered close to levels of untreated Jurkat T cells in the presence of Z-VAD- FMK. In conclusion, this study demonstrates cardamonin, cardamonin-Cu(II) and cardamonin-Fe(II) induced apoptotic cell death in Jurkat T cells via an oxidative stress mediated intrinsic mitochondrial pathway that was caspase-dependent.
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Marenda, Flávia Roberta Buss. "CITOTOXICIDADE DE PECTINAS DO ALBEDO DE MARACUJÁ (Passiflora edulis flavicarpa) EM LINHAGENS TUMORAIS". UNIVERSIDADE ESTADUAL DE PONTA GROSSA, 2015. http://tede2.uepg.br/jspui/handle/prefix/640.
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Previous issue date: 2015-02-03Conselho Nacional de Desenvolvimento Científico e Tecnológico
The passion fruit industrial use reach only 25% of the total fruit and passion fruit peel, representing 50% of the total, are discarded, but can be used in the extraction of pectin. Recent studies indicate that pectin, modified so as native, has antitumor activity. This study aimed to evaluate the cytotoxicity of pectin of passion fruit peel in tumor cell lines. Extraction has been made and the chemical modification of pectin of passion fruit peel, subjected to three different treatments. Both the raw material and pectin were characterized by specific analyzes. The cytotoxicity of untreated pectins, modified autoclaved and autoclaved were evaluated in tumor lines Jurkat, HeLa and HRT-18. The peel of passion fruit represented 54.7% of total fruit. The passion fruit peel flour bleached untreated and shown to be rich in soluble and insoluble fibers. The flour autoclaved pectin showed higher content of phenolic compounds; however, bleached pectin retained more phenolic compounds from the raw material. The modified pectins had a lower degree of methoxylation and lower molecular weight compared to native pectins, confirming the modification process. The best effect Cytotoxicity in Jurkat cells treated with autoclaved pectin modified with IC50 of 2.63 mg mL-1. The calculation of the selectivity index indicated that the modified autoclaved pectin has a low toxicity to healthy cells. In conclusion, the results demonstrate a potential antitumor promising for autoclaved modified pectin, that needs to be further exploited.
O aproveitamento industrial do maracujá atinge apenas 25% do total do fruto e as cascas do maracujá, que representam 50% desse total, são descartadas, mas podem ser utilizadas na extração de pectina. Estudos recentes indicam que a pectina, tanto nativa quanto modificada, apresenta atividade antitumoral. Assim, este trabalho teve por objetivo avaliar a citotoxicidade de pectinas do albedo do maracujá em linhagens tumorais. Foi feita a extração e a modificação química da pectina do albedo de maracujá, submetido a três diferentes tratamentos. Tanto a matéria-prima quanto a pectina foram caracterizadas por análises específicas. A citotoxicidade das pectinas sem tratamento, autoclavada e autoclavada modificada, foram avaliadas em linhagens tumorais Jurkat, HeLa e HRT-18. A casca do maracujá representou 54,7% do total do fruto. As farinhas do albedo do maracujá sem tratamento e branqueada mostraram-se ricas em fibras solúveis e insolúveis. A farinha e a pectina autoclavada apresentaram maior teor de compostos fenólicos; no entanto, a pectina branqueada reteve mais compostos fenólicos provenientes da matéria prima. As pectinas modificadas apresentaram menor grau de metoxilação e menor massa molar, comparada às pectinas nativas, confirmando o processo de modificação. O melhor efeito de citotoxicidade foi obtido em células Jurkat tratadas com pectina autoclavada modificada, com IC50 de 2,63 mg mL-1. O cálculo do Índice de Seletividade (IS) indicou que que a pectina autoclavada modificada apresenta baixa toxicidade para células saudáveis. Em conclusão, os resultados demonstram promissor potencial antitumoral para a pectina autoclavada modificada, que precisa ser melhor explorado.
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Lebogo, Kgomotso Welheminah. "The evaluation of the effects of semi-purified extracts of Commelina benghalensis on the molecular events associated with the growth, apoptosis and cell cycle progression of Jurkat-T cells". Thesis, University of Limpopo (Turfloop Campus), 2007. http://hdl.handle.net/10386/914.
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Lindholm, Cecilia. "Shb and Its Homologues: Signaling in T Lymphocytes and Fibroblasts". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1813.
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Stimulation of the T cell receptor (TCR) induces tyrosine phosphorylation of numerous intracellular proteins, leading to activation of the interleukin-2 (IL-2) gene in T lymphocytes. Shb is a ubiquitously expressed adapter protein, with the ability to associate with the T cell receptor and several signaling proteins in T cells, including: the TCR ζ-chain, LAT, PLC-γ1, Vav, SLP-76 and Gads. Jurkat T cells expressing Shb with a mutation in the SH2 domain, exhibited reduced phosphorylation of several proteins and abolished activation of the MAP kinases ERK1, ERK2 and JNK, upon CD3 stimulation. The TCR induced Ca2+ response in these cells was abolished, together with the activation of the IL-2 promoter via the transcription factor NFAT. Consequently, IL-2 production was also perturbed in these cells, compared to normal Jurkat T cells. Shb was also seen to associate with the β and γ chains of the IL-2 receptor, upon IL-2 stimulation, in T and NK cells. This association occurred between the Shb SH2 domain and Tyr-510 of the IL-2R β chain. The proline-rich domains of Shb were found to associate with the tyrosine kinases JAK1 and JAK3, which are important for STAT-mediated proliferation of T and NK cells upon IL-2 stimulation. Shb was also found to be involved in IL-2 mediated regulation of apoptosis. These findings indicate a dual role for Shb in T cells, where Shb is involved in both T cell receptor and IL-2 receptor signaling.
A Shb homologue, Shf was identified, and seen to associate with the PDGF-α-receptor. Shf shares high sequence homology with Shb and a Shd (also of the Shb family) in the SH2 domain and in four motifs containing putative tyrosine phosphorylation sites. When Shf was overexpressed in fibroblasts, these cells displayed significantly lower rates of apoptosis than control cells in the presence of PDGF-AA. These findings suggest a role for the novel adapter Shf in PDGF-receptor signaling and regulation of apoptosis.
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Cipelli, Riccardo. "Endocrine disruption and human health : from populations to cells : an integrated approach in the study of bisphenol A". Thesis, University of Exeter, 2013. http://hdl.handle.net/10871/14145.
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Background. Endocrine disruptors (EDC) are exogenous compounds that mimic the action of natural hormones and alter the normal endocrine system. Life-long chronic exposure to Bisphenol A (BPA), a putative EDC, has been linked with risk of metabolic disorders in epidemiological studies. Objectives. The aim was to study the human health effects of exposure to BPA, using an integrated approach combining environmental epidemiology and toxicology. Methods. Urinary levels of BPA exposure were measured in participants of the InChianti longitudinal study, a representative population-based study of Italian adults, at the Baseline (1998-00) and nine years later (3rd Wave, 2007-09). Hormones levels and the gene expression of specific target genes were the end points considered. Results were validated in laboratory studies on a human leukemic T-cell line (Jurkat cells). Results. In general, urinary BPA (uBPA) concentrations were higher among men and younger respondents, and within subjects uBPA concentrations were correlated (r=0.58; p=0.013, model adjusted for age, sex, urinary creatinine). At baseline, uBPA concentration were associated with higher total testosterone concentrations in men (β = 0.05; 95% CI, 0.02–0.08). In the 3rd wave, gene expression analysis revealed positive associations between uBPA concentrations and ESR2 (estrogen receptor beta) expression (β=0.18; 95% CI: 0.04, 0.32) and ESRRA (estrogen related receptor alpha) expression (β= 0.17; 95% CI: 0.02, 0.32). In a following in vitro study, BPA exposure (0.001-1 micro molar) led to enhanced expression of ESRRA and ESR2 in Jurkat cells over a period of 72 hours. Conclusions. Results indicate that BPA is bioactive in the human body and is able to alter circulating hormone concentrations and estrogen receptor/estrogen-related receptr gene expression. In particular, given the role of ERRα as a major control point for oxidative metabolism and heart development, this research provides indications on the possible molecular mechanisms of action of BPA in metabolic diseases.
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Majdalawieh, Amin F. "Isolation and characterization of Jurkat-derived signaling-deficient T cell lines". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79040.
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In this study, we describe the isolation and characterization of a functionally signaling-deficient Galpha16-negative somatic mutant (hereafter referred to clone 43) derived from the wildtype Jurkat T cell line by means of an activation-induced cell death resistance-based selection strategy. The catalytic activity of Lck in abrogated in clone 43 most likely due to a lack of autophosphorylation at the stimulatory site within the kinase domain of Lck, Y394. Based on Galpha16 cDNA sequencing data, the deficiency presented in clone 43 is most likely due to one or two point mutations located at amino acid residues 26 and 300 of the Galpha16 subunit. Importantly, these signaling defects were fully reversed by re-introduction of wildtype Galpha16 version into clone 43. Indeed, our findings are the first of their kind to validate the proposed model by which the Galpha subunit modulates the activity of Src family of protein tyrosine kinases. These studies underscore the integral role played by Galpha 16 in TCR-mediated signaling and offer a powerful genetic tool to strengthen our knowledge about the regulation and function of G proteins in T lymphocytes. We also describe the phenotype of two other signaling-deficient, Jurkat-derived clones, named clone 15 and clone 21. (Abstract shortened by UMI.)
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Murrell, Rachel Nichole. "Effect of Brevetoxin and Brevetoxin ANtagonists on Jurkat E6-1 Cell Proliferation, Survival, and Gene Expression". NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-07302008-152733/.
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Brevetoxins (PbTx) are potent lipid soluble polyether neurotoxins produced by the marine dinoflagellate Karenia brevis, an organism linked to periodic red tide blooms. Brevetoxins have been linked to deaths in marine mammals, which are exposed through ingestion of organisms harboring high brevetoxin concentrations and through the inhalation of aerosolized brevetoxins. Humans are also at risk through the same routes of exposure. Evidence suggests that respiratory exposure to brevetoxins can lead to a severe inflammatory response. Brevetoxins exert their toxicity by interacting with neurotoxin receptor site five associated with domain IV of the alpha subunit of the voltage gated sodium channel. Brevetoxin binding to tissues that contain voltage gated sodium channels on excitable cells results in membrane depolarization, repetitive firing, and increase in sodium currents. The goal of the current research project is to determine how these marine toxins evoke an immune response, specifically by examining the effects of brevetoxin and brevetoxin antagonists on T cells. The hypothesis is that brevetoxins alter cell proliferation, cause DNA damage, disrupt normal signal transduction, and ultimately cause cell death, possibly through an apoptotic mechanism, and the natural and synthetic brevetoxin antagonists are able to prevent and reverse these deleterious effects, making them a useful pharmaceutical agent not only for brevetoxin exposure treatment, but also for human diseases exhibiting similar inflammatory congestion, like Asthma and Cystic Fibrosis. The effects of brevetoxins and antagonists were determined by cell proliferation assays, comet assays and examination of caspase activation, Poly ADP- ribose polymerase (PARP) cleavage and gene expression. Exposure of Jurkat E6-1 Cells to Brevetoxin 2, 3, 6, and 9 at doses of 10-5M severely inhibited proliferation. Further analysis revealed positive staining for apoptosis, PARP cleavage, caspase 3/7 and caspase 8 activation, decreased intracellular sodium and increased intracellular calcium concentrations. PCR array gene expression analysis revealed significant change in gene expression. The apoptosis PCR array yielded 30 up-regulated and 4 down-regulated genes divided into the following families: TNF ligand, TNF receptor, Bcl-2, caspase, IAP, CARD, death domain, CIDE, p53 and DNA damage response, and anti-apoptosis. The DNA Damage Signaling Pathway Array had 20 up-regulated genes and 5 down-regulated genes from the following families: apoptosis, cell cycle arrest, cell cycle checkpoint, DNA repair-damaged DNA binding, DNA repair-double strand break repair, DNA repair-mismatch repair, and other genes related to DNA repair. The Common Cytokine PCR array had 50 up-regulated genes from the following gene families: interferons, interleukins, bone morphogenic protein and TGF-ï¢, PDGF/VEGF, TNF Superfamily, and other growth factors/cytokines. Exposure of Jurkat E6-1 cells to brevetoxin in combination with the antagonists brevenal, alpha naphthoyl, and beta naphthoyl did not improve cell proliferation, which is in stark contrast to experiments conducted with CHO-K1 BH4 cells. This disparity may be due to the difference in voltage gated sodium channel subtypes that these cells possess. The results demonstrate that brevetoxins can induce apoptosis and DNA damage and that the antagonists may show selectivity based on VGSC subtype.
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Matsui, Hiroyuki. "CAGE-seq reveals that HIV-1 latent infection does not trigger unique cellular responses in a Jurkat T cell model". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/265190.
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Brown, Nicole Chantae. "The mechanism of T cell dysfunction induced by Diethylstilbestrol". VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1321.
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Estrogens have the ability to alter the immune system. Diethylstilbestrol (DES), asynthetic estrogen, is known to have estrogenic activity and induce thymic alterations.We investigated the mechanism by which DES is able to alter T cells and thus theimmune system. First, we studied the effect of DES on mature T cells by using the T cellleukemia cell line, Jurkat. We found that DES treatment reduced cell viability andincreased apoptosis. Additionally, apoptosis was found to involve both death receptorand mitochondria1 pathways. Furthermore, estrogen receptor beta was found to beexpressed in these cells and increased following DES treatment. Secondly, we studiedthe effect of DES on developing T cells using two different mouse models, timed pregnant and HY-TCR transgenic. The pregnant mouse model showed that DESexposure in utero reduced thymic cell viability and induced apoptosis at gestational day(gd)-17. Apoptosis was found to involve the death receptor pathway. Additionally,alterations in T cell subsets was most pronounced at gd-17 as well. The HY-TCR tgmouse model showed that DES exposure altered both positive and negative selection of Tcells. Furthermore, DES was found to alter the ability of T cells to proliferate during animmune response. Finally, we studied the intrathymic interaction between thymicstromal cells and thymic T cells. We found that cel1:cell interaction was important forinducing T cell apoptosis in the thymus. Additionally, FasL expression was increased onthymic stromal cells following DES exposure. Furthermore, the presence of both FasL onstromal cells and Fas on T cells was important for inducing T cell apoptosis in thethymus.
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Patel, Shakil. "The role of membrane potential dynamics in cell behaviours : investigating the membrane potential dynamics in the Jurkat and HMEC-1 cell lines using the continuous wavelet transform". Thesis, Lancaster University, 2016. http://eprints.lancs.ac.uk/84813/.
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The role of the plasma membrane potential is most commonly associated with the generation of action potentials in excitable cells, however, experimental evidence suggests that this membrane potential is also linked to various behaviours in all cells (Blackiston et al., 2009). These cell behaviours include cell proliferation, cell migration and even cell survival. The membrane potential has been thought to influence these cell behaviours upstream of the classical transduction pathways. Recent evidence suggests that the membrane potential is dynamic rather than static and this dynamic behaviour may encode information on cell behaviours. The whole cell patch clamping technique coupled with the continuous wavelet transform (CWT) technique was used to investigate the presence of fluctuations and oscillations in the membrane potential of Jurkat cells and HMEC-1 cells. The underlying nature of the membrane potential dynamics of Jurkat cells was investigated by perturbing the extracellular concentration of either K+ , Na+ or Cl- . The membrane potential dynamics of proliferating, non-proliferating and activated Jurkat cells was investigated by either varying the culture medium or treating the cells with the concavalin A mitogen. The membrane potential dynamics of HMEC-1 endothelial cells was also investigated. The magnitude of the static membrane potential of proliferating Jurkat cells was significantly more depolarised that non-proliferating Jurkat cells – a trend which has been observed in a wide range of cell types. The membrane potential dynamics appear to be driven by the conductance of ions rather than the magnitude of the static membrane potential per se. In summary, this thesis has proven that the membrane potential varies with cell state and the CWT technique can be used to interrogate recordings of the membrane potential to ascertain information on the membrane potential dynamics that cannot be currently determined by other techniques.
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Mbazima, Vusi G. "The Effects of Crude Methanolic Extract of Commelina benghalensis Linn on the Expression of Apoptotic and Cell Division Cycle Genes in Jurkat T and Wil-2 NSCancer Cell Lines". Thesis, University of Limpopo (Turfloop Campus), 2009. http://hdl.handle.net/10386/937.
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Thesis (Ph.D. (Biochemistry)) --University of Limpopo, 2009Commelina benghalensis Linn is used in traditional medicine in several Asian and African countries for the treatment of various ailments such as stomach irritations, burns, sore throat and feet, diarrhoea and as an anti-inflammatory agent. Recently, our laboratory showed that the crude methanolic extract of Commelina benghalensis L (CMECB) exhibits growth inhibitory and proapoptotic effects in Jurkat T and Wil-2 NS cancer cell lines. In this study, the precise molecular mechanism(s) associated with CMECB-induced growth inhibitory and apoptosis inducing effects in Jurkat T and Wil-2 NS cell lines were investigated. This was achieved by investigating the effects of the extract on the cell division cycle distribution profile as well as its effects on various cell division cycle and apoptosis regulatory genes. Ground stems of C. benghalensis L were extracted with absolute methanol to obtain a crude extract. To assess the effect of CMECB on cancer cell growth, experimental cell cultures were exposed to various concentrations (0 to 600 μg/ml) of CMECB for up to 72 hours. The results demonstrated a significant reduction in cell viability and inhibition of proliferation of experimental cell cultures as determined by the trypan blue dye exclusion assay and the Coulter counter method, respectively. Analysis of nuclear morphological changes in cells stained with Hoechst 33258 confirmed apoptosis as the mode of cell death that is associated with the growth inhibitory effects of CMECB in both the Jurkat T and Wil-2 NS cell lines. This assertion was based on the observed presence of nuclear morphological changes such as chromatin condensation and fragmentation and apoptotic bodies in cells exposed to CMECB. In order to get an insight on the pro-apoptotic mechanisms of CMECB, Western blot xxi and quantitative real-time PCR (qrt-PCR) were used to investigate the expression profiles of various apoptosis and cell division cycle regulatory genes. Qrt-PCR results showed a lack of a clear up- and/or down-regulatory effects of CMECB on the mRNA expression levels of bax and bcl-2 in both Jurkat T and Wil-2 NS cells. Western blot analyses demonstrated that CMECB induced apoptosis by facilitating Bax protein translocation from the cytosol to the mitochondria in both Jurkat T and Wil-2 NS cells. In addition, CMECB down-regulated Bcl-2 protein expression which, as a result, led to the shift in the Bax/Bcl-2 protein ratio at certain time points and concentration in both Jurkat T and Wil-2 NS cells. The modulation of the Bcl-2 family members led to mitochondrial cytochrome c release into the cytosol and activation of caspases-9 and -3; this was also confirmed by caspase activity assays and eventual degradation of PARP. Furthermore, CMECB induced Jurkat T and Wil-2 NS cell division cycle arrest at the G2/M phase as determined by flow cytometric analysis. Western blot analyses of G2/M phase regulatory proteins demonstrated that the CMECB-induced cell division cycle arrest was associated with the downregulation of cyclin B1 and Cdc2 protein expression levels. Western blot analyses results further revealed that the arrest of Wil-2 NS cells at the G2/M phase was independent of p21 protein activity. However, Jurkat T cell division cycle arrest was found to be mediated, in part, by p21. Quantitative real-time PCR results did not show a clear trend in terms of the down- or up-regulatory effects of the extracts on the G2/M phase regulatory genes. The CMECBinduced apoptosis and G2/M arrest was found to occur in a p53-independent xxii manner due to the lack and down-regulation of p53 protein levels in both Jurkat T and Wil-2 NS cells, respectively. In conclusion, CMECB induces its anticancer activity by inducing G2/M phase arrest and mitochondrial-mediated apoptosis independent of p53 protein activity. Although the study did not perform in vivo experiments to ascertain the efficacy of extracts of CMECB against specific tumour types in animal models, the present findings somehow validate the traditional use of C. benghalensis L as an anticancer agent. A more definitive study needs to be done to ascertain this assertion.
National Research Foundation and the University of Limpopo research office
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C?rdoba, Mar?a Ang?lica Mera. "Avalia??o da atividade citot?xica in vitro dos extratos vegetais de Pseudobrickellia brasiliensis (Spreng) R. M. King & H. Rob, Miconia ferruginata DC e Ageratum fastigiatum (Gardn.) R. M. King sobre c?lulas tumorais Jurkat". UFVJM, 2017. http://acervo.ufvjm.edu.br/jspui/handle/1/1564.
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?rea de concentra??o: Ci?ncias farmac?uticas.Incluir como ag?ncias financiadoras: Grupo Coimbra das Universidades Brasileiras (GCUB) e Organiza??o dos Estados Americanos (OEA).
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O Cerrado mineiro possui muitas esp?cies vegetais utilizadas na medicina popular, dentre elas est?o a Pseudobrickellia brasilensis , a Miconia ferruginata e Ageratum fastigiatum, plantas popularmente usadas como analg?sico, cicatrizante e anti-inflamat?rio. Estudos realizados no Laborat?rio de Imunologia da UFVJM indicaram que extratos destas plantas possuem efeito inibit?rio sobre a ativa??o de linf?citos humanos in vitro. Em virtude disso, e com base em relatos populares sobre uma poss?vel a??o antitumoral, o objetivo principal deste trabalho foi pesquisar se estes extratos apresentariam ou n?o efeito citot?xico sobre a linhagem tumoral Jurkat, utilizando-se concentra??es n?o t?xicas, j? avaliadas sobre c?lulas mononucleares do sangue perif?rico humano (PBMC). Uma vez que os extratos vegetais foram dilu?dos no solvente Dimetilsulf?xido (DMSO), inicialmente investigou-se a concentra??o m?xima de DMSO que n?o alteraria a viabilidade das c?lulas Jurkat ap?s 24, 48 e 72 horas de cultura. O efeito citot?xico dos extratos foi avaliado sobre linf?citos tumorais (Jurkat) e sobre linf?citos humanos de volunt?rios h?gidos pelo m?todo de exclus?o com azul de tripan, com exce??o das culturas tratadas com P.brasilensis, onde a viabilidade foi avaliada por citometria de fluxo. Tamb?m foram calculados os ?ndices de seletividade e percentuais de efic?cia dos extratos com rela??o ao f?rmaco antineopl?sico Paclitaxel. Foi avaliada tamb?m a interfer?ncia desses extratos sobre as fases do ciclo celular das c?lulas Jurkat, bem como os mecanismos de morte envolvidos na a??o citot?xica dos extratos. De acordo com os resultados obtidos, o DMSO n?o apresentou efeito t?xico sobre as c?lulas Jurkat na concentra??o de 1%v/v nos tr?s tempos de incuba??o, sendo esta a concentra??o de solvente utilizada em todos os ensaios realizados. Extratos etan?licos das folhas da P. brasilensis (PBf) a 200?g/mL, das partes a?reas da A. fastigiatum (Afpa) a 50?g/mL e extratos etan?licos e aquosos da M. ferruginata (Mfet, Mfaq) a 125?g/mL mostraram maior toxicidade sobre as c?lulas Jurkat principalmente ap?s 72h de tratamento. O tratamento, por 24h, com extrato Afpa 50 ?g/mL mostrou ser o mais seletivo e eficaz com rela??o aos outros extratos. Foi evidenciado em todos os extratos, que nas maiores concentra??es, ap?s de 24 horas de tratamento, houve uma inibi??o na progress?o da fase G2M do ciclo celular. O extrato das partes a?reas de Ageratum fastigiatum tamb?m produziu uma reten??o dessas c?lulas na fase G0-G1. Todos os extratos induziram a apoptose as c?lulas Jurkat, onde o n?mero de c?lulas em apoptose tardio foi predominante em rela??o aos processos necr?ticos.
Disserta??o (Mestrado) ? Programa de P?s-gradua??o em Ci?ncias Farmac?uticas, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2017.
The Cerrado Mineiro has many vegetable species used in folk medicine. Plants like Pseudobrickellia Brasilensis, Miconia ferruginata and Ageratum fastigiatum are widely used as analgesic, healing or anti-inflammatory. Studies carried on the Immunology Laboratory (UFVJM) shown that extracts from these plants has inhibitory effects in the activation of in-vitro-cultured human lymphocytes. In this way, and based on folk stories related with their anti-tumor action, the main objective of this work was research about the cytotoxic effect of this plants on Jurkat tumor line-cell cultures, using as first experiment non-toxic extract concentrations previously proved on peripheral blood mononuclear cells (PBCM). Once the vegetable extracts were diluted in dimetilsulfoxide (DMSO), previously, the maximum DMSO concentration not-altering cell viability was determined after 24, 48 and 72 hours. Cytotoxic effect was studied using the exclusion method with tripam blue on tumor lymphocytes (Jukart) and human lymphocytes, donated by healthy volunteers, except for P.brasilensis treated line cells, for which cell viability was studied by flux cytometer. The selectivity index and extracts efficiency percentage were calculated and related with the antineoplastic Paclitaxel drug. The extracts interference on the Jukart cell cycle phases and the cell death mechanisms related with the cytotoxic activity were evaluated. According to the obtained results, DMSO does not show cytotoxic effects on Jukart cells in 1% (v/v) concentration at the three incubation times, being this the solvent concentration used in all the experiments. Ethanol extracts of P. brasilensis leaves (PBf) at 200?g / mL, aerial parts of A. fastigiatum (Afpa) at 50?g / mL and M. ferruginata aqueous and ethanolic extracts (Mfet, Mfaq) at 125?g / mL showed higher Toxicity on Jurkat cells mainly after 72h of treatment. The 24 h treatment with Afpa at 50 ?g/mL was the most selective and effective in comparison with the other tested extracts. It was evidenced in all extracts, that at the highest concentrations, after 24 hours of treatment, there was an inhibition in the progression of the G2M phase of the cell cycle. The extract of Ageratum fastigiatum aerial parts also produced the G0-G1 phase retention. All extracts induced Jukart cell apoptosis, and cell number on late apoptotic phase predominated on the necrotic ones.
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Pluchart, Claire. "Etude des vésicules extracellulaires procoagulantes au cours du traitement d'induction des leucémies aigues lymphoblastiques de l'enfant. Vincristine induces procoagulant activity of the human lymphoblastic leukemia cell line Jurkat through the release of extracellular vesicles". Thesis, Reims, 2020. http://www.theses.fr/2020REIMM207.
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La leucémie aigue lymphoblastique (LAL) est le cancer le plus fréquent de l’enfant, représentant 25% des cancers pédiatriques. Les complications thromboemboliques veineuses sont des complications sévères et fréquentes, estimées à 6,1% dans une étude prospective récente. La pathogénie de cette complication n’est toujours pas complètement élucidée. Elle pourrait impliquer l’interaction des cellules circulantes et des vésicules extracellulaires (VEC) avec les chimiothérapies. Nous avons tout d’abord démontré via un modèle in vitro l’activité procoagulante des blastes lymphoïdes et des VEC blastiques, dépendante des phosphatidylsérines. Nous avons également observé dans cette même étude l’effet procoagulant inattendu de la vincristine. Nous avons ensuite réalisé une étude clinique portant sur l’analyse des VEC plasmatiques pendant le traitement d’induction. Nous avons observé que les VEC, majoritairement d’origine plasmatique augmentaient en nombre tout au long de l’induction. Elles présentent une activité procoagulante. Il existe une association significative entre leur nombre/ activité prooagulante et les taux de plaquettes et de leucocytes. Ces résultats sont en faveur d’une activation plaquettaire durant le traitement d’induction à l’origine de la production de VEC. De ce fait dans un troisième article nous avons étudié sur les mêmes patients l’évolution du taux plasmatique de P-sélectine, marqueur d’activation plaquettaire. Le taux de P-sélectine augmente pendant l’induction et le taux est corrélé au nombre des VEC et au taux de leucocytes et de plaquettes. De ce fait la P-sélectine apparait comme un potentiel biomarqueur de la thrombose dans les LAL de l’enfantAcute lymphoblastic leukaemia (ALL) is the most common childhood malignancy, representing 25% of all paediatric malignancies. Venous thromboembolism (VTE) is a common and severe complication of ALL treatment. The reported incidence rate of VTE in children is 6.1% in a recent prospective study. Pathogenesis of this complication is still not fully understood but may involve interactions between circulating cells and extracellular vesicles (EV) and chemotherapy. We first demonstrated in an in-vitro model that lymphoid blasts and derived EV could have a procoagulant activity through phospholipid exposure. Another result of this study was to show an unexpected procoagulant effect of Vincristine (VCR) on lymphoid blasts and EV. We next conducted a prospective clinical study on ALL in paediatric patients aiming at evaluating EV during induction treatment. We observed that EV were mainly from platelet origin. Their number increased during induction treatment. They showed a procoagulant activity. EV number and procoagulant activity were associated with leucocyte and platelet number. These results suggest a platelet activation during the induction treatment of ALL, leading to platelet EV generation. We next studied the level of P-selectin in the same group of patients. We observed that P-selectin level increased during the induction course and that its level was associated with EV, leucocyte and platelet number. P-selectin may be a potential biomarker in thrombosis in paediatric ALL
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Chieh, Li-Yi y 李怡潔. "Effect of Berberine on Interleukin-2 Secretion from Jurkat Cells". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/48024239693480043394.
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碩士長庚大學
基礎醫學研究所
93
Berberine is an isoquinoline alkaloid isolated from herb plants, such as Cortex phellodendri (Huangbai) and Rhizoma coptidis (Huanglian). Huanglian and Huangbai have used as “heat-removing” agents. In addition, berberine has been reported to anti-inflammatory effect both in vivo and in vitro. Inflammatory is tightly related to immunity. However, the effect of berberine on the immune systems is still unknown. We proposed that berberine could exert immunoregulatory effects on immune cells by cytokine release. In this study, we investigate the effect of berberine on interleukin-2 (IL-2) secretion from Jurkat cell lines, a kind of human lymphocytes. In 12-well plate, Jurkat cells (1×106 /mL) were cultured in RPMI-1640 with 10% fetal calf serum (FCS), glutamate, 100 U penicillin at 37℃, 5% CO2 incubator. Different concentrations of berberine (5,8,10,15,20 μg/mL) with or without PHA (5 μg/ml) were added. Twenty-four hours later, media were collected, centrifuged, and stored in –20℃ for IL-2 enzyme immunoassay (EIA). The expression of IL-2 mRNA was detected by RT-PCR. Also, the effect of berberine on the MAPK signal pathway in Jurkat cells was detected by Western blot. Our results indicated that: (1) decreased secretion of IL-2 from Jurkat cells treated with PHA and berberine was observed after 24 h incubation. This inhibition is not due to necrosis or apoptosis of Jurkat cells as demonstrated by LDH test; (2) berberine (25 μg/ml) attenuated the IL-2 mRNA level in Jurkat cells; (3) PHA induced ERK, one of the MAPK, phosphorylation was observed from 10 minutes to 24 hrs, but not JNK or p38 phosphorylation; (4) PHA-induced ERK phosphorylation was inhibited by berberine (1, 10, 25 μg/ml) from 6 to 24 hrs. In contrast, berberine enhanced p38 phosphorylation and had no effect on JNK phosphorylation. In summary, these results suggest that berberine inhibited IL-2 secretion in Jurkat cells may mediated through the blunted IL-2 mRNA level and ERK phosphorylation
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Hwang, Guey-Shyang y 黃桂祥. "Effects of Arecoline on Interleukin-2 Secretion in Jurkat Cells". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/22545646432519355345.
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博士國立陽明大學
生理學研究所
102
Abstract Chewing betel quid is a recreation for many individuals in Taiwan. Arecoline (ARC; 1,2,5,6-tetrahydrol-1-methyl-3-pyridinecarboxylic acid methyl ester) is an alkaloid extracted from betel nut (Areca catechu L.). BQ chewing is one of the major risk factor of epatocarcinoma, oropharyngeal, and esophagus cancers in Taiwan, India, and Southeast Asian countries. Recently, keratinocyte inflammation has been shown to be crucial for tissue fibrosis and chemical carcinogenesis . Various inflammatory mediators such as prostaglandins (PGs), interleukin-1, interleukin-6 (IL-6) and tumor necrosis factorα (TNF-α) are associated to these pathogenic processes . Four major alkaloids are found in betel nut: arecoline, arecaidine, guvacoline and guvacine. Arecoline is the most important alkaloid in areca nut. Epidemiological studies showed a strong correlation between oral cancer and betel nut-chewing habit. Arecoline and/or its alkaloids have been shown to be characterized by carcinogenicity, immunotoxicity, genotoxicity, and teratogenicity in animal model system. In addition, arecoline has been shown to be mutagenic in mammalian cells, especially in oral mucosal fibroblasts. The increased frequency of micronucleated cells, chromosomal aberrations, and sister chromatid exchanges in exfoliated cells of the buccal mucosa was observed in areca-nut consumers. In addition, arecoline has been shown to enhanced the frequency of chromosomal aberrations and frequency of micronuclei in mouse bone marrow cells in vivo. However, the interaction between arecoline/ arecaidine and immune/endocrine system are still unclear. Therefore, this study was to investigate the effect of arecoline on the secretion of interleukin-2 (IL-2) by Jurkat cells. Jurkat cells were cultured in RPMI-1640 with 10% FBS. Different concentrations of arecoline were added to the culture medium with or without phytohemagglutinin (PHA). The IL-2 and prostaglandin E2 (PGE2) concentrations in collected media were then determined by enzyme-linked immunosorbent assay (ELISA). In addition, expression at the protein level of phosphorylated extracellular signal-regulated kinase (ERK), α7-nicotinic acetylcholine receptors (α7-nAChRs) and cyclooxygenase-2(COX-2) in the Jurkat cells were determined by Western blotting, while the level of IL-2 mRNA was determined by reverse-transcription polymerase chain reaction (RT-PCR). Arecoline, in a dose-dependent manner, significantly decreased IL-2 secretion by Jurkat cells incubated with 0 or 5 g/ml PHA. PGE2 significantly inhibited IL-2 secretion by Jurkat cells in a dose-dependent manner. PHA-induced ERK phosphorylation was attenuated in Jurkat cells treated with arecoline. PHA-enhanced IL-2 mRNA expression was also inhibited by arecoline. Taken together, these results imply that arecoline inhibits the protein expression of α7-nAChRs , the release of PGE2 and PHA-induced IL-2 secretion by Jurkat cells.
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Hoffmann, Ruth [Verfasser]. "Investigation of helenalin-induced cell death in Bcl-2 overexpressing Jurkat cells / Ruth Hoffmann". 2010. http://d-nb.info/1008340561/34.
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Audain, Keiron A. "The effects of Sutherlandia frutescens and Fumonisin B1 on Jurkat cells". Thesis, 2011. http://hdl.handle.net/10413/5625.
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The medicinal plant Sutherlandia frutescens (SF) is commonly consumed in South Africa,
and is traditionally applied to a range of ailments. Yet its popularity stems from the use of SF
as a cancer treatment. This plant contains a range of active compounds including L-canavanine
(L-CAV), D-pinitol and gamma (γ)-aminobutyric acid, all of which contribute to
the therapeutic properties of SF. It is also endorsed by the South African Ministry of Health
as a supplementary treatment for HIV/AIDS.
Maize is the staple crop of South Africa, and can be frequently contaminated by the
mycotoxin fumonisin B1 (FB1). The mycotoxin is linked to an extensive list of livestock
diseases. Although little is known about its role in human disease, FB1 has been
epidemiologically linked to oesophageal cancer in South Africa.
Both SF and FB1 have been shown to promote apoptosis, and the effect(s) of consuming both
in combination is currently unknown.
The principle aim of this study was to determine whether SF and FB1 had either synergistic or
antagonising effects in combination, by investigating immune cell toxicity Jurkat cells.
Apoptotic parameters such as caspase activation, mitochondrial depolarisation,
phosphatidylserine (PS) externalisation and ATP quantification were analysed. Levels of
caspase activation were highest in cells treated with SF only (caspase-3: 86.79 RLU, no
significance compared to other treatments; caspase-8: 40.1 RLU, significance compared to
other treatments [p<0.05]; caspase-9: 11.07 RLU, significance compared to FB1 and control
treatments [p<0.05]). ATP levels were significantly highest in SF-treated cells compared to
other treatments (8.17 RLU, [p<0.05]). Mitochondrial depolarisation was also highest in SF-treated
Jurkat cells at 18.5% depolarisation with no significance compared to other
treatments, however PS externalisation were significantly lower in SF-treated cells compared
with other treatments (3.69% [p<0.05]).
Oxidative stress parameters were also investigated, including thiobutyric acid reactive species
(TBARS), Glutathione (GSH) and Reactive Nitrogen Species (RNS) assays. TBARS levels
were significantly higher in FB1 treated cells (OD 1.95, [p<0.05]) compared to SF and
control. Glutathione and RNS levels were also lowest in FB1-treated cells.
The data suggests that SF induces apoptosis, characteristic of its nature as an anti-cancer
treatment, and FB1 induces oxidative stress, which is characteristic of its carcinogenic
properties. Based on this preliminary study, it appears that FB1 and SF both synergises and
antagonises the other in combination, yet further investigation is needed into its effects in
vivo.Thesis (M.Med.Sc.)-University of KwaZulu-Natal, 2011.
33
"Cyclic nucleotide regulated calcium signaling in vascular and jurkat T cells". Thesis, 2011. http://library.cuhk.edu.hk/record=b6075141.
Texto completoResumen
cAMP-elevating agents such as adenosine and epinephrine (after binding to beta-adrenergic receptor) contribute to local vascular dilation and some of these dilations are endothelium-dependent. Previous intracellular Ca 2+ imaging studies in mouse microvessel endothelial cells reported that addition of adenosine or epinephrine induced a Ca2+ influx which is blocked by CNG channel blockers such as L-cis-diltiazem or LY83583. Inside-out patch clamp studies confirmed the existence of a cAMP-activated current in endothelial cells, strongly suggesting a functional role of CNG, in particular CNGA2, channels in endothelial cells. The current study went further to show that similar Ca2+ influx in response to adenosine or epinephrine occurred in endothelial cells in freshly isolated mouse aortic strips and was again blocked by L-cis-diltiazem. By measuring the isometric force developed in mouse aortic strips, we showed that CNGA2 channel-mediated Ca2+ influx in endothelial cells contributed to the endothelium-dependent vascular dilatation in response to adenosine and epinephrine.In conclusion, cyclic nucleotides playa vital role in the regulation of intracellular Ca2+ concentration in vascular cells and Jurket T cells.
In Jurkat T cells, cyclic nucleotides regulated Ca2+ mobilization in a different way. Fluorescence-imaging studies showed that cGMP inhibited store-operated Ca2+ influx and histamine-induced Ca 2+ rise in Jurkat T cells through activation of PKG.
Thromboxane A2 (TxA2)-induced smooth muscle contraction has been implicated in cardiovascular, renal and respiratory diseases. This contraction can partly be attributed to TxA2-induced Ca2+ influx, which activates the Ca2+-calmodulin-MLCK pathway. This study aims to identify the channels that mediate TxA2-induced Ca2+ influx in vascular smooth muscle cells. Application of U-46619, a thromboxane A2 mimic, resulted in a constriction in endothelium-denuded small mesenteric artery segments. The constriction relied on the presence of extracellular Ca2+, because removal of extracellular Ca2+ abolished the constriction. This constriction was partially inhibited by a L-type Ca2+ channel inhibitor nifedipine (0.5-1 muM). The remaining component was inhibited by L-cis-diltiazem, a selective inhibitor for CNG channels, in a dose-dependent manner, Another CNG channel blocker LY83583 [6-(phenylamino)-5,8-quinolinedione] had similar effect. In primary cultured smooth muscle cells derived from rat aorta, application of U46619 (100 nM) induced a rise in cytosolic Ca2+, which was inhibited by L-cis-diltiazem. Immunoblot experiments confirmed the presence Of CNGA2 protein in vascular smooth muscle cells, These data suggest a functional role of CNG channels in U-46619-induced Ca 2+ influx and contraction of smooth muscle cells.
Leung, Yuk Ki.
"August 2010."
Adviser: Yao Xiaoxiang.
Source: Dissertation Abstracts International, Volume: 73-04, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 116-132).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
34
Mackenzie, Jared Stuart. "The effects of Tulbaghia violacea leaf, bulb and stalk extracts on Jurkat cells". Thesis, 2012. http://hdl.handle.net/10413/9627.
Texto completoResumen
Studies have shown that the traditional healers have used Tulbaghia violacea (TV) (also
known as ‘wild garlic’) for the treatment of a number of ailments including fever,
tuberculosis, stomach problems, and oesophageal cancer. However, little is known with
regards to the anticancer and antiproliferative properties of this plant. Therefore, this
study investigated the effects of TV and domesticated garlic extracts on Jurkat cells, in
order to determine whether or not these extracts possess anti-proliferative properties.
Cultured Jurkat cells were treated with IC50 concentrations of garlic (14μg/ml), TV leaf
(256μg/ml), TV bulb (225μg/ml) and TV stalk (216μg/ml) extracts as determined by the
methylthiazol tetrazolium assay. Free radical production was measured using the
thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) assays, while
glutathione (GSH) concentration was measured using the GSH-Glo™ assay. The
apoptosis inducing properties of each extract were measured using flow cytometry
(Annexin V- Fluos and JC-1 assays) and luminometry (caspases 3/7, 8, 9 and ATP).
Western blots were run to determine protein expression, while comet and DNA
fragmentation assays were used to determine the level of DNA damage induced. Wild
and domesticated garlic extracts induced a significant increase in malondialdehyde
concentration ([MDA]), with TV bulb extract inducing the highest concentration
(p<0.0001). A significant increase in NO concentration was observed in the bulb
(p<0.0001) and stalk (p<0.001) extracts, and leaf (p<0.05) and stalk (p<0.05) TV
extracts significantly increasing GSH concentration. The longest comet tails were
observed in TV bulb extracts (p<0.0001) and comprised mainly of single strand breaks,
while the comets induced following garlic exposure contained double strand breaks. All
extracts, except TV leaf, increased the percentage of cells undergoing apoptosis.
Tulbaghia violacea leaf induced a significant (p<0.0001) increase in percentage of cells
undergoing necrosis, whereas TV bulb resulted in a significant (p<0.0001) decrease.
All TV extracts induced caspase 3/7 and 9 activity, with the most significant increase in
caspase 9 activity observed for TV leaf and bulb. No significant change in caspase 3/7
activity was evident for domesticated garlic. Cleavage of PARP and expression of
NF B and HSP 70 occured for all extracts. However, HSP 70 was not differentially
expressed. Exposure to wild and domesticated garlic extracts induced peroxidative lipid
and DNA damage within the cells, indicating oxidative stress. This damage occurred in
conjunction with increased percentage of cells undergoing apoptosis and expression of
caspase 3/7. Therefore, these findings suggest that TV is inducing cell death through
apoptosis in Jurkat cells using a number of mechanisms, including the induction of
oxidative stress. This is of clinical significance, as cell death through apoptosis is the
preferred method of action for anti-cancer drugs.Thesis (M.Med.)-University of KwaZulu-Natal, Durban, 2012.
35
Chien-Yu y 林建佑. "The mechanisms of peptidylarginine deiminases-induced apoptosis in acute T leukemia Jurkat cells". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/03884985715255505815.
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碩士中山醫學大學
免疫學研究所
95
Peptidylarginine deiminase IV (PADI4) posttranslationally converts peptidylarginine to citrulline. It plays the essential role in immune cell differentiation and apoptosis. A haplotype of single-nucleotide polymorphisms (SNPs) in PADI4 is functionally relevant as a rheumatoid arthritis (RA) gene. It could increase enzyme activity leading to raised levels of citrullinated protein and stimulating autoantibody. Previous our study exposes that inducible PADI4 causes haematopoietic cell death (Liu, et al, 2006 Apoptosis). Herein, we further investigate whether RA risk PADI4 haplotype (SNP PADI4; S55G, A82V and A112G) and the increase of its enzymatic activity induce apoptosis. In the tetracycline (Tet)-On Jurkat T cells, ionomycin (Ion) only treatment didn’t induce apoptosis however it promoted inducible PADI4-decreased cell viability and –enhanced apoptosis. In vitro and in vivo PADI enzyme activity assay, we demonstrated PADI4 enzyme activity of SNP PADI4 was higher than RA non-risk PADI4 haplotype (WT PADI4). The effect of SNP PADI4-induced apoptosis was superior to WT PADI4. In addition, both Ion and SNP PADI4 synergistically provoked apoptosis compared with both Ion and WT PADI4. Concurrently, in the conditionally inducible SNP PADI4 cells of Ion treatment-induced apoptosis, not only the expression of Bcl-xL was down-regulated and Bax up-regulated, but also cytochrome c released from mitochondria to cytoplasm significantly. Western blotting data showed the increase of apoptosomal caspase activation during the programming cell death in the inducible SNP PADI4 cells subsequent to Ion treatment. These data demonstrated that both SNP PADI4 and increasing its enzyme activity could enhance apoptosis through mitochondrial pathway and further provide a conceivable explanation in the pathogenesis of RA following the upregulation of PADI4 activity in its SNPs. The early study revealed that PADI4 was shown to be associated with RA, but PADI2 appeared the feasible role. In addition, we examine whether inducible overexpression of PADI2 enhances apoptotic cell death. PADI2 reduced the viability in a does- and time-dependent manner of Jurkat-Tet-On system cells. The apoptosis-inducing activities were determined by nuclear condensation and DNA fragmentation.
36
Wen, Yu Feng y 溫玉鳳. "The Action of Glycyrrhizin on the Secretion of Interleukin-2 from Jurkat cells". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/50014607778276337772.
Texto completoResumen
碩士長庚大學
基礎醫學研究所
93
Glycyrrhizin, extracted from the licorice root, is a Chinese traditional herb medicine for 2500 years. Studies showed glycyrrhizin could regulate the specific and non-specific immunity in mice and human beings. In addition, glycyrrhizin inhibits bacterial infection, virus replication, attenuates skin allergy and inactivates B-hepatitis virus. Also, glycyrrhizin has shown to destroy the HIV virus by inhibiting the replication of this virus. Recent study indicated glycyrrhizin prevents the replication of SARS virus in vitro. However, the effect of glycyrrhizin on the immune systems is still unknown. In this study, we investigate the effect of glycyrrhizin on interleukin-2 (IL-2) secretion from Jurkat cell, a kind of human lymphocytes tumor cell lines from food industry research and development institute in Hsinchu were maintained in RPMI 1640 medium supplemented with 10 % FCS, 100 units/ml penicillin /streptomycin /antimycotics cultured at 37℃, 5% CO2 incubator. Different concentrations of glycyrrhizin (10-7 ~ 10-6 M) with PHA (2μg/ml) were added. Twenty-four hours later, culture suspended were collected, and stored in -20℃ for later IL-2 EIA. The expression of IL-2 mRNA was detected by RT-PCR. Meanwhile, different inhibitors with glycyrrhizin (10-6 M) and PHA (2μg/ml) were added into the media. The phosphorylation of MAPK, including JNK, ERK, and p38, were analyzed by western blot. Our results indicated that: (1) decreased secretion of IL-2 from Jurkat cells treated with PHA and glycyrrhizin (10-7 ~10-6 M) was observed after 24 hours incubation; (2) glycyrrhizin attenuated the IL-2 mRNA level in Jurkat cells treated with PHA at 5 hours. Also, decreased phosphorylation of ERK was observed at 24 hours in Jurkat cells treated with glycyrrhizin and PHA. Taken together, these results suggest that the decreased IL-2 secretion in Jurkat cells treated with glycyrrhizin may mediate through the blunted IL-2 mRNA level anddecreased ERK phosphorylation.
37
Yang, Ren-ming y 楊仁銘. "The induction and suppression of 1,4-dichlorobenzene on apoptosis in Human T-Lymphoma Cell Line (Jurkat Cells)". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/t7kmh4.
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碩士東吳大學
微生物學系
93
1,4-Dichlorobenzene (DCB), widely used as a moth repellent and a space deodorant, is one kind of chlorobenzene that is classified by the International Agency for Research on Cancer among chemicals possibly carcinogenic to humans on the basis of a sufficient evidence for carcinogenicity to rodents. DCB has been found to cause renal tubular-cell adenocarcinomas in rats and hepatocellular carcinomas in mice. Since it lacks roles in DNA fragmentation, clastogenic effects and genotoxicity, DCB has been anticipated as a nongenotoxic carcinogen, especially as a hepatocarcinogen. The liver homeostasis, so as other organs, is controlled by the balance between cell proliferation and cell death by apoptosis. Some hepatocarcinogen suppress apoptosis under stress to induce cancer. DCB has been found to suppress the hepatocyte apoptosis induced by transforming growth factor β1. Apoptosis can be initiated by the release of cytochrome c from mitochondria that required the uptake of calcium from endoplasmic reticulum. In our preliminary experiments, DCB has been found to disturb the cellular calcium homeostasis. In this study, we investigated the correlation between the characters of DCB on calcium homeostasis and apoptosis by using human T-lymphoma cell Line (Jurkat Cells).We found that DCB can release calcium from endoplasmic reticulum in human T-lymphoma cell line.DCB can’t induce apoptosis and suppress staurosporine- induced apoptosis.DCB reduce mitochondrial membrane potential loss induced by staurosporine,inhibit casapse 3 activation and block DNA fragmentation.
38
Rao, Tian-lin y 饒天霖. "Measurements of The Interactive Force Between Jurkat Cells Using a Single-Beam Optical Tweezer". Thesis, 2011. http://ndltd.ncl.edu.tw/handle/ncwjuj.
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碩士國立虎尾科技大學
機械與機電工程研究所
99
This paper presents a single beam optical tweezers used to measure the interactive force between Jurkat cells (the diseased white blood cells with a diameter of 14.0 μm). Optical trapping of beads and Jurkat cells using a single-beam optical tweezer have been achieved. The experimental results show that a laser power of 2.4 mW is sufficient to trap 3-μm-diameter polystyrene beads, while a laser power of 1.5 mW is sufficient to trap individual Jurkat cells. Since the laser (λ=532 nm) can cause large damage when used in biological manipulation. Therefore, the Jurkat cells were trapped using a laser (λ=671 nm) with a low laser power condition. Separating two mutually attached Jurkat cells requires a laser power of 4 mW. Experimental results show that as the adhesion time of the two Jurkat cells is increased, the separation power also increases. Compared with two mutually attached Jurkat cells, three mutually attached Jurkat cells require a large separation power. The Jurkat cells adhered to the PDMS structure has also been investigated. Experimental indicate that as the adhesion time is increased between the Jurkat cells and the PDMS structure, the separation power also increases.
39
Wang, Hsiao-Chiu y 王筱秋. "The action of Gossypol on the secretion of Interleukin-2 from human lymphocytic Jurkat cells". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/60953453135455490719.
Texto completoResumen
碩士長庚大學
基礎醫學研究所
95
Gossypol is a polyphenolic compound extracted from the cotton plant (Gossypium species). It functions as a natural insecticide that renders the plant resistant to pathogens and insects. The pharmacological interest in gossypol primarily originated as a consequence of its antifertility action. Also, gossypol possesses the anticancer, antiviral, and antioxidant actions. T cell can regulate and coordinate the overall immune response by secreting lymphokines. The studies indicated that gossypol can induce the lymphocytes apoptosis through the activation of caspase3 and the expression of Bak, but the effect of gossypol on the cytokine secretion form lymphocytes is still unknown. Interleukin-2 (IL-2), also called T-cell growth factor, is the main cytokine that T cell uses to regulate the immune system in human body. In this study, we investigate the effect of gossypol on IL-2 secretion from Jurkat cells, a kind of human lymphocytic tumor cell line. Jurkat cells were maintained in RPMI- 1640 with 10% FBS. The media IL-2 were determined with ELISA. The IL-2 mRNA expression was determined by RT-PCR. The phosphorylated ERK1/2 and JNK1/2 will be determined by western blot. Our research indicated that: (1) inhibited IL-2 secretion from Jurkat cells pretreated with gossypol for 3 h and PHA for 12 h later; (2) attenuated IL-2 mRNA expression in dose-dependent manner were observed in Jurkat cells pretreated with gossypol 3hr and PHA 2hr later; (3) reduced ERK1/2 and JNK1/2 phosphorylation were found in Jurkat cells pretreated with gossypol 3hr and PHA 25 to 30 min; (4) reduced cell number were observed in Jurkat cells after 24 to 72 hr treatment of gossypol. In conclusion, the inhibitory effect of gossypol on IL-2 secretion form human lymphocytic Jurkat cells is through the reduced IL-2 mRNA expression, the attenuated of ERK1/2 and JNK1/2 phosphorylation. In addition, gossypol inhibits the cell proliferation after 24 to 72 hr incubation.
40
Elhousiny, Moustafa. "The effect of substance P (SP) on adhesion of Jurkat leukemia cells and squamous carcinoma cells (SCC) to vascular endothelial cells and role in metastasis". Thesis, 2019. https://researchonline.jcu.edu.au/60366/1/JCU_60366_Elhousiny_2019_thesis.pdf.
Texto completoResumen
Metastasis is the leading cause of fatality in 90% of cancers, and approximately 60% of all cancer cases will have either regional or distant metastasis at initial diagnosis. Global data shows that survival rates drop significantly with the advance of disease stage and metastatic activity; therefore, patients with localised disease have a far better prognosis than those with disseminated tumours. In this aspect, Leukaemia and oral squamous-cell carcinoma (OSCC) are invasive neoplasms. Both cancers are considered the worst prognosis cancers with an overall survival rate of 50% or slightly higher.
The accumulating research suggests that inflammation is more likely to act in favour of tumour initiation and metastasis. The striking similarity which exists between the out flux of tumour mass in the circulation and that of inflammatory exudates in wound healing points to the possibility that the same mediators might be utilised for both purposes. Substance P (SP) is a primary regulator of neurogenic inflammation mainly acting as a trigger for vasodilatation, plasma protein extravasation and leukocyte adhesion to vascular endothelial cells. SP has been proposed as a model that can explain the inflammation-tumour relationship. Therefore, the link between the role of SP and the extravasation of tumour cells into the circulation represents an attractive opportunity for unravelling the metastatic mechanisms.
We carried a systematic review which identified nine inflammatory mediators associated with metastasis. The 16 articles reported lymph node metastasis and one article reported both lymph node and distant metastasis. The inflammatory mediators identified were CXCR4 (six studies), CXCL12 (SDF-1), CCR7, IL-6 (two studies each), IL-18, CCL20 (MIP-3), CXCL1 (GRO-1), CCL3, CXCR2 (one study each). This review systematically summarises the evidence of the prognostic role of inflammatory mediators in predicting metastasis/metastatic stages in OSCC. Additionally, it compares the available evidence from clinical and experimental animal settings.
Our experimental results showed that SP increased the adhesion of Jurkat Leukaemia cell lines in a time-course treatment with a peak adhesion increase at three-four hours. SP increased the adhesion of H157, CAL27, and DOK cells to HUVEC endothelial cells (P < 0.001), significantly, in a time-dependent treatment with peak adhesion at three hours. It has been demonstrated that SP is expressed by several tumours and several roles have been proposed for its action in tumour growth and progression. Our study describes a new role for SP in stimulating an early onset adhesion of tumour-endothelial adhesion.
We found that treating endothelial cells with either stimulating factor or inhibitor produces more potent levels of adhesion which may 1) explain the organ-specific metastasis of cancers; and 2) highlight the active interaction of tumour-endothelial cells during adhesion. Moreover, our data suggests that inhibition of adhesion levels – achieved using cycloheximide, which blocks translation of messenger RNA on the cytosolic 80S ribosomes but does not inhibit the organelle protein synthesis – did not achieve higher levels such as the one inflicted with monoclonal antibodies. This might suggest that tumour cells highly express adhesion molecules as well as inflammatory receptors.
Our data also suggests that in Jurkat cells, CAL27 and BICR22, SP 1mcg/ml treatment has increased both CD 11 (not significant) and CD 49 (P < 0.05), but not CD15s expression in 1-48 hour time-scale treatment, as indicated by the FACS analysis. Anti-human monoclonal antibodies to VCAM or ICAM significantly inhibited adhesion levels to below the untreated baseline levels. The NK-1R antagonist was only effective in inhibiting adhesion molecule expression in Jurkat and CAL27. No other effect was noted in the other OSCC cell lines.
We hypothesised that adhesion molecules were the main requirement of the adhesion process, and adhesion molecule expression followed the pattern predicted which increased from no expression in the normal oral keratinocytes to the lymph node positive cell line H157 and declined in the metastatic cells BICR22, for the three adhesion molecules. The pre-cancer cell line DOK had an elevated expression profile which agrees with previous studies, suggesting an early invasive/metastatic phenotype in the tumour cycle.
Our results did not prove any significant effect for SP on the release of MMP-2 in either Jurkat cells or OSCC cell lines. This was against the predicted pattern in which we hypothesised that SP would trigger up-regulation of MMP enzymes to facilitate the
transmigration of tumour cells through the endothelium.
The resulting model represents a novel approach in cancer treatment where the main target is prevention of metastasis. This paradigm shift has a powerful potential to develop effective anti-metastatic therapies through interfering with the metastatic cycle. The data resulting from the systematic review as well as the experimental findings can be integrated for future implementation in two main categories.
In conclusion, the study identifies a new role for Substance P in mediating an early onset adhesion of cancer cells to endothelial cells. The study also highlights the role of the NK-1R antagonist as a novel therapy in inhibiting this adhesion in those cell lines. A combined therapy of the NK-1R antagonist and monoclonal anti-adhesion molecule would be powerful in preventing the onset of metastasis. These primary data warrant further research through animal models to confirm this role for Substance P.
41
Hasan, Raisa. "Characterising heterogeneity in the T-cell acute lymphoblastic leukaemia jurkat cell line in the context of the TAL1 locus". Thesis, 2019. http://hdl.handle.net/1959.7/uws:55445.
Texto completoResumen
T-cell acute lymphoblastic leukaemia (T-ALL) is the hyperproliferative transformation of T-cell lymphoid progenitor cells within the blood and bone marrow and is extremely heterogeneous. T-ALL has been linked to the overexpression of transcription factors, such as TAL1, that is specific within the late-cortical subtype of T-ALL. This project has utilised clonal cell line populations for testing phenotypic intra-tumoural heterogeneity seen within cancer cell lines, such as the Jurkat cell line, to generate clonal populations relative to the parental cell line they are derived from at passages 1, 5 and 9 as a cost-effective model. We tested the phenotype of proliferation using a carboxyfluorescein succinimidyl ester (CFSE) assay which identified Jurkat clonal populations as highly proliferative and displayed lower expression of the TAL1 gene, relative to the parental cell line using real-time PCR analysis. We also identified four differentially bound putative regulatory element sites using bioinformatics analysis of publicly available data. This analysis displayed a Jurkat-specific predicted intragenic regulatory element and intergenic enhancer regions that map to the known upstream TAL1 Jurkat super-enhancer as stated by Mansour et al. (2014). DNA methylation is known to fine-tune intragenic and intergenic enhancer-mediated transcription. Thus, we used a methylation-sensitive restriction endonuclease (MSRE) assay that provided insight of dynamic and stable DNA methylation patterns at the intragenic and intergenic sites across the TAL1 locus between Jurkat clonal populations, respectively, at passages 1 and 9. Finally, using MinION nanopore sequencing, we identified single-nucleotide variants common between Jurkat clonal populations tested at passages 1 and 9, which map to regulatory elements, SNPs in linkage disequilibrium across the TAL1 locus and sites of predicted transcription factor binding, therefore suggesting regulatory functionality of these SNVs in the context of the TAL1-mediated T-ALL.
42
Chao, Ho-Hsin y 趙賀欣. "Effects of catechin and epigallocatechin gallate (EGCG)on the secretion of interleukin-2 by Jurkat cells". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/21341763962807735451.
Texto completoResumen
碩士長庚大學
基礎醫學研究所
93
Green tea has been a popular beverage in China and Japan for centuries. It is thought that green tea has a lot of health-promoting benefits. (+)-Catechin and (-)-epigallocatechin gallate (EGCG) are the major and the most abundant components found in green tea leaves (Camellia sinensis). Previous studies showed that catechin and EGCG have anti-carcinogenic, anti-inflammatory, anti-atherogenic, thermogenic and anti-microbial activities. Moreover, the inflammatory cytokines (i.e. TNF-αand IFN-γ), and RA-specific IgG were decreased in the animal treated with green tea polyphenols (GrTP). However, the effect of catechin and EGCG on the immune systems is still unknown. In this study, we investigate the effect of catechin and EGCG on interleukin-2 (IL-2) secretion from human T-lymphoblastoid Jurkat cell lines. Different concentrations of catechin and EGCG (10-7 ～ 10-4 M) with or without PHA (5μg/ml) were added. Twenty-four hours later, media were collected, centrifuged, and stored in –20℃ for IL-2 EIA. The expression of IL-2 mRNA was detected by RT-PCR. Also, the effect of catechin and EGCG on the MAPK signal pathway in Jurkat cells was detected by Western blot. Our results indicated that: (1) decreased secretion of IL-2 from Jurkat cells treated with PHA and catechin and EGCG was observed after 24 h incubation; (2) catechin and EGCG were found no toxic effects on Jurkat cells in range 0.25～25 and 2.5～50 μM, respectively, as assessed by LDH assay; (3) both catechin and EGCG significantly attenuated the IL-2 mRNA level at 6h; (4) PHA-induced ERK, one of the MAPK, phosphorylation was inhibited by catechin. Taken together, these results suggest that catechin and EGCG inhibited IL-2 secretion in Jurkat cells may be mediated through the blunted IL-2 mRNA level and ERK phosphorylation.
43
heng-kai, lin y 林亨鍇. "The Transcription Element of IL-10 promoter Mediating the Expression of IL-10 in Jurkat Cells". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/45187145272520330379.
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碩士國立成功大學
微生物暨免疫學研究所
91
IL-10 plays a crucial role in immune regulation. Our previous study showed that IL-10 level was increased in Jurkat cells by coculture with U-118MG or forskolin-treatment. In this study, we intended to investigate the regulation of IL-10 gene in Jurkat cells in detail. Two fragments of IL-10 promoter were amplified with polymerase chain reaction (PCR) and used as probes in electrophoresis mobility shift assay (EMSA) to analyze the involved transcription factors for the transcription of IL-10 gene. EMSA data showed that nuclear extracts of Jurkat and BJAB cells had different binding capabilities on IL-10 promoter region. A particular band, designated as E, being a complex of nuclear extracts and IL-10 promoter region from —1120 to —986, disappeared after treated with forskolin or coculture with U-118MG. It implied a negative regulatory role of this complex on IL-10 gene. PKA inhibitor (KT5720) can inhibit the CREB phosphorylation and IL-10 production. In addition, treatment with forskolin enhanced CREB phosphorylation (Western immunoblot) and CRE binding activity (EMSA) in Jurkat cell. However, coculture with U-118MG did not significantly induce the phosphorylation of CREB and CRE binding activity in Jurkat cells. Therefore, PKA may not be the major pathway for IL-10 expression in Jurkat cells upon coculture with U-118MG. Moreover, we found that casepase 8 might not involve in U-118MG induced IL-10 production. In summary, our results indicated that direct activation of PKA pathway can stimulate the transcription of IL-10 gene. However, PKA pathway does not mediate U-118MG induced IL-10 production.
44
Yu, Ju Wen y 余主文. "Effects of Berberine, Glycyrrhizin and Gossypol on the Expression of MAPK, Sirt1, Sirt2, and Cyclooxygenase-2 in Jurkat Cells". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/58114562131294093011.
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碩士長庚大學
生物醫學研究所
102
Glycyrrhizin and berberine have been used as Chinese traditional herb medicine for 2500 years. Studies indicated that glycyrrhizin, berberine and gossypol possess as anticancer, analgesic, anti-inflammatory, febrifuge, hypolipidemic, anti-cancer, and vasodilation effect. In addition, these materials inhibit bacterial infection, destroy the Leishmania donovani by interaction in vitro with nuclear DNA from this bacterial, regulate immune system, and glucose metabolism. Cyclooxygenase (COX) 1, 2 and prostaglandin (PG)-E2 have been demonstrated to be existed in leukocytes, and they were the downstream products of the NF-κB signaling pathway. Previous studies from our laboratory showed these herbs inhibit the IL-2 secretion from Jurkat cells in part through the attenuated MAPK phosphorylation. However, it is still unknown the mechanism of these herbs on decreased MAPK and COX2 expression from Jurkat cells. Studies indicate that sirtuins have more relavant with cell cycle, stable of the genomic, energy metabolism, anti-inflammatory and anti-aging. Regucalcin can be pro-inflammatory factor and regulates the energy metabolism. Our hypothesis is that glycyrrhizin, berberine and gossypol may affect the IL-2 secretion from Jurkat cells through the expression of COX2, MAPK, sirtuins, regucalcin, and the cell cycle regulation. Our results showed that: (1) increased expression of phosphorylated ERK1/2 (p-ERK1/2), p-p38, SIRT1, and regucalcin proteins in Jurkat cells treated with glycyrrhizin and PHA were found; (2) berberine inhibited the expression of p-JNK, COX2, SIRT2, and regucalcin proteins in Jurkat cells treated with PHA; (3) gossypol increased SIRT2 expression, not significant, in Jurkat cells treated with PHA; (4) glycyrrhizin (0.1 and 0.5 M) promotes G0/G1 arrest; 20 g/ml berberine results in G2/M arrest; G0/G1 arrest was found in Jurkat cells treated with gossypol (10-6 M) and PHA (1 g). Taken together, these results indicated that: (1) the inhibition of PHA-induced IL-2 secretion from Jurkat cells by glycyrrhizin is in part via an inhibited expression of MAPK through the increased SIRT1; (2) berberine inhibited the PHA-induced IL-2 secretion through the attenuated expression of p-JNK, SIRT1, and regucalcin; (3) decreased secretion of PHA-induced IL-2 from Jurkat cells treated with gossypol is through the increased SIRT2.
45
Kajstura, Małgorzata. "Effects of geldanamycin, a ligand of heat shock protein 90, on cell cycle progression and induction of apoptosis in human lymphocytes and jurkat cells". Praca doktorska, 2019. https://ruj.uj.edu.pl/xmlui/handle/item/69784.
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Heat shock protein 90 (HSP90), which is implicated in post-translational folding, stability, and maturation of proteins, controls several key cell cycle regulators. Thus, the hypothesis was raised that geldanamycin, a specific and potent inhibitor of HSP90 function, may have pronounced effects on cell cycle progression. The objective of this study was to test this hypothesis in normal and cancer cells of human origin. The experiments performed on human lymphocytes mitogenically stimulated by phytohemagglutinin (PHA) indicated that 100 nM or 150 nM geldanamycin induces transition of cells to the G0 state of cell cycle. This was documented utilizing acridine orange, a metachromatic dye which differentially stains DNA versus RNA. The same experimental protocol allowed demonstration that geldanamycin is a potent inducer of apoptosis in PHA-activated cells. Importantly, both the block in G0 and induction of apoptosis were reversible and returned to control values upon removal of geldanamycin. Similar conclusions were reached when cell number in cultures was analyzed, excluding the possibility that a relevant fraction of cells was disintegrated during the incubation period. Experiments on Jurkat line of acute T-cell leukemia were performed next. Jurkat cells were used here as a model system in which the cytostatic and cytotoxic properties of geldanamycin on cancer cells can be tested. Initial experiments determined the time course and concentration-dependence of geldanamycin-induced alterations in cell cycle distribution and apoptosis. In contrast to human lymphocytes, geldanamycin did not induce G0 arrest in Jurkat cells, but inhibited them initially in the G2 phase, and at later time points in the G1 phase. The G2 was distinguished from mitosis by the absence of phosphorylation of histone H3, a specific marker of mitotic cells. The inhibition of Jurkat cells in G1 was linked to a decrease in phosphorylation of retinoblastoma protein. Finally, the exposure of Jurkat cells to geldanamycin resulted in induction of apoptosis, predominantly in cells being arrested in G1 and G2/M phases of the cell cycle. Finally, to address the possibility that stimulation of nuclear factor kappa-B (NF-kB), downstream of HSP90, modulates the effects of geldanamycin on cancer cells, Jurkat IkBaM line was employed. These cells cannot activate their NF-kB-mediated responses because of the mutation in its inhibitory protein, IkB. In the absence of functional NF-kB, geldanamycin-mediated induction of apoptosis and loss of cycling cells were markedly higher than when NF-kB was functional. These results were further corroborated by experiments in which parthenolide, a plant-derived inhibitor of NF-kB was employed. Geldanamycin-treated Jurkat cells responded to the parthenolide challenge by partial arrest in S phase and increased cell death by apoptosis. In conclusion, inhibition of HSP90 by geldanamycin blocks cell cycle progression and induces apoptosis of Jurkat cells, and NF-kB mediates these effects. The newly identified network of interactions may facilitate understanding of the mechanism of cytostatic and cytotoxic action of geldanamycin derivatives used currently in clinical trials.
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Kirschke, Stephanie Olivia [Verfasser]. "Investigation of the apoptosis signal transduction mediated by the marine pyridoacridine alkaloid Ascididemin in human leukemic Jurkat T cells / Stephanie Olivia Kirschke". 2002. http://d-nb.info/967056535/34.
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Lucas, Bethany R. "Ectopic expression of TAL-1 increases resistance to TNF[alpha]-induced apoptosis in Jurkat cells via changes in the NF-kB signaling pathway". 2011. http://liblink.bsu.edu/uhtbin/catkey/1642170.
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TAL-1, ectopically expressed in 60% of T-cell acute lymphoblastic leukemia (T-ALL) patients, may contribute to poor chemotherapy response. This research sought to determine if TAL-1 influences expression of proteins involved in the NF-kB signaling pathway and thus, resistance to cell death. NF-kB, IKKy, and TRAF-2 expression levels were found to be TAL-1 dependent. Cell death levels were higher in staurosporine-treated cells compared to tumor necrosis factor a-treated or dual-treated cells. TAL-1, NF-kB, IKKy, and TRAF-2 expression levels were elevated in tumor necrosis factor a-treated cells and reduced in staurosporine-treated or dual treated cells compared to untreated cells. These results suggest TAL-1 influences expression of proteins involved in the NF-kB signaling pathway, thus inducing an anti-apoptotic response in the cell.Department of Biology
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Alves, MN. "Nanoparticle and cell modifications using capillary electrophoresis". Thesis, 2020. https://eprints.utas.edu.au/35173/1/Neves_Mo%C3%A7o_Alves_whole_thesis_ex_pub_mat.pdf.
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Particle separation and manipulation is a strength of electrophoresis. In this dissertation, firstly, the power of electrophoresis as a microanalytical technique is demonstrated by separations of bare magnetic nanoparticles provided for the first time electropherograms exhibiting symmetrical and highly reproducible peaks, free of spurious spikes characteristic of nanoparticle clusters. This was achieved using non-complexing (nitrate) and complexing (chloride, citrate and phosphate) electrolyte ions with additions of tetramethylammonium hydroxide. This enabled the separation of bare and functionalised magnetic nanoparticles. Secondly, CE was coupled to a magnetic field and trapping of magnetic nanoparticles was demonstrated using purposely selected electrolyte compositions.
Just like nanoparticles, cells exhibit an electric surface charge due to exposed charged or chargeable functional groups. Therefore, they migrate under the influence of an electric field. Through isotachophoretic focusing, the electrostatic adsorption of functionalised magnetic nanoparticles to the cell wall of Escherichia coli TOP10 and their cellular uptake was studied. The same strategy was applied for the ITP transformation of E. coli TOP10 with plasmid DNA. Counter pressure-assisted isotachophoresis brought a large excess of plasmid DNA in contact with the cell surface allowing for a transformation rate 1,000-fold higher compared to electroporation and chemical transfection at survival rates greater than 60%. Based on the findings, the ITP method was adjusted for effective transfection of mammalian cells (Jurkat T) showing similar robustness to electroporation. This opens possibilities of using the developed method for the delivery of many other membrane impermeable solutes for screening of genes and drugs.
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Li, Hui-Ru y 李蕙如. "A high-throughput system for screening of human interleukin-2 inducers and/or repressors based on the expression of a reporter gene in Jurkat T cells". Thesis, 2000. http://ndltd.ncl.edu.tw/handle/87601919924944552693.
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碩士國立陽明大學
藥理學研究所
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Abstract Human interleukin-2 (IL-2) is a pleiotropic cytokine that regulates many essential immune functions, including the growth and differentiation of lymphocytes. Recent reports indicate that IL-2 is effective in metastatic melanoma and renal cell carcinoma therapies, and also capable of diminishing the pool of latently infected CD4+ T cells in HIV-infected patients receiving antiviral therapy. However, clinical applications of IL-2 were restricted by the severe side effects resulting from direct administration of this cytokine. In this regard, selective small molecule IL-2 inducers may be good replacements because administration of these agents might result in an effective but not a toxic level of this cytokine in the circulation. For this purpose, we constructed a high-throughput model cell system and examined its responsiveness to a variety of immuno- stimulators and immunosuppressants. Our system was based on the production of secreted alkaline phosphatase (SEAP) from Jurkat cells stably transfected with its corresponding gene whose expression was under control of a human IL-2 promoter. A clone whose SEAP production was increased dramatically after PMA plus calcimycin (A23187) treatment was identified and named JKHR-1. The increase in enzyme activity in these cells was preceded by an increase in its mRNA, indicating activation of the reporter gene occurring mainly at the level of transcription. Induction of SEAP synthesis was also observed when this clone was treated with T-cell mitogens PHA, Con A, jacalin, PMA/PHA, and anti-CD3/anti-CD28 antibodies. In contrast, SEAP production from JKHR-1 cells activated by PMA plus PHA was completely abolished by pretreatment with cyclosporin A, FK-506, U0126, or SB203580, but not dexamethasone or mycophenolic acid. Taken together, this stable T-cell line appeared to be useful in high-throughput screening for both inducers and repressors of human IL-2 production.
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Charette, Nicholle Jeanine. "INVOLVEMENT OF DIFFERENT RAB GTPASES IN THE TRAFFICKING OF CXCR4 AND CCR5 HOMO- AND HETERODIMERS BETWEEN THE ENDOPLASMIC RETICULUM AND PLASMA MEMBRANE IN HEK293 AND JURKAT CELLS". 2011. http://hdl.handle.net/10222/14023.
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Little is known about the outward trafficking of receptor dimers from the endoplasmic reticulum to the plasma membrane, or the role that trafficking plays in assembly, targeting and specificity of receptor signalling. Bimolecular fluorescence complementation was used to follow prescribed receptor homo/heterodimers in Jurkat cells and clarify the trafficking itineraries those receptors follow to reach the plasma membrane. Chemokine receptors CXCR4 and CCR5 were chosen due to their implication in numerous pathologies including, HIV and cancer, and their ability to form homo and hetero-oligomers. This study demonstrates that although the individual receptors composing heterodimeric complexes are the same as in homodimeric complexes, the heterodimer traffics and signals independently of its constituent homodimers. The presence of CD4 affects the trafficking of CCR5 containing dimers but not the CXCR4 homodimer. These observations demonstrate the importance of considering receptor heterodimers as distinct signalling entities that should be more carefully and individually characterized.