Relevant bibliographies by topics / CysLT2

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  2. Dissertations / Theses
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  4. Book chapters
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Academic literature on the topic 'CysLT2'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "CysLT2"

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Bandeira-Melo, Christianne, Lesley J. Woods, Mojabeng Phoofolo, and Peter F. Weller. "Intracrine Cysteinyl Leukotriene Receptor–mediated Signaling of Eosinophil Vesicular Transport–mediated Interleukin-4 Secretion." Journal of Experimental Medicine 196, no. 6 (September 16, 2002): 841–50. http://dx.doi.org/10.1084/jem.20020516.

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We investigated whether cysteinyl leukotrienes (cysLT) are intracrine signal transducers that regulate human eosinophil degranulation mechanisms. Interleukin (IL)-16, eotaxin, and RANTES stimulate vesicular transport–mediated release of preformed, granule-derived IL-4 and RANTES from eosinophils and the synthesis at intracellular lipid bodies of LTC4, the dominant 5-lipoxygenase–derived eicosanoid in eosinophils. 5-Lipoxygenase inhibitors blocked IL-16–, eotaxin-, and RANTES-induced IL-4 release; but neither exogenous LTC4, LTD4, nor LTE4 elicited IL-4 release. Only after membrane permeabilization enabled cysLTs to enter eosinophils did LTC4 and LTD4 stimulate IL-4, but not RANTES, release. LTC4-elicited IL-4 release was pertussis toxin inhibitable, but inhibitors of the two known G protein–coupled cysLT receptors (cysLTRs) (CysLT1 and CysLT2) did not block LTC4-elicited IL-4 release. LTC4 was 10-fold more potent than LTD4 and at low concentrations (0.3–3 nM) elicited, and at higher concentrations (>3 nM) inhibited, IL-4 release from permeabilized eosinophils. Likewise with intact eosinophils, LTC4 export inhibitors, which increased intracellular LTC4, inhibited eotaxin-elicited IL-4 release. Thus, LTC4 acts, via an intracellular cysLTR distinct from CysLT1 or CysLT2, as a signal transducer to selectively regulate IL-4 release. These results demonstrate that LTC4, well recognized as a paracrine mediator, may also dynamically govern inflammatory and immune responses as an intracrine mediator of eosinophil cytokine secretion.
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Jiang, Yongfeng, Laura A. Borrelli, Yoshihide Kanaoka, Brian J. Bacskai, and Joshua A. Boyce. "CysLT2 receptors interact with CysLT1 receptors and down-modulate cysteinyl leukotriene–dependent mitogenic responses of mast cells." Blood 110, no. 9 (November 1, 2007): 3263–70. http://dx.doi.org/10.1182/blood-2007-07-100453.

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Abstract Cysteinyl leukotrienes (cys-LTs) induce inflammation through 2 G protein–coupled receptors (GPCRs), CysLT1 and CysLT2, which are coexpressed by most myeloid cells. Cys-LTs induce proliferation of mast cells (MCs), transactivate c-Kit, and phosphorylate extracellular signal-regulated kinase (ERK). Although MCs express CysLT2, their responses to cys-LTs are blocked by antagonists of CysLT1. We demonstrate that CysLT2 interacts with CysLT1, and that knockdown of CysLT2 increases CysLT1 surface expression and CysLT1-dependent proliferation of cord blood–derived human MCs (hMCs). Cys-LT–mediated responses were absent in MCs from mice lacking CysLT1 receptors, but enhanced by the absence of CysLT2 receptors. CysLT1 and CysLT2 receptors colocalized to the plasma membranes and nuclei of a human MC line, LAD2. Antibody-based fluorescent lifetime imaging microscopy confirmed complexes containing both receptors based on fluorescence energy transfer. Negative regulation of CysLT1-induced mitogenic signaling responses of MCs by CysLT2 demonstrates physiologically relevant functions for GPCR heterodimers on primary cells central to inflammation.
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Drost, Adriana, Mirjam Funk, Karoline Norz, Anne Zipfel, Lothar Kanz, and Robert Mohle. "Cysteinyl Leukotrienes Signal Via Overexpressed CysLT1, but Not CysLT2 Receptor In Chronic Lymphocytic Leukemia." Blood 116, no. 21 (November 19, 2010): 3612. http://dx.doi.org/10.1182/blood.v116.21.3612.3612.

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Abstract Abstract 3612 The G Protein-coupled receptors (GPCRs) CysLT1 and CysLT2 are both expressed in peripheral blood mononuclear cells (PBMNC). Their ligands are inflammatory mediators of the cysteinyl leukotriene (cysLT) family and contribute, together with ligands of other GPCRs such as chemokines, to migration and proliferation of a variety of cell types. In the present study, we demonstrate by real-time RT-PCR that CysLT1 mRNA is overexpressed in B-CLL cells compared to both normal PBMNC and normal CD19+ B cells, whereas only low levels of CysLT2 mRNA are present. GPCR-typical cellular responses such as intracellular calcium fluxes and actin polymerization, which were induced by the cysLT LTD4 in CLL cells in a dose-dependent manner, were suppressed by the CysLT1 antagonist MK571, the prototype of the lukast family of drugs used in asthma treatment (e.g., montelukast). However, MK571 and other lukasts also block the leukotriene transporter MRP. The fact that the CysLT1 antagonist LY171883, which has no effect on MRP, also abrogated the responses of CLL cells indicates that the effects of cysLTs are mediated solely by CysLT1. Moreover, also chemotaxis was induced by the cysLT LTD4 in B-CLL cells (optimum at low nanomolar concentrations) and could be blocked by MK571. We further observed inhibiting effects of MK571 on cysLT-induced Erk/MAP kinase phosphorylation in B-CLL cells, which suggests an involvement of CysLT1 in cell proliferation. Indeed, MK571 significantly induced apoptosis of CLL cells in vitro and reduced survival of cultured B-CLL cells. However, the concentrations for a significant reduction of cell viability were higher (1-10 μM) than the concentration required for efficient CysLT1 receptor inhibition (0.1 μM). Thus, the influence of MK571 on B-CLL cell survival may mainly be due to direct effects on apoptosis occuring at the higher dose level and/or blocking of the leukotriene transporter MRP. Accordingly, LY171883 and the combined CysLT1/2 antagonist Bay-u9773 did not induce CLL apoptosis. Our results suggest that CysLT1 is overexpressed in B-CLL cells and involved in cell trafficking, similar to the chemokine receptor CXCR4. Considering the redundancy among GPCRs and the limited effect of MK571 on cell survival, CysLT1 for its own represents a less attractive therapeutic target using the currently available CysLT1 antagonists of the lukast family. However, combined inhibition of several GPCRs highly expressed in CLL cells including cysLT1 and CXCR4 may constitute a promising therapeutic approach and should be further evaluated. Disclosures: No relevant conflicts of interest to declare.
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Ballerini, P., P. Di Iorio, R. Ciccarelli, F. Caciagli, A. Polp, A. Beraudi, S. Buccella, et al. "P2Y1 and Cysteinyl Leukotriene Receptors Mediate Purine and Cysteinyl Leukotriene Co-Release in Primary Cultures of Rat Microglia." International Journal of Immunopathology and Pharmacology 18, no. 2 (April 2005): 255–68. http://dx.doi.org/10.1177/039463200501800208.

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Inflammation is widely recognized as contributing to the pathology of acute and chronic neurodegenerative conditions. Microglial cells are pathologic sensors in the brain and activated microglia have been viewed as detrimental. Leukotriene, including cysteinyl leukotrienes (CysLTs) are suggested to be involved in brain inflammation and neurological diseases and ATP, by its receptors is a candidate for microglia activation. A23187 (10μM) stimulated microglia to co-release CysLTs and [3H]adenine based purines ([3H]ABPs), mainly ATP. The biosynthetic production of CysLTs was abolished by 10μM MK-886, an inhibitor of 5-lipoxygenase-activating protein activity. RT-PCR analysis showed that microglia expressed both CysLT1 / CysLT2 receptors, P2Y1 ATP-receptors and several members of the ATP binding cassette (ABC) transporters including MRP1, MRP4 and Pgp. The increase in [Ca2+]i elicited by LTD4 (0.1 μM) and 2MeSATP (100μM), agonists for CysLT- and P2Y1-receptors, was abolished by the respective antagonists, BAYu9773 (0.5 μM) and suramin (50 μM). The stimulation of both receptor subtypes, induced a concomitant increase in the release of both [3H]ABPs and CysLTs that was blocked by the antagonists and significantly reduced by a cocktail of ABC transporter inhibitors, BAPTA/AM (intracellular Ca2+ chelator) and staurosporine (0.1 μM, PKC blocker). P2Y antagonist was unable to antagonise the effects of LTD4 and BAYu9773 did not reduce the effects of 2MeSATP. These data suggest that: i) the efflux of purines and cysteinyl-leukotrienes is specifically and independently controlled by the two receptor types, ii) calcium, PKC and the ABC transporter system can reasonably be considered common mechanisms underlying the release of ABPs and CysLTs from microglia. The blockade of P2Y1 or CysLT1/CysLT2 receptors by specific antagonists that abolished the raise in [Ca2+]i and drastically reduced the concomitant efflux of both compounds, as well as the effects of BAPTA and staurosporine support this hypothesis. In conclusion, the data of the present study suggest a cross talk between the purine and leukotriene systems in a possible autocrine/paracrine control of the microglia-mediated initiation and progression of an inflammatory response.
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Sasaki, Fumiyuki, and Takehiko Yokomizo. "The leukotriene receptors as therapeutic targets of inflammatory diseases." International Immunology 31, no. 9 (May 28, 2019): 607–15. http://dx.doi.org/10.1093/intimm/dxz044.

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Abstract Leukotrienes (LTs) are inflammatory mediators derived from arachidonic acid. LTs include the di-hydroxy acid LT (LTB4) and the cysteinyl LTs (CysLTs; LTC4, LTD4 and LTE4), all of which are involved in both acute and chronic inflammation. We and other groups identified a high-affinity LTB4 receptor, BLT1; the LTC4 and LTD4 receptors, CysLT1 and CysLT2; and the LTE4 receptor, GPR99. Pharmacological studies have shown that BLT1 signaling stimulates degranulation, chemotaxis and phagocytosis of neutrophils, whereas CysLT1 and CysLT2 signaling induces airway inflammation by increasing vascular permeability and the contraction of bronchial smooth muscle. Recently, we and other groups suggested that the LTB4–BLT1 axis and the cysteinyl LTs–CysLT1/2 axis are involved in chronic inflammatory diseases including asthma, atopic dermatitis, psoriasis, atherosclerosis, arthritis, obesity, cancer and age-related macular degeneration using animal models for disease and gene knockout mice. This review describes the classical and novel functions of LTs and their receptors in several inflammatory diseases and discusses the potential clinical applications of antagonists for LT receptors and inhibitors of LT biosynthesis.
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Slater, Kayleigh, Aisling B. Heeran, Sandra Garcia-Mulero, Helen Kalirai, Rebeca Sanz-Pamplona, Arman Rahman, Nebras Al-Attar, et al. "High Cysteinyl Leukotriene Receptor 1 Expression Correlates with Poor Survival of Uveal Melanoma Patients and Cognate Antagonist Drugs Modulate the Growth, Cancer Secretome, and Metabolism of Uveal Melanoma Cells." Cancers 12, no. 10 (October 13, 2020): 2950. http://dx.doi.org/10.3390/cancers12102950.

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Metastatic uveal melanoma (UM) is a rare, but often lethal, form of ocular cancer arising from melanocytes within the uveal tract. UM has a high propensity to spread hematogenously to the liver, with up to 50% of patients developing liver metastases. Unfortunately, once liver metastasis occurs, patient prognosis is extremely poor with as few as 8% of patients surviving beyond two years. There are no standard-of-care therapies available for the treatment of metastatic UM, hence it is a clinical area of urgent unmet need. Here, the clinical relevance and therapeutic potential of cysteinyl leukotriene receptors (CysLT1 and CysLT2) in UM was evaluated. High expression of CYSLTR1 or CYSLTR2 transcripts is significantly associated with poor disease-free survival and poor overall survival in UM patients. Digital pathology analysis identified that high expression of CysLT1 in primary UM is associated with reduced disease-specific survival (p = 0.012; HR 2.76; 95% CI 1.21–6.3) and overall survival (p = 0.011; HR 1.46; 95% CI 0.67–3.17). High CysLT1 expression shows a statistically significant (p = 0.041) correlation with ciliary body involvement, a poor prognostic indicator in UM. Small molecule drugs targeting CysLT1 were vastly superior at exerting anti-cancer phenotypes in UM cell lines and zebrafish xenografts than drugs targeting CysLT2. Quininib, a selective CysLT1 antagonist, significantly inhibits survival (p < 0.0001), long-term proliferation (p < 0.0001), and oxidative phosphorylation (p < 0.001), but not glycolysis, in primary and metastatic UM cell lines. Quininib exerts opposing effects on the secretion of inflammatory markers in primary versus metastatic UM cell lines. Quininib significantly downregulated IL-2 and IL-6 in Mel285 cells (p < 0.05) but significantly upregulated IL-10, IL-1β, IL-2 (p < 0.0001), IL-13, IL-8 (p < 0.001), IL-12p70 and IL-6 (p < 0.05) in OMM2.5 cells. Finally, quininib significantly inhibits tumour growth in orthotopic zebrafish xenograft models of UM. These preclinical data suggest that antagonism of CysLT1, but not CysLT2, may be of therapeutic interest in the treatment of UM.
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Voisin, Tiphaine, Caroline Perner, Marie-Angele Messou, Stephanie Shiers, Saltanat Ualiyeva, Yoshihide Kanaoka, Theodore J. Price, et al. "The CysLT2R receptor mediates leukotriene C4-driven acute and chronic itch." Proceedings of the National Academy of Sciences 118, no. 13 (March 22, 2021): e2022087118. http://dx.doi.org/10.1073/pnas.2022087118.

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Acute and chronic itch are burdensome manifestations of skin pathologies including allergic skin diseases and atopic dermatitis, but the underlying molecular mechanisms are not well understood. Cysteinyl leukotrienes (CysLTs), comprising LTC4, LTD4, and LTE4, are produced by immune cells during type 2 inflammation. Here, we uncover a role for LTC4 and its signaling through the CysLT receptor 2 (CysLT2R) in itch. Cysltr2 transcript is highly expressed in dorsal root ganglia (DRG) neurons linked to itch in mice. We also detected CYSLTR2 in a broad population of human DRG neurons. Injection of leukotriene C4 (LTC4) or its nonhydrolyzable form NMLTC4, but neither LTD4 nor LTE4, induced dose-dependent itch but not pain behaviors in mice. LTC4-mediated itch differed in bout duration and kinetics from pruritogens histamine, compound 48/80, and chloroquine. NMLTC4-induced itch was abrogated in mice deficient for Cysltr2 or when deficiency was restricted to radioresistant cells. Itch was unaffected in mice deficient for Cysltr1, Trpv1, or mast cells (WSh mice). CysLT2R played a role in itch in the MC903 mouse model of chronic itch and dermatitis, but not in models of dry skin or compound 48/80- or Alternaria-induced itch. In MC903-treated mice, CysLT levels increased in skin over time, and Cysltr2−/− mice showed decreased itch in the chronic phase of inflammation. Collectively, our study reveals that LTC4 acts through CysLT2R as its physiological receptor to induce itch, and CysLT2R contributes to itch in a model of dermatitis. Therefore, targeting CysLT signaling may be a promising approach to treat inflammatory itch.
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Nettis, Eustachio, Maddalena D'Erasmo, Elisabetta Di Leo, Gianfranco Calogiuri, Vincenzo Montinaro, Antonio Ferrannini, and Angelo Vacca. "The Employment of Leukotriene Antagonists in Cutaneous Diseases Belonging to Allergological Field." Mediators of Inflammation 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/628171.

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Leukotrienes (LTs) are potent biological proinflammatory mediators. LTC4, LTD4, and LTE4 are more frequently involved in chronic inflammatory responses and exert their actions binding to a cysteinyl-LT 1 (CysLT1) receptor and a cysteinyl-LT 2 (CysLT2) receptor. LTs receptor antagonists available for clinical use demonstrate high-affinity binding to the CysLT1 receptor. In this paper the employment of anti-LTs in allergic cutaneous diseases is analyzed showing that several studies have recently reported a beneficial effects of these agents (montelukast and zafirlukast as well as zileuton) for the treatment of some allergic cutaneous related diseases-like chronic urticaria and atopic eczema although their proper application remains to be established.
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Sjoberg, Jan, Frida Schain, Ylva Tryselius, Linda Backman, Anna Porwit, Cheng Liu, Dawei Xu, et al. "Novel Findings Support a Patophysiological Role of the Arachidonic Cascade in Hodgkin Lymphoma." Blood 110, no. 11 (November 16, 2007): 2269. http://dx.doi.org/10.1182/blood.v110.11.2269.2269.

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Abstract Lipoxygenases (LO) are a family of structurally related enzymes which catalyze the conversion of the fatty acid arachidonic acid to biologically active metabolites. The key enzyme in leukotriene synthesis, 5- LO, catalyzes the first step in the metabolism of arachidonic acid to leukotriene (LT) C4. This compound and its metabolites LTD4 and LTE4, collectively called cysteinyl leukotrienes (cysLT), can bind to two high-affinity receptors, named cysLT1 and cysLT2. A sister enzyme to 5-LO is 15-LO-1 which also can catalyze the formation of bioactive metabolites. Arachidonic acid metabolites have traditionally been linked to inflammation and asthma but several studies also indicate a role of these metabolites in carcinogenesis In our studies of arachidonic acid metabolism in human lymphomas, we have identified the expression of 15-LO-1 and receptors for cysLT in primary as well as cultured Hodgkin-Reed Sternberg (H-RS) cells. In tumor tissue, H-RS cells positive for 15-LO-1 and the cysLT1 receptor were detected immunohistochemically in 13/15 and 12/16 cases, respectively. The presence of mRNA for 15-LO-1 and the cysLT1 and 2 receptors was confirmed by microarray analysis of laser dissected H-RS cells. Studies of 15-LO-1 gene transcription revealed that STAT6 activation and chromatin remodeling by DNA demethylation and histone acetylation are crucial for transcriptional activation of this gene in cultured H-RS cells. Incubation of the Hodgkin lymphoma-derived cell lines KMH2 and L1236 with LTD4 led to a robust calcium response that was completely abolished in presence of the cysLT1 receptor inhibitor zafirlukast. In L1236 cells, LTD4 induced increased DNA synthesis, interleukin-13 transcription and release of TNF-alpha, interleukin-6 and interleukin-8 in a dose-dependent manner, all of which were inhibited by zafirlukast. Thus, as the H-RS cells lack the expression of 5-LO, we hypothesize that that tumor-associated cysLT-producing inflammatory cells, such as eosinophils and mast cells, contribute to the pathogenesis of Hodgkin lymphoma through induction of tumor cell proliferation and cytokine release. Furthermore, immunohistochemical studies of 20 non-Hodgkin lymphomas revealed the expression of cysLT1 receptors also in primary mediastinal B cell lymphomas (PMBCL), and the functionality of these receptors was confirmed in the PMBCL-derived cell line MedB1. Taken together, these novel findings support a role for arachidonic acid metabolites in the pathogenesis of lymphoma.
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Sekioka, Tomohiko, Michiaki Kadode, Noriko Osakada, Manabu Fujita, Naoya Matsumura, Yoshiyuki Yamaura, Shinji Nakade, Takeshi Nabe, and Kazuhito Kawabata. "A new CysLT1 and CysLT2 receptors-mediated anaphylaxis guinea pig model." Prostaglandins, Leukotrienes and Essential Fatty Acids 119 (April 2017): 18–24. http://dx.doi.org/10.1016/j.plefa.2017.03.002.

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Dissertations / Theses on the topic "CysLT2"

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Fleck, Juliana. "MONTELUCASTE DIMINUI AS CRISES CONVULSIVAS EM ANIMAIS ABRASADOS E POTENCIALIZA O EFEITO ANTICONVULSIVANTE DO FENOBARBITAL." Universidade Federal de Santa Maria, 2015. http://repositorio.ufsm.br/handle/1/3855.

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Epilepsy is a chronic neurological disease characterized by recurrent, unprovoked seizures. Evidence suggests that inflammation plays a role in the pathophysiology of seizures. Although cysteinyl leukotrienes (CysLTs) have been implicated in seizures, no study has investigated whether blocking of CysLT1 receptors potentiates the anticonvulsant action of classic antiepileptic drugs, as well as the expression of CysLT receptors is altered by inflammation. In this study we showed that the inverse agonist of CysLT1 receptor, montelukast, synergistically increases the anticonvulsant action of phenobarbital against seizures induced in a model of acute injection of pentylenetetrazole (PTZ). Furthermore, it is shown that LTD4 (leukotriene D4) prevents the effect of montelukast. Isobolographic analysis revealed an ED50 mix value for a fixed-ratio combination (1:1 proportion) of montelukast plus phenobarbital of 0.06 ± 0.02 μmol, whereas the calculated ED50 add value was 0.49 ± 0.03 μmol. The interaction index was 0.12, indicating a synergistic interaction. Montelukast significantly decreased the antiseizure DE50 for phenobarbital (0.74 and 0.04 μmol in the absence and presence of montelukast, respectively) and, consequently, phenobarbital-induced sedation at equieffective doses. We also investigated whether the CysLT1 inverse agonist montelukast and a classical anticonvulsant, phenobarbital, decrease seizures in PTZ-kindled mice and CysLT receptor expression. Montelukast (10 mg/kg, s.c.) and phenobarbital (20 mg/kg, s.c.) increased the latency to generalized seizures in kindled mice. Montelukast increased CysLT1 immunoreactivity only in non-kindled PTZ-challenged mice. Interestingly, PTZ challenge decreased CysLT2 immunoreactivity only in kindled mice. CysLT1 antagonists seem to emerge as promising adjunct therapeutic agents in the treatment of refractory seizures. Notwithstanding, additional studies are necessary to evaluate the clinical implications of this work.
A epilepsia é uma doença que se manifesta por crises epilépticas recorrentes, não provocadas. Evidências sugerem que a inflamação desempenha um papel na patofisiologia destas crises. Embora os leucotrienos cisteínicos (CysLTs) tenham sido implicados no desenvolvimento de crises convulsivas, nenhum estudo investigou se o bloqueio dos receptores CysLT1 potencializa a ação anticonvulsivante de antiepilépticos clássicos, assim como se a expressão dos receptores de CysLT é alterada por inflamação. Neste estudo mostramos que o agonista inverso de CysLT1, montelucaste, sinergicamente aumenta a ação anticonvulsivante do fenobarbital contra crises convulsivas induzidas em um modelo de injeção aguda de pentilenotetrazol (PTZ). Além disso, é mostrado que o LTD4 (leucotrieno D4) previne o efeito do montelucaste. A análise isobolográfica revelou que o valor de DE50 mix, calculado experimentalmente para uma combinação de proporção 1: 1 de montelucaste e fenobarbital foi de 0,06 ± 0,02 umol, ao passo que o valor de DE50 add, calculado foi de 0,49 ± 0,03 umol. O índice de interação encontrado foi de 0,12, indicando uma interação sinérgica. A associação dos fármacos diminuiu significativamente o DE50 para o efeito anticonvulsivante do fenobarbital de 0,74 para 0,04 umol (na ausência e na presença de montelucaste, respectivamente) e, consequentemente, a sedação induzida por fenobarbital em doses equieficazes. Posteriormente foi avaliado se o montelucaste e o fenobarbital diminuem as crises convulsivas em animais previamente abrasados, assim como se o tratamento farmacológico ou o abrasamento alteram a expressão de receptores CysLTs. O montelucaste (10 mg/kg; s.c.) e o fenobarbital (20 mg/kg, s.c.) aumentaram a latência para crises convulsivas generalizadas em camundongos abrasados. O montelucaste aumentou a imunorreatividade do receptor CysLT1 em camundongos não abrasados e que foram desafiados por PTZ que não foram abrasados. Entretanto, o desafio de PTZ diminuiu a imunorreatividade do receptor CysLT2 apenas em camundongos abrasados. Antagonistas do receptor CysLT1 parecem emergir como agentes terapêuticos adjuntos promissores no tratamento de crises refratárias. Não obstante, estudos adicionais são necessários para avaliar as implicações clínicas deste trabalho.
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Thompson, Charles. "Signalisation des récepteurs CYSLT1 et CYSLT2 et activation transcriptionnelle induite par les cystéinylleucotriènes dans l'asthme." Thèse, Université de Sherbrooke, 2006. http://savoirs.usherbrooke.ca/handle/11143/4229.

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Depuis quelques années, une population croissante d’enfants et d’adultes est touchée par l’asthme. L’étendue des recherches sur le sujet reflète sans doute la complexité de cette maladie. En effet, la pathogenèse de l’asthme est sous le contrôle de plusieurs médiateurs, générés par une multitude de cellules (inflammatoires et structurelles) qui s’organisent et interagissent entre elles. L’aspect multifactoriel et hétérogène de cette pathologie en fait une cible difficile à atteindre. Parmi ses principales caractéristiques, on retrouve le broncospasme, l’hypersécrétion de mucus, l’hyper-réactivité bronchique, l’inflammation et le remodelage pulmonaire. À la fin des années 1990, les antagonistes classiques des leucotriènes font leur apparition sur le marché et sont prescrits pour le traitement de l’asthme. Il s’agit d’antagonistes spécifiques du récepteur CysLT 1, le premier de deux récepteurs de hautes affinités pour les cystéinyl-leucotriènes (cysLT). Les cysLT sont des médiateurs lipidiques impliqués dans plusieurs processus inflammatoires. En plus d’être augmentés dans l’asthme, ils ont la capacité de mimer les principaux symptômes asthmatiques. Malgré l’utilisation clinique des antagonistes classiques des leucotriènes, plusieurs mécanismes moléculaires et cellulaires des cysLT demeurent inconnus. Dans la présente thèse, nous avons initialement abordé le rôle des cysLT dans le processus inflammatoire impliqué dans les cas plus sévères d’asthme. Nous avons par conséquent étudié la capacité des cysLT à induire la production d’une chimiokine. L’asthme sévère étant caractérisé par un influx neutrophilique, nous nous sommes principalement concentré sur l’expression de l’IL-8, le chimioattractant par excellence de ce type cellulaire. Nous avons observé une très forte induction de l’IL-8 en réponse aux cysLT et ce, par l’intermédiaire du récepteur CysLTl et CysLT2. Un des objectifs principaux de ce travail était l’étude de la signalisation induite par les récepteurs CysLTl et CysLT2. Les deux récepteurs répondant aux mêmes agonistes, nous avons par conséquent généré deux modèles cellulaires, afin d’étudier chacun spécifiquement. Le premier modèle exprime de façon stable le CysLTl, alors que le second exprime le CysLT2. Nous avons donc mis en lumière les mécanismes de régulation transcriptionelle impliqués dans l’expression de l’L-8 par les cysLT. Les voies de signalisation NF-kB et AP-1 sont fortement impliquées dans la transduction de signal de chaque récepteur CysLT. Nous avons donc approfondi l’étude de ces voies de signalisation en réponse au cysLT. Des études récentes proposent un rôle pour les cysLT dans le remodelage pulmonaire. Les changements structuraux des voies aériennes impliquent la participation de plusieurs molécules fibrogéniques et angiogéniques. Parmi ces facteurs, plusieurs sont synthétisés sous forme de précurseur qui nécessite une activation/maturation par clivage endoprotéolytique. Cette tâche peut être accomplie par la furine, une convertase de proprotéine. Ainsi, nous avons étudié l’effet des cysLT sur l’expression de la furine et les mécanismes de régulation concernés. Nous démontrons en fait que le LTD4, via le récepteur CysLTl, induit l’expression de la furine, autant au niveau de l’ARNm que la protéine. De plus, l’augmentation de la furine coïncide avec une hausse de l’activation de la métalloprotéinase MT1-MMP et du TGF|3, deux facteurs impliqués dans le remodelage pulmonaire. Enfin, cette thèse propose de nouveaux mécanismes par lesquels les cysLT et leurs récepteurs participent à la pathogénèse asthmatique. Ainsi, nous démontrons que les cysLT jouent un rôle dans l’inflammation pulmonaire en stimulant la production de chimiokines. Nous avons également approfondi les connaissances sur les voies de signalisation menant à la production d’L-8 en réponse au cysLT. Finalement, nous suggérons l’implication des cysLT dans le remodelage pulmonaire via l’induction de la convertase de proprotéine furine. [Symboles non conformes]
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Audette, Karine. "Internalisation différentielle des récepteurs Cysteinyl leucotriène 1 et 2 (CysLT1 et CysLT2) bla voie dépendante des vésicules de clathrine est nécessaire à l'endocytose du CysLT1. /." [S.l. : s.n.], 2007.

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Audette, Karine. "Internalisation différentielle des récepteurs Cysteinyl leucotriène 1 et 2 (CysLT1 et CysLT2) la voie dépendante des vésicules de clathrine est nécessaire à l'endocytose du CysLT1." Mémoire, Université de Sherbrooke, 2007. http://savoirs.usherbrooke.ca/handle/11143/3869.

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Les récepteurs cystéinyl-leucotriène 1 et 2 font partie de la grande famille des récepteurs couplés aux protéines G. Ces deux récepteurs partagent une homologie de séquence de 38%, cette homologie étant particulièrement faible dans la région C-terminale. Tout d'abord, nous avons étudié la localisation et l'internalisation des deux récepteurs chez des lignées cellulaires HEK293 exprimant de façon stable l'un ou l'autre des deux récepteurs. Le récepteur CysLT1, localisé principalement au niveau de la membrane plasmique, s'internalise fortement (60%) au cours de la première heure de stimulation au LTD[indice inférieur 4] (Leucotriène D4) et s'accumule dans la région péri-nucléaire. L'internalisation reste soutenue même après 4 heures de stimulation et est bloquée par le Montélukast, un antagoniste spécifique du récepteur CysLT1. Par contre, le récepteur CysLT2 est situé majoritairement à l'intérieur de la cellule et très faiblement à la surface cellulaire à l'état non-stimulé. Une faible internalisation, soit près de 5%, est observée à des temps de stimulation inférieurs à 1 heure. Toutefois, une augmentation de l'expression à la surface des cellules est observée lorsque les cellules sont stimulées pendant plus de 2 heures au LTC[indice inférieur 4] (Leucotriène C4). Ce phénomène d'externalisation étant intriguant, nous avons étudié la fonctionnalité des récepteurs à la surface via des essais de production d'inositol phosphates après 2 et 4 heures de prétraitement au LTC[indice inférieur 4]. Nous avons obtenu des hausses de 4 fois de la production des inositol phosphates après 2 et 4 heures de prétraitement au LTC[indice inférieur 4] comparativement à un ratio de 2 fois lorsque prétraité à l'EtOH. L'autre partie du projet consistait à mieux définir l'internalisation du récepteur CysLT1 ainsi que les molécules impliquées. Premièrement, nous avons observé que les acides aminés 304 à 321 de la queue C-terminale du CysLT1 étaient cruciaux pour l'internalisation du récepteur. La cotransfection de mutants et dominants négatifs d'arrestines 2 et 3 a suggéré l'indépendance des arrestines pour l'internalisation du récepteur CysLT1. Nous avons aussi montré que les GRK (kinases de RCPG) 2, 5 et 6, la PKA ainsi que la caséine kinase 2 ne semblent pas nécessaires pour l'internalisation du récepteur CysLT1 contrairement aux PKC et à la caséine kinase 1 qui sont importantes dans ce processus. Ensuite, nous avons démontré que la cotransfection d'un dominant négatif de la dynamine 1A (K44A) empêche l'internalisation du récepteur CysLT1. Étant donné que le potentiel de signalisation du récepteur peut dépendre de la voie d'internalisation empruntée, nous avons étudié les voies d'internalisation possibles. Des prétraitements avec le sucrose hyperosmotique et la concanavaline A ont inhibé l'internalisation du CysLT1 respectivement de 90% et 70%, indiquant la participation des vésicules de clathrine. La baisse d'internalisation induite par certains agents désorganisant le cholestérol membranaire a amené certaines évidences de la participation des radeaux lipidiques. De plus, nous avons démontré l'importance d'un réseau d'actine intact dans le processus d'internalisation du récepteur CysLT1 via des agents qui induisent la dépolymérisation de l'actine. Nous avons obtenu des baisses significatives de l'internalisation de 57% et 43% suite à des prétraitements avec respectivement la cytochalasine D et la latrunculine B. Finalement, la réexpression rapide à la surface des récepteurs CysLT1 suite au retrait de l'agoniste suggère un recyclage rapide des récepteurs via les endosomes précoces. Les résultats de ce mémoire exposent des divergences au niveau de la localisation et de l'internalisation des récepteurs CysLT1 et CysLT2. Nos résultats suggèrent également que l'internalisation du récepteur CysLT1 est dépendante de l'activité de la dynamine et du réseau d'actine et qu'elle s'effectue via les vésicules de clathrine et possiblement via les radeaux lipidiques.
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Brochu-Bourque, Ariane. "Caractérisation fonctionnelle de la mutation M201V du récepteur CysLT[indice inférieur 2]." Mémoire, Université de Sherbrooke, 2011. http://savoirs.usherbrooke.ca/handle/11143/4080.

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Les cystéinyl-leucotriènes (cysLTs), qui inclut [i.e. incluent] le LTC[indice inférieur 4], le LTD[indice inférieur 4] et le LTE[indice inférieur 4] , sont impliqués dans une variété de maladies inflammatoires (ex : l'asthme) et agissent sur au moins deux récepteurs couplés aux protéines G distincts, nommé [i.e.] le CysLT[indice inférieur 1] et le CysLT[indice inférieur 2]. Des antagonistes spécifiques du récepteur CysLT[indice inférieur 1] ont été élaborés et sont utilisés pour contrôler la bronchoconstriction et l'inflammation chez le patient asthmatique. Le récepteur CysLT[indice inférieur 2] semblerait également impliqué dans l'asthme bien que son rôle et sa signalisation soient encore mal compris. Un polymorphisme dans le gène du CysLT[indice inférieur 2], produisant la substitution d'un acide aminé (M201V), a été associé à l'asthme au sein de trois différentes populations étudiées. Le but de cette étude était donc de déterminer si la mutation M201V affecte l'affinité du CysLT[indice inférieur 2] pour ses ligands naturels et son efficacité de signalisation. Pour ce faire, des cellules HEK293 ont été transfectées de façon stable soit avec le récepteur CysLT[indice inférieur 2] de type « sauvage » ou avec le CysLT[indice inférieur 2] contenant la mutation (M201V). Nous avons démontré que l'affinité pour le LTC[indice inférieur 4] est diminuée de 50% par la présence de la mutation M201V alors que l'affinité pour le LTD[indice inférieur 4] est essentiellement perdue. Chez les cellules CysLT[indice inférieur 2] M201V, la production d'inositol phosphate (IP) induite par le LTC[indice inférieur 4] est diminuée aux plus faibles concentrations de ligand utilisées mais revient à la normale à la concentration maximale de LTC[indice inférieur 4] utilisée (100 nM). Par contre, la production d'IP induite par le LTD[indice inférieur 4] est significativement diminuée par la mutation, et ce, pour l'ensemble des concentrations utilisées. Des résultats similaires ont également été observés avec la transactivation du promoteur de l'IL-8 induite par le LTC[indice inférieur 4] ou le LTD[indice inférieur 4] . Enfin, nous avons étudié les différentes voies de signalisation impliquées dans l'activation du promoteur de l'IL-8. Lors d'une stimulation au LTC[indice inférieur 4], nous avons observé que la phosphorylation de JNK et de p65 est davantage affectée par la mutation M201V que la phosphorylation de ERK et de p38. Pour ce qui est d'une stimulation au LTD[indice inférieur 4], la phosphorylation de p65 est totalement affectée par la mutation M201V. Similairement, cette mutation abolit complètement la phosphorylation de JNK ainsi que l'activation de ERK et de p38 aux plus faibles concentrations de LTD[indice inférieur 4] utilisées. Cependant, l'activation de ERK et de p38 est maintenue à un niveau semblable aux cellules CysLT[indice inférieur 2] lorsqu'on utilise de plus fortes concentrations de LTD[indice inférieur 4] . Ainsi, nos résultats indiquent que le polymorphisme M201V affecte davantage la réponse du CysLT[indice inférieur 2] au LTD[indice inférieur 4] qu'au LTC[indice inférieur 4] et affecte plus particulièrement certaines voies de signalisation que d'autres. Ces résultats confirment ceux précédemment obtenus et permettent de mieux comprendre comment la mutation M201V affecte les voies de signalisation du CysLT[indice inférieur 2] et son affinité pour le LTC[indice inférieur 4] et le LTD[indice inférieur 4].
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García, Murria María Jesús. "Regulación redox de la Rubisco: Contribución estructural y funcional del par de residuos conservados Cys172 y Cys192." Doctoral thesis, Universitat de València, 2006. http://hdl.handle.net/10803/9536.

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La Ribulosa 1,5-bisfosfato carboxilasa oxigenasa (Rubisco) cataliza el primer paso en la fijación fotosintética del CO2 a través del ciclo de Calvin. La estructura del holoenzima activo en organismos eucariotas es un hexadecámero compuesto por 8 subunidades grandes (de 51-58KDa) y 8 subunidades pequeñas (de 12-18KDa). En condiciones de senescencia natural o inducida por estrés la Rubisco sufre una degradación rápida y selectiva. Una de las respuestas más generalizadas ante diferentes tipos de estrés en distintos organismos es la oxidación de grupos tioles de la Rubisco, que se ha relacionado in vitro e in vivo con la inactivación y susceptibilización proteolítica del enzima. Los residuos de cisteínas filogenéticamente conservados de la Rubisco son candidatos potenciales a mediar esta regulación redox. Con estos antecedentes, el objetivo general del presente trabajo ha sido evaluar la implicación de los residuos Cys172 y Cys192 (altamente conservados en eucariotas y cianobacterias) en la actividad, modulación redox, y en la organización estructural del holoenzima. Para ello se han abordado los siguientes aspectos:I. Obtención y caracterización de las Rubiscos mutantes C172S, C192S y C172S/C192S Las funciones de los residuos Cys172 y Cys192 se han investigado estudiando el fenotipo de mutantes en los que dichos residuos se han sustituido por serina mediante mutagénesis dirigida del gen rbcL en el alga unicelular Chlamydomonas reinhardtii. El enzima C172S posee un factor de especificidad mayor que el silvestre, con unas constantes aparentes de Michaelis para el CO2 y O2 aumentadas. La Rubisco C192S presenta una especial sensibilidad a la inactivación por agentes modificadores de grupos sulfhidrilo. Ello parece responder al carácter crítico de la modificación de la Cys172 en la actividad enzimática y al efecto protector que sobre este residuo ejerce la Cys192. El estudio del ensayo de la sensibilidad térmica, de los cambios en la sensibilidad proteolítica y de la movilidad del holoenzima en geles nativos indica que la sustitución de las Cys172 y/o Cys192 afecta a la estructura de los enzimas. II. Determinación de la estructura de las Rubiscos C172S y C192S por difracción de rayos X Se ha determinado la estructura tridimensional de la Rubisco de los mutantes C172S y C192S. Como diferencia más significativa se ha detectado un desplazamiento de la hebra β1 del barril α/β en el enzima C172S en relación a la estructura del enzima silvestre. III. Estudio de la respuesta de los mutantes a diferentes tipos de estrés El mutante C172S sometido a estrés salino degrada la Rubisco de forma más lenta que la cepa silvestre o los demás mutantes. Además, bajo un estrés por diamida específicamente dirigido a la oxidación de los grupos sulfhidrilo, el mutante C172S se muestra resistente a la inactivación que sufren las demás cepas. Ello apunta a un papel singular del residuo Cys172 en la modulación del catabolismo de la Rubisco en respuesta a situaciones de estrés. En condiciones de estrés por diamida, todas las cepas mutantes (C172S, C192S y C172S/C192S) presentan una degradación retardada de la Rubisco por comparación con la cepa silvestre. Ello sugiere que, en estas condiciones de oxidación directa de los tioles celulares, la formación de un puente disulfuro entre la Cys172 y la Cys192 podría actuar como una señal condicionante de la degradación del enzima.
Cysteines 172 and 192 from the large subunit of the photosynthetic enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) are a pair of vicinal residues evolutively conserved among cyanobacteria, algae and higher plants. In the present study, it has been analyzed the effect of the substitution of Cys172 and Cys192 by serine on the catalytic properties, thermostability, three-dimensional structure of the mutant enzymes, and the in vivo turnover and inactivation of Rubisco enzymes in stressed cells.1. Site-directed mutagenesis of conserved cysteine residues (Cys172 and Cys192) of Rubisco in Chlamydomonas reinhardtii and Rubisco mutants characterization.The most remarkable effect of the C172S mutant was a 15% increase in the value of the specificity factor compared to the wild-type enzyme, while the specificity factor of C192S Rubisco was identical to wild-type.The C192S enzyme was more sensitive to inactivation through oxidation of cysteines than the wild type and the rest of the enzymes. The results suggest that the Cys192 protects the critical modification of the Cys172. The results of thermal stability, proteolytic susceptibility assays and holoenzyme mobility in native electrophoresis show that the substitution of Cys172 and/or Cys192 affect to the enzyme structure. 2. Crystallization and Structure determination of C172S and C192S Rubisco mutants.X-ray structures of the mutant enzymes reveal that the substitution at position 172 causes a significant shift of the main chain backbone atoms of β-strand1 of the α/β-barrel.3. In Vivo turnover and inactivation of the C172S, C192S, C172S/C192S and wild-type Rubisco Enzymes in stressed Cells.The absence of Cys172 protects Rubisco from degradation under saline stress conditions. The C172S mutant enzyme is more resistant to inactivation under oxidative (diamide induced) stress.In a oxidative conditions (diamide stress) Cys172-Cys192 disulfide bond formation could act as a redox signaling pathway.
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Duta, Dana-Nicoleta. "Interaction of CysLT1 receptor with importin [alpha] proteins." Mémoire, Sherbrooke : Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/3367.

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Yaddaden, Louiza. "Caractérisation de variants du récepteur des cystéinyl leucotriènes de type 1, CysLT[indice inférieur 1]-G300S et CysLT[indice inférieur 1]-I206S." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/7515.

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Les cystéinyl-leucotriènes (cysLTs) sont des médiateurs lipidiques pro-inflammatoires impliqués dans l'asthme, liant trois récepteurs couplés aux protéines G: CysLT[indice inférieur 1], CysLT[indice inférieur 2] et GPR99. Des polymorphismes de deux de ces récepteurs, CysLT[indice inférieur 1]-G300S et CysLT[indice inférieur 2]-M201V, ont été fortement associés à l’atopie, une prédisposition aux allergies, alors que le polymorphisme CysLT[indice inférieur 1]-I206S n’y est pas significativement associé. Il a été montré précédemment que le variant CysLT[indice inférieur 2]-M201V avait une signalisation diminuée. L'objectif du projet était d'étudier la signalisation cellulaire des variants CysLT[indice inférieur 1]-G300S et CysLT[indice inférieur 1]-I206S, ainsi que l’interaction du variant CysLT[indice inférieur 1]-G300S avec le récepteur CysLT[indice inférieur 2]-M201V. La lignée cellulaire HEK-293 a été transfectée avec les ADNs plasmidiques codant pour des récepteurs de type sauvage et mutants. L’expression de surface des récepteurs a été vérifiée par cytométrie en flux. La production d’inositol phosphates (IPs) et la transactivation des promoteurs de l’IL-8 et de l’IL-13 ont été mesurées par essai IP-1 et essai luciférase, respectivement, en réponse au LTD[indice inférieur 4] et LTC[indice inférieur 4]. Ensuite, la phosphorylation de principaux effecteurs de signalisation (Erk1/2, p65, p38 et c-Jun) suite à l’activation des récepteurs par le LTD[indice inférieur 4], a été évaluée par immunobuvardage Western. Enfin, l’interaction entre les récepteurs a été étudiée par des expériences de BRET (Bioluminescence Resonance Energy Transfer) et BiFC (Bimolecular Fluorescent Complementation), en plus d’expériences de type fonctionnel en co-expression. L’expression de surface des récepteurs mutants et de type sauvage est équivalente. Le variant CysLT[indice inférieur 1]-G300S induit une plus forte production d’IPs et une plus grande transactivation des promoteurs de l’IL-8 et de l'IL-13 que le récepteur de type sauvage. De plus, la phosphorylation de Erk1/2 est également augmentée par l’activation de ce variant. Par contre, le récepteur CysLT[indice inférieur 1]-I206S ne montre pas de différence significative dans sa transduction de signal. La co-expression des récepteurs CysLT[indice inférieur 1]-G300S et CysLT[indice inférieur 2]-M201V n’affecte pas leur expression de surface, mais résulte en une faible transactivation du promoteur de l’IL-8 et une production réduite d’IPs en réponse au LTD[indice inférieur 4]. Enfin, les récepteurs ont la capacité d’interagir et de dimériser entre eux. En conclusion, ces résultats suggèrent que le variant CysLT[indice inférieur 1]-G300S induit une plus forte réponse que le récepteur de type sauvage. Cependant, bien qu’il puisse dimériser et interagir avec le variant CysLT[indice inférieur 2]-M201V, ce dernier domine la réponse combinée lorsqu’il est co-exprimé avec le variant CysLT[indice inférieur 1]-G300S.
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Poulin, Sébastien. "Modulation de l'expression du facteur angiogénique VEGF (vascular endothelial growth factor) par les cysteinyl-leucotriènes." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4007.

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Les cysteinyl-leucotriènes (cysLTs) ont des rôles majeurs dans la pathophysiologie de l'asthme et sont impliqués dans le remodelage des voies respiratoires, un processus caractérisé par plusieurs changements structuraux incluant entre autre [i.e. autres] la fibrogenèse et l'hyperplasie des cellules musculaires lisses. Dans cette étude, nous avons investigué le rôle potentiel des cysLTs dans la modulation du « vascular endothelial growth factor » (VEGF), un facteur de croissance connu pour être important dans une autre facette du remodelage, c'est-à-dire l'angiogenèse. Nous avons montré que le LTD[indice inférieur 4] induit l'expression du VEGF chez les monocytes humains et les cellules musculaires lisses bronchiques humaines avec une inhibition complète par un antagoniste spécifique du récepteur CysLT1. De plus, des cellules de reins embryonnaires humaines (HEK-293) transfectées d'une façon stable avec CysLT1 ont été utilisées pour étudier la régulation transcriptionnelle du promoteur du VEGF. La stimulation de ces cellules avec des cysLTs mène à l'activation du promoteur du VEGF d'une façon dépendante de la concentration et résistante à la Bordetella pertussis toxin (PTX). Aussi, il en résulte une augmentation de l'expression de l'ARNm et de la protéine du VEGF d'une façon dépendante du temps de stimulation. L'utilisation de mutants tronqués en 5' de la construction du promoteur du VEGF de type sauvage démontre que la région en amont de -90 Pb n'est pas requise pour sa régulation transcriptionnelle par les cysLTs. De plus, un prétraitement avec des inhibiteurs pharmacologiques des MAPKs suggère l'implication de JNK et ERK, mais pas de p38 dans l'activation du promoteur du VEGF par LTD[indice inférieur 4]. Également, l'inhibition partielle de l'activation du promoteur du VEGF via la surexpression des formes dominantes négatives des protéines JunD, FosB et Ras suggère un rôle actif pour le complexe AP-1. Cependant, puisqu'un mutant du promoteur avec des substitutions dans le site de liaison d'AP-1 maintient toujours sa transactivation par LTD[indice inférieur 4], le complexe AP-1 semble agir d'une façon indirecte. En fait, l'inhibition complète de l'activation du promoteur du VEGF et de l'augmentation subséquente de son ARNm par un prétraitement avec la mithramycine, un inhibiteur de la transcription Sp1-dépendante, suggère que AP-1 pourrait agir indirectement sur Sp1 pour la modulation du VEGF par les cysLTs. Par surcroît, des expériences utilisant un promoteur du VEGF (-123 +50 pb) avec tous ses sites Sp1 mutés (4) ont montré que ces régions étaient nécessaires à la transactivation du VEGF par LTD[indice inférieur 4]. Bref, nos résultats indiquent pour la première fois que les cysLTs peuvent activer transcriptionnellement la production du VEGF via le récepteur CysLT1, avec l'implication de JNK, ERK, AP-1 et Sp1. Ces résultats proposent que les cysLTs pourraient être importants dans le processus d'angiogenèse associé au remodelage des voies respiratoires et indiquent un possible bénéfice jusqu'à maintenant insoupçonné dans l'utilisation des antagonistes des récepteurs CysLT1 dans la prévention ou le traitement du remodelage dans l'asthme.
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Maia, Viviane Alves de Oliveira. "Imunoexpress?o do EGFR e da podoplanina em cistos radiculares e dent?geros." Universidade Federal do Rio Grande do Norte, 2014. http://repositorio.ufrn.br:8080/jspui/handle/123456789/17132.

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The radicular cysts (RCs) and dentigerous (DCs), despite having different etiologies, form a pathological cavity lined by epithelium, which grows due to the buildup of fluid inside, as the surrounding bone is reabsorbed and the epithelium will being induced to proliferate. The epithelial proliferation, which has been identified as one of the key processes in the growth of odontogenic cystic lesions, is influenced by growth factors such as EGFR (epidermal growth receptor factor) and podoplanin (PDPN), many of which may have its production stimulated mainly during inflammatory processes. The objective of this research was to evaluate and compare the immunohistochemical expression of EGFR and PDPN in 30 cases of RCs and 30 cases of DCs, semiquantitatively, in light microscopy, associating it with the degree of inflammation, cellular localization of immunostaining and with the immunostained epithelial layers. Data were statistically analyzed by Chi-square test and Fisher exact test, considering a significance level of 5 %. The results showed high immunoreactivity of both proteins in the lesions studied, only statistically significant difference was observed in immunostaining of PDPN (p=0.033), which proved higher in RCs. The other analyzed parameters showed no relevant significant differences. We conclude that, as EGFR and PDPN showed high immunoreactivity in cystic lesions analyzed, these proteins participate the pathogenesis of these lesions through the epithelial stimulation process, despite having different etiologies. Furthermore, it can infer that the higher immunostaining of PDNP in RCs that DCs showed no distinction indicator between the two lesions, regarding their etiologies, once this protein also showed a considerable expression in DCs, independent of the intensity of the inflammatory infiltrate
Os cistos radiculares (CRs) e dent?geros (CDs), apesar de possu?rem etiologias diferentes, formam uma cavidade patol?gica revestida por epit?lio, a qual cresce em fun??o do ac?mulo de l?quido em seu interior, ? medida que o osso ao redor ? reabsorvido e o epit?lio vai sendo induzido a proliferar. A prolifera??o epitelial, que tem sido apontada como um dos processos determinantes no crescimento das les?es c?sticas odontog?nicas, ? influenciada por fatores de crescimento como o EGFR (receptor do fator de crescimento epid?rmico) e a podoplanina (PDPN), muitos dos quais podem ter sua produ??o estimulada principalmente durante processos inflamat?rios. O objetivo desta pesquisa foi avaliar e comparar a express?o imunoistoqu?mica do EGFR e da PDPN em 30 casos de CRs e 30 casos de CDs, de forma semiquantitativa, em microscopia de luz, associando-a com o grau de inflama??o, localiza??o celular da imunocolora??o e com as camadas epiteliais imunomarcadas. Os dados foram avaliados estatisticamente por meio de testes do Qui-quadrado e Exato de Fisher, considerando-se um n?vel de signific?ncia de 5%. Os resultados mostraram que houve elevada imunorreatividade das duas prote?nas nas les?es estudadas, sendo observada apenas diferen?a estat?stica significativa na imunoexpress?o da PDPN (p=0,033), que se mostrou mais elevada nos CRs. Os demais par?metros analisados n?o demonstraram diferen?as significativas relevantes. Conclui-se que, como o EGFR e a PDPN apresentaram elevada imunoexpress?o nas les?es c?sticas analisadas, essas prote?nas participam da patog?nese dessas les?es atrav?s da estimula??o epitelial, apesar de apresentarem etiologias diferentes. Al?m disso, pode-se inferir que a maior imunomarca??o da PDPN em CRs do que em CDs n?o se mostrou indicador de distin??o entre as duas les?es, com rela??o ?s suas etiologias, uma vez que nestes ?ltimos essa prote?na tamb?m apresentou express?o consider?vel, independente da intensidade do infiltrado inflamat?rio
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Books on the topic "CysLT2"

1

James, Grant. Dermoid cyst of the ovary. [S.l: s.n., 1987.

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A, Zeeb Barbara, Smol J. P, and Wilkinson Anna N, eds. Atlas of chrysophycean cysts. Dordrecht: Kluwer Academic Publishers, 1995.

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Orr, Tamra. Ovarian tumors and cysts. New York: Rosen Pub. Group, 2009.

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Duff, Katharine E., Barbara A. Zeeb, and John P. Smol. Atlas of Chrysophycean Cysts. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-017-0809-8.

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Wilkinson, Anna N., Barbara A. Zeeb, and John P. Smol. Atlas of Chrysophycean Cysts. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0811-1.

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NATO Advanced Study Institute on Cyst Nematodes (1985 Martina Franca, Italy). Cyst nematodes. New YorK: Plenum Press, 1986.

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NATO Advanced Study Institute on Cyst Nematodes (1985 Martina Franca). Cyst nematodes. New York: Plenum in cooperation with NATO Scientific Affairs Division, 1986.

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NATO Advanced Study Institute on Cyst Nematodes (1985 Martina Franca, Italy). Cyst nematodes. New YorK: Plenum Press, 1986.

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Lamberti, F., and C. E. Taylor, eds. Cyst Nematodes. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2251-1.

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Perry, R. N., M. Moens, and J. T. Jones, eds. Cyst nematodes. Wallingford: CABI, 2018. http://dx.doi.org/10.1079/9781786390837.0000.

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Book chapters on the topic "CysLT2"

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Barua, Ranadhir. "Cysts (Skene’s Duct Cyst)." In Tumours of the Female Lower Genital Tract, 394–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74828-8_26.

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Arnold, M., and J. W. Lotz. "Hydatid Cysts (Echinococcus Cyst)." In ABC of Pediatric Surgical Imaging, 64–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-89385-1_32.

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Barua, Ranadhir. "Cysts and Cyst-like Conditions." In Tumours of the Female Lower Genital Tract, 270–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74828-8_21.

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Malik, Neelima. "Cysts of the “Oro-Maxillofacial Region”." In Oral and Maxillofacial Surgery for the Clinician, 549–75. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-1346-6_27.

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AbstractCysts of the Oro-Maxillofacial region have common occurrence in comparison to any other parts of the body. These can be true cysts or pseudocysts and can be found in the jaw bones or in the soft tissues. Cysts are of various types, and over the years, various classifications are put forward, which are helpful to identify each cyst, based on its origin and its clinical and histopathological presentation. Based on the classification, one can also decide the treatment plan accordingly. The classifications are given by various researchers and also by WHO. In this chapter, various odontogenic and nonodontogenic cysts and their treatment aspect are discussed in detail.
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Mazabraud, André. "Idiopathic cyst, juxta-articular and related cysts, epidermoid cyst, hydatid cyst." In Pathology of bone tumours, 317–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-95839-7_29.

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Larheim, Tore A. "Jaw Cysts and Cyst-Like Conditions." In Maxillofacial Imaging, 23–56. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53319-3_2.

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Teller, Peter, Hermann König, Ulrich Weber, and Peter Hertel. "Baker’s Cysts, Ganglion Cysts." In MRI Atlas of Orthopedics and Traumatology of the Knee, 175–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55620-3_11.

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Ishikawa, Kinya. "Cysts." In Adnexal Tumors of the Skin, 64–69. Tokyo: Springer Japan, 1987. http://dx.doi.org/10.1007/978-4-431-68054-3_4.

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Rossi, Armando, and Giorgio Rossi. "Cysts." In CT of the Peritoneum, 279–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56488-8_11.

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Braun-Falco, Otto, Gerd Plewig, Helmut H. Wolff, and Richard K. Winkelmann. "Cysts." In Dermatology, 977–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-00181-3_53.

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Conference papers on the topic "CysLT2"

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Lagemaat, M. W., L. G. E. Cox, M. L. Reilingh, C. C. van Donkelaar, B. van Rietbergen, L. Blankevoort, C. N. van Dijk, and K. Ito. "Fluid Pressure May Lead to Subchondral Bone Cyst Development via Mechanoregulated Bone Remodeling." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19582.

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Ankle trauma associated with an osteochondral defect (OD) of the talus often leads to subchondral bone cysts (Fig. 1, left). These cysts are associated with persistent ankle pain, thereby limiting the patients’ mobility [1]. Histology suggests that bone cyst development may occur in different stages, since some cysts are found to contain fluid, while others contain soft tissues. In addition, talar cysts may grow or shrink in time, and develop a sclerotic rim. The exact mechanism behind the development of talar cysts is unclear, but it has been proposed that fluid intrusion from the joint space through the OD plays a key role [1,2]. Pressurization of this fluid may have an osteolytic effect on the surrounding bone, thereby enlarging the cyst cavity.
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Elangovan, Shreehari, and Gregory M. Odegard. "Finite Element Modeling of Intraneural Ganglion Cysts of the Common Peroneal Nerve." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11637.

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Intraneural Ganglion Cysts [IGC] are a set of medical conditions that result in denervation of the muscles innervated by the cystic nerve leading to pain and loss of function. Current treatment approaches only temporarily alleviate pain and denervation which, however, does not prevent cyst recurrence. Hence, a mechanistic understanding of the pathogenesis of IGC can help clinicians understand them better and therefore device more effective treatment options. In this study, a preliminary analysis methodology is established to investigate the pathogenesis of IGC.
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Chahal, Amandeep, and Pushpa Dahiya. "Evaluation of ovarian reserve in women undergoing ovarian cystectomy by laparoscopy and laparotomy." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685295.

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Ovarian cysts are one of the commonest problems encountered in the gynecological field. Majority of these cysts are functional i.e., disappear spontaneously, while few need cystectomy. Ovarian cystectomy is done by laparotomy and laparoscopic technique. The method to achieve haemostasis in the ovarian bed after cyst removal varies with the type of technique. Electrocoagulation is used to achieve haemostasis in laparoscopic cystectomy while the bleeding vessels are sutured for haemostasis in cystectomy by laparotomy. Both the modalities of management varies in terms of compromise of ovarian reserve. The study was carried out to evaluate the surgical impact of benign ovarian masses on ovarian reserve as measured by serum levels of antimullerian harmone. In this prospective study on 30 women of reproductive age group with benign ovarian masses, 15 women were enrolled for laparoscopic ovarian cystectomy and another 15 women were enrolled for cystectomy by laparotomy and ovarian reserve was measured by levels of serum AMH preoperatively, postoperative one week and postoperative 3 months using standard ELISA assay kit. The preoperative, postoperative one week and postoperative 3 months levels of mean AMH were 4.74 ± 1.86 ng/ml, 2.92 ± 1.45 ng/ml and 2.64 ± 0.96 ng/ml respectively, in women undergoing laparoscopic cystectomy and 3.98 ± 1.35 ng/ml, 2.48 ± 0.64 ng/ml and 2.11 ± 0.63 ng/ml respectively in women undergoing ovarian cystectomy by laparotomy. So there was decline of mean AMH levels in postoperative one week and postoperative 3 months samples in both of the groups of enrolled women. However, this decline varied with the type of cyst removed and is insignificantly greater in laparoscopy group, wherein electrocoagulation may cause extensive and sustained damage to ovarian tissue.
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Deshpande, Deepak A., Capre Mitchell, Junyan Gu, Colin Funk, and Raymond B. Penn. "Regulation Of Cysteinyl Leukotriene (CysL) Type 1 Receptor (CysLT1R) By Protein Kinase C (PKC)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6360.

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Moyer, Matthew T., Setareh Sharzehi, Charles E. Dye, Wafik El-Deiry, Thomas J. McGarrity, Abraham Mathew, Niraj Gusani, Raquel E. Davila, and Brooke Ancrile. "Abstract B95: Is ethanol required for cyst ablation in patients with premalignant type pancreatic cysts?" In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b95.

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Lu, Victor, Avital Perry, Christopher Graffeo, Krishnan Ravindran, and Jamie Van Gompel. "Recurrence of Rathke’s Cleft Cysts Based on Gross Total Resection of Cyst Wall: A Meta-analysis." In 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702442.

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Ramachandran, Rajesh, Larry Siu, Vadim Kurbatov, Evan Grossman, Frank Gress, and Laura Martello. "Abstract B33: Classification of pancreatic cysts in a minority population through cytokine profiling of cyst fluid fine-needle aspirate." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b33.

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Iankov, Georgi, Mihail Plochev, Anatoli Semkov, Eluar Goranov, Vladimir Stanoev, and Danail Petrov. "Primary extrapulmonary intrathoracic hydatid cysts." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2530.

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Farzana Shahar Banu, A., M. Kayalvizhi, Banumathi Arumugam, and Ulaganathan Gurunathan. "Texture based classification of dental cysts." In 2014 International Conference on Control, Instrumentation, Communication and Computational Technologies (ICCICCT). IEEE, 2014. http://dx.doi.org/10.1109/iccicct.2014.6993152.

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Mestan, Hüseyin, Kenan Can Ceylan, and Şeyda Örs Kaya. "Surgery outcomes of the bronchogenic cysts." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1094.

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Reports on the topic "CysLT2"

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Fensome, R. A., and G. L. Williams. Dinoflagellate cyst PalyAtlas. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2019. http://dx.doi.org/10.4095/313575.

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Nelson, Brenda L. Solitary Bone Cyst. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada520056.

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Bissonnette, Kaitlyn, Travis Faske, and Albert Tenuta. Soybean Cyst Nematode. United States: Crop Protection Netework, April 2021. http://dx.doi.org/10.31274/cpn-20210423-0.

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Davies, E. H., and T. P. Poulton. Upper Jurassic Dinoflagellate Cysts From Strata of northeastern British Columbia. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1986. http://dx.doi.org/10.4095/120664.

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Lawson, Vincent, Gregory L. Tylka, Christopher C. Marett, and Gregory D. Gebhart. Soybean Cyst Nematode Resistant Soybean Trial. Ames: Iowa State University, Digital Repository, 2007. http://dx.doi.org/10.31274/farmprogressreports-180814-938.

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Fan, Ying. Total Cyst Excision of Type I Choledochal Cyst 2 Years After Roux-enY Hepatocholangiojejunostomy: Report of a Case. Science Repository OÜ, April 2019. http://dx.doi.org/10.31487/j.scr.2018.10.001.

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Ioannides, N. S. Dinoflagellate cysts from upper cretaceous-lower tertiary sections, Bylot and Devon Islands, Arctic Archipelago. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1986. http://dx.doi.org/10.4095/123641.

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Kurita, H., and T. Uchida. Dinoflagellate cysts from the JAPEX/JNOC/GSC Mallik 2L-38 gas hydrate research well. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1999. http://dx.doi.org/10.4095/210750.

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Tylka, Gregory L., Gregory D. Gebhart, Christopher C. Marett, Mark P. Mullaney, and Stith N. Wiggs. Evaluation of Soybean Varieties Resistant to Soybean Cyst Nematode. Ames: Iowa State University, Digital Repository, 2011. http://dx.doi.org/10.31274/farmprogressreports-180814-1142.

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Tylka, Gregory L., Gregory D. Gebhart, and Christopher C. Marett. Evaluation of Soybean Varieties Resistant to Soybean Cyst Nematode. Ames: Iowa State University, Digital Repository, 2010. http://dx.doi.org/10.31274/farmprogressreports-180814-569.

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