Готові списки джерел за темами / Senescence markers

Добірка наукової літератури з теми "Senescence markers"

Автор: Grafiati

Опубліковано: 13 квітня 2024

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Статті в журналах з теми "Senescence markers":

Adewoye, Adeolu Badi, Dimitris Tampakis, Antonia Follenzi, and Alexandra Stolzing. "Multiparameter flow cytometric detection and quantification of senescent cells in vitro." Biogerontology 21, no. 6 (August 10, 2020): 773–86. http://dx.doi.org/10.1007/s10522-020-09893-9.

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Abstract It has been over half a century since cellular senescence was first noted and characterized, and yet no consensus senescent marker has been reliably established. This challenge is compounded by the complexity and heterogenic phenotypes of senescent cells. This necessitates the use of multiple biomarkers to confidently characterise senescent cells. Despite cytochemical staining of senescence associated-beta-galactosidase being a single marker approach, as well as being time and labour-intensive, it remains the most popular detection method. We have developed an alternative flow cytometry-based method that simultaneously quantifies multiple senescence markers at a single-cell resolution. In this study, we applied this assay to the quantification of both replicative and induced senescent primary cells. Using this assay, we were able to quantify the activity level of SA β-galactosidase, the expression level of p16INK4a and γH2AX in these cell populations. Our results show this flow cytometric approach to be sensitive, robust, and consistent in discriminating senescent cells in different cell senescence models. A strong positive correlation between these commonly- used senescence markers was demonstrated. The method described in this paper can easily be scaled up to accommodate high-throughput screening of senescent cells in applications such as therapeutic cell preparation, and in therapy-induced senescence following cancer treatment.

Bojko, Agnieszka, Joanna Czarnecka-Herok, Agata Charzynska, Michal Dabrowski, and Ewa Sikora. "Diversity of the Senescence Phenotype of Cancer Cells Treated with Chemotherapeutic Agents." Cells 8, no. 12 (November 23, 2019): 1501. http://dx.doi.org/10.3390/cells8121501.

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It is acknowledged that cancer cells are able to undergo senescence in response to clinically used chemotherapeutics. Moreover, recent years have provided evidence that some drugs can selectively remove senescent cells. Therefore, it is essential to properly identify and characterize senescent cells, especially when it comes to cancer. Senescence was induced in various cancer cell lines (A549, SH-SY-5Y, HCT116, MDA-MB-231, and MCF-7) following treatment with doxorubicin, irinotecan, methotrexate, 5-fluorouracil, oxaliplatin, or paclitaxel. Treatment with tested chemotherapeutics resulted in upregulation of p21 and proliferation arrest without cytotoxicity. A comparative analysis with the use of common senescence markers (i.e., morphology, SA-β-galactosidase, granularity, secretory phenotype, and the level of double-stranded DNA damage) revealed a large diversity in response to the chemotherapeutics used. The strongest senescence inducers were doxorubicin, irinotecan, and methotrexate; paclitaxel had an intermediate effect and oxaliplatin and 5-fluorouracil did not induce senescence. In addition, different susceptibility of cancer cells to senescence was observed. A statistical analysis aimed at finding any relationship between the senescence markers applied did not show clear correlations. Moreover, increased SA-β-gal activity coupled with p21 expression proved not to be an unequivocal senescence marker. This points to a need to simultaneously analyze multiple markers, given their individual limitations.

Verma, Dinesh Kumar, Bo Am Seo, Anurupa Ghosh, Shi-Xun Ma, Karina Hernandez-Quijada, Julie K. Andersen, Han Seok Ko, and Yong-Hwan Kim. "Alpha-Synuclein Preformed Fibrils Induce Cellular Senescence in Parkinson’s Disease Models." Cells 10, no. 7 (July 5, 2021): 1694. http://dx.doi.org/10.3390/cells10071694.

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Emerging evidence indicates that cellular senescence could be a critical inducing factor for aging-associated neurodegenerative disorders. However, the involvement of cellular senescence remains unclear in Parkinson’s disease (PD). To determine this, we assessed the effects of α-synuclein preformed fibrils (α-syn PFF) or 1-methyl-4-phenylpyridinium (MPP+) on changes in cellular senescence markers, employing α-syn PFF treated-dopaminergic N27 cells, primary cortical neurons, astrocytes and microglia and α-syn PFF-injected mouse brain tissues, as well as human PD patient brains. Our results demonstrate that α-syn PFF-induced toxicity reduces the levels of Lamin B1 and HMGB1, both established markers of cellular senescence, in correlation with an increase in the levels of p21, a cell cycle-arrester and senescence marker, in both reactive astrocytes and microglia in mouse brains. Using Western blot and immunohistochemistry, we found these cellular senescence markers in reactive astrocytes as indicated by enlarged cell bodies within GFAP-positive cells and Iba1-positive activated microglia in α-syn PFF injected mouse brains. These results indicate that PFF-induced pathology could lead to astrocyte and/or microglia senescence in PD brains, which may contribute to neuropathology in this model. Targeting senescent cells using senolytics could therefore constitute a viable therapeutic option for the treatment of PD.

Kim, Seo Rin, Kai Jiang, Christopher M. Ferguson, Hui Tang, Xiaojun Chen, XiangYang Zhu, LaTonya J. Hickson, Tamara Tchkonia, James L. Kirkland, and Lilach O. Lerman. "Transplanted senescent renal scattered tubular-like cells induce injury in the mouse kidney." American Journal of Physiology-Renal Physiology 318, no. 5 (May 1, 2020): F1167—F1176. http://dx.doi.org/10.1152/ajprenal.00535.2019.

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Cellular senescence, a permanent arrest of cell proliferation, is characterized by a senescence-associated secretory phenotype (SASP), which reinforces senescence and exerts noxious effects on adjacent cells. Recent studies have suggested that transplanting small numbers of senescent cells suffices to provoke tissue inflammation. We hypothesized that senescent cells can directly augment renal injury. Primary scattered tubular-like cells (STCs) acquired from pig kidneys were irradiated by 10 Gy of cesium radiation, and 3 wk later cells were characterized for levels of senescence and SASP markers. Control or senescent STCs were then prelabeled and injected (5 × 105 cells) into the aorta of C57BL/6J mice. Four weeks later, renal oxygenation was studied in vivo using 16.4-T magnetic resonance imaging and function by plasma creatinine level. Renal markers of SASP, fibrosis, and microvascular density were evaluated ex vivo. Per flow cytometry, irradiation induced senescence in 80–99% of STCs, which showed increased gene expression of senescence and SASP markers, senescence-associated β-galactosidase staining, and cytokine levels (especially IL-6) secreted in conditioned medium. Four weeks after injection, cells were detected engrafted in the mouse kidneys with no evidence for rejection. Plasma creatinine and renal tissue hypoxia increased in senescent compared with control cells. Senescent kidneys were more fibrotic, with fewer CD31+ endothelial cells, and showed upregulation of IL-6 gene expression. Therefore, exogenously delivered senescent renal STCs directly injure healthy mouse kidneys. Additional studies are needed to determine the role of endogenous cellular senescence in the pathogenesis of kidney injury and evaluate the utility of senolytic therapy.

Kritsilis, Marios, Sophia V. Rizou, Paraskevi Koutsoudaki, Konstantinos Evangelou, Vassilis Gorgoulis, and Dimitrios Papadopoulos. "Ageing, Cellular Senescence and Neurodegenerative Disease." International Journal of Molecular Sciences 19, no. 10 (September 27, 2018): 2937. http://dx.doi.org/10.3390/ijms19102937.

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Ageing is a major risk factor for developing many neurodegenerative diseases. Cellular senescence is a homeostatic biological process that has a key role in driving ageing. There is evidence that senescent cells accumulate in the nervous system with ageing and neurodegenerative disease and may predispose a person to the appearance of a neurodegenerative condition or may aggravate its course. Research into senescence has long been hindered by its variable and cell-type specific features and the lack of a universal marker to unequivocally detect senescent cells. Recent advances in senescence markers and genetically modified animal models have boosted our knowledge on the role of cellular senescence in ageing and age-related disease. The aim now is to fully elucidate its role in neurodegeneration in order to efficiently and safely exploit cellular senescence as a therapeutic target. Here, we review evidence of cellular senescence in neurons and glial cells and we discuss its putative role in Alzheimer’s disease, Parkinson’s disease and multiple sclerosis and we provide, for the first time, evidence of senescence in neurons and glia in multiple sclerosis, using the novel GL13 lipofuscin stain as a marker of cellular senescence.

Coates, Philip J. "Markers of senescence?" Journal of Pathology 196, no. 4 (2002): 371–73. http://dx.doi.org/10.1002/path.1073.

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Wagner, Kay-Dietrich, and Nicole Wagner. "The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis." Cells 11, no. 12 (June 19, 2022): 1966. http://dx.doi.org/10.3390/cells11121966.

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It is widely accepted that senescent cells accumulate with aging. They are characterized by replicative arrest and the release of a myriad of factors commonly called the senescence-associated secretory phenotype. Despite the replicative cell cycle arrest, these cells are metabolically active and functional. The release of SASP factors is mostly thought to cause tissue dysfunction and to induce senescence in surrounding cells. As major markers for aging and senescence, p16INK4, p14ARF/p19ARF, and p21 are established. Importantly, senescence is also implicated in development, cancer, and tissue homeostasis. While many markers of senescence have been identified, none are able to unambiguously identify all senescent cells. However, increased levels of the cyclin-dependent kinase inhibitors p16INK4A and p21 are often used to identify cells with senescence-associated phenotypes. We review here the knowledge of senescence, p16INK4A, p14ARF/p19ARF, and p21 in embryonic and postnatal development and potential functions in pathophysiology and homeostasis. The establishment of senolytic therapies with the ultimate goal to improve healthy aging requires care and detailed knowledge about the involvement of senescence and senescence-associated proteins in developmental processes and homeostatic mechanism. The review contributes to these topics, summarizes open questions, and provides some directions for future research.

Kim, Gee-Hye, Yun Kyung Bae, Ji Hye Kwon, Miyeon Kim, Soo Jin Choi, Wonil Oh, Soyoun Um, and Hye Jin Jin. "Positively Correlated CD47 Activation and Autophagy in Umbilical Cord Blood-Derived Mesenchymal Stem Cells during Senescence." Stem Cells International 2021 (April 15, 2021): 1–13. http://dx.doi.org/10.1155/2021/5582792.

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Autophagy plays a critical role in stem cell maintenance and is related to cell growth and cellular senescence. It is important to find a quality-control marker for predicting senescent cells. This study verified that CD47 could be a candidate to select efficient mesenchymal stem cells (MSCs) to enhance the therapeutic effects of stem cell therapy by analyzing the antibody surface array. CD47 expression was significantly decreased during the expansion of MSCs in vitro ( p < 0.01 ), with decreased CD47 expression correlated with accelerated senescence phenotype, which affected cell growth. UCB-MSCs transfected with CD47 siRNA significantly triggered the downregulation of pRB and upregulation of pp38, which are senescence-related markers. Additionally, autophagy-related markers, ATG5, ATG12, Beclin1, and LC3B, revealed significant downregulation with CD47 siRNA transfection. Furthermore, autophagy flux following treatment with an autophagy inducer, rapamycin, has shown that CD47 is a key player in autophagy and senescence to maintain and regulate the growth of MSCs, suggesting that CD47 may be a critical key marker for the selection of effective stem cells in cell therapy.

Rossi, Clara, Marco Venturin, Jakub Gubala, Angelisa Frasca, Alberto Corsini, Cristina Battaglia, and Stefano Bellosta. "PURPL and NEAT1 Long Non-Coding RNAs Are Modulated in Vascular Smooth Muscle Cell Replicative Senescence." Biomedicines 11, no. 12 (December 6, 2023): 3228. http://dx.doi.org/10.3390/biomedicines11123228.

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Cellular senescence is characterized by proliferation and migration exhaustion, senescence-associated secretory phenotype (SASP), and oxidative stress. Senescent vascular smooth muscle cells (VSMCs) contribute to cardiovascular diseases and atherosclerotic plaque instability. Since there are no unanimously agreed senescence markers in human VSMCs, to improve our knowledge, we looked for new possible senescence markers. To this end, we first established and characterized a model of replicative senescence (RS) in human aortic VSMCs. Old cells displayed several established senescence-associated markers. They stained positive for the senescence-associated β-galactosidase, showed a deranged proliferation rate, a dramatically reduced expression of PCNA, an altered migratory activity, increased levels of TP53 and cell-cycle inhibitors p21/p16, and accumulated in the G1 phase. Old cells showed an altered cellular and nuclear morphology, downregulation of the expression of LMNB1 and HMGB1, and increased expression of SASP molecules (IL1β, IL6, IL8, and MMP3). In these senescent VSMCs, among a set of 12 manually selected long non-coding RNAs (lncRNAs), we detected significant upregulation of PURPL and NEAT1. We observed also, for the first time, increased levels of RRAD mRNA. The detection of modulated levels of RRAD, PURPL, and NEAT1 during VSMC senescence could be helpful for future studies on potential anti-aging factors.

Galvis, Daniel, Darren Walsh, Lorna W. Harries, Eva Latorre, and James Rankin. "A dynamical systems model for the measurement of cellular senescence." Journal of The Royal Society Interface 16, no. 159 (October 9, 2019): 20190311. http://dx.doi.org/10.1098/rsif.2019.0311.

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Senescent cells provide a good in vitro model to study ageing. However, cultures of ‘senescent’ cells consist of a mix of cell subtypes (proliferative, senescent, growth-arrested and apoptotic). Determining the proportion of senescent cells is crucial for studying ageing and developing new anti-degenerative therapies. Commonly used markers such as doubling population, senescence-associated β-galactosidase, Ki-67, γH2AX and TUNEL assays capture diverse and overlapping cellular populations and are not purely specific to senescence. A newly developed dynamical systems model follows the transition of an initial culture to senescence tracking population doubling, and the proportion of cells in proliferating, growth-arrested, apoptotic and senescent states. Our model provides a parsimonious description of transitions between these states accruing towards a predominantly senescent population. Using a genetic algorithm, these model parameters are well constrained by an in vitro human primary fibroblast dataset recording five markers at 16 time points. The computational model accurately fits to the data and translates these joint markers into the first complete description of the proportion of cells in different states over the lifetime. The high temporal resolution of the dataset demonstrates the efficacy of strategies for reconstructing the trajectory towards replicative senescence with a minimal number of experimental recordings.

Більше джерел

Дисертації з теми "Senescence markers":

dos, Santos Soares Martins de Castro Alicia Maria. "A mechanistic investigation into candidate markers of telomere-induced senescence in normal human epidermal keratinocytes." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8034.

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Telomere dysfunction is one mechanism of cellular and tissue ageing. Dysfunctional telomeres in fibroblasts are recognised as DNA double-strand breaks (DSBs) and trigger the DNA damage pathway of senescence. However, telomere uncapping in normal human epidermal keratinocytes, via expression of the dominant negative mutant of the telomere repeat-binding factor 2 (TRF2!B!M), resulted in a senescent-like arrest without a significant DNA damage response (DDR). This suggests that either keratinocytes are unusually sensitive to telomere uncapping and the low DDR is sufficient to induce senescence or that dysfunctional telomeres may also be signalled through an alternative pathway. Subsequent analysis revealed genes HIST2H2BE, ICEBERG, S100A7 and HOPX as potential markers for telomere dysfunction-induced senescence (TDIS) since they were induced by telomere uncapping and seemed to be regulated by telomerase. The aim of this project was to assess the specificity of these candidate markers for TDIS and to select the most promising for use as a biomarker. To this end, keratinocytes were exposed to doses of ionising radiation, capable of generating transient or permanent damage to the DNA, or transduced with retroviral constructs expressing p14ARF, p16INK4a, p53 or TRF2!B!M and the gene expression levels of the candidates assessed after a recovery period or at the early stages of senescence. Whilst S100A7, HOPX or ICEBERG were not induced by a transient or persistent DDR or by p16INK4a, ICEBERG and HOPX were induced by p53 and p14ARF when these were ectopically expressed at higher levels. Thus, S100A7 seems to be the most specific early marker for telomere dysfunction in keratinocytes since it was selectively induced by telomere uncapping via expression of TRF2!B!M and not by DSBs or by over expression of p14ARF, p53 or p16INK4a. S100A7 may have the potential to identify cells with telomere dysfunction in human epithelia and body fluids.

Althubiti, Mohammad Ahmad M. "Characterisation of novel markers and effectors of senescence and their role in cancer and ageing." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/39408.

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Cellular senescence is a reversible cell cycle arrest that has been shown to play a role in aging and cancer. Senescent cells accumulation can occur prematurely, as seen in response of stress and oncogenic insults, or normally, as observed in organismal aging. Thus, identification and studying senescent cells in vivo and in vitro have an important diagnostic and therapeutic potential. In addition, the molecular mechanisms involved in establishing and maintaining senescence are not fully understood. Consequently, the current approach that is used for senescent identification has limitations. For this reason, we characterized a list of potential markers of senescence from a proteomic screening of plasma membrane of senescent cells. From the list, we have validated 10 of them, namely, DEP1, NTAL, EBP50, STX4, VAMP3, ARMCX3, B2MG, LANCL1, VPS26A and PLD3 that are differently expressed in different model of cell senescence. These markers can be combined to detect senescent cells in vitro or in tissue sections. We also proposed a FACS based method using two markers (DEP1 and B2MG) with known extracellular epitopes. This could facilitate the senescence detection and studying. From the proteomic screening, we also found that BTK is elevated in senescent cells. BTK was induced in response of p53 activation due to different stimuli. Moreover, phosphorylation of ATM, p53 at ser15 and γH2AX was increased after BTK overexpression, which suggested the involvement of BTK in DNA damage pathways. BTK was able to phosphorylate p53 directly at N-terminus. BTK inhibition with chemicals or RNAi depletion was sufficient to bypass senescence. In addition, BTK inhibitors were also able to extend life span in flies. p53 KO flies did not show any difference in life span after using BTK inhibitors, which showed the importance of BTK in p53-mediated senescence. BTK inhibition also decreased the senescent cells accumulation in flies. All these data collectively suggest the possibility of using BTK inhibitors to ameliorate aging-associated disorders.

Xia, Chen. "Genetic typing of the Senescence-Accelerated immunoreactivity in the Mouse (SAM) strains with Microsatellite markers." Kyoto University, 1999. http://hdl.handle.net/2433/181698.

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要旨pdfファイル:タイトル「Genetic typing of the Senescence-Accelerated the Mouse (SAM) strains with Microsatellite markers」
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第7729号
医博第2082号
新制||医||707(附属図書館)
UT51-99-G323
京都大学大学院医学研究科脳統御医科学専攻
(主査)教授芹川忠夫, 教授日合弘, 教授笹井芳樹
学位規則第4条第1項該当

Targa, Laurie. "Contribution to the study of mesenchymal stromal / stem cells heterogeneity, focus on surface markers and senescence." Thesis, Université de Lorraine, 2019. https://docnum.univ-lorraine.fr/ulprive/DDOC_T_2019_0353_TARGA.pdf.

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Les Cellules Stromales / Souches Mésenchymateuses (CSM) ont un grand potentiel pour de nombreuses applications. Elles sont les cellules les plus utilisées pour les essais cliniques développant des thérapies cellulaires. L’efficacité thérapeutique des CSM est influencée par leur amplification in vitro et d’autres facteurs tels que les paramètres liés au donneur de cellules. Pour améliorer les thérapies à base de CSM, cette étude a ciblé l’étude de leur hétérogénéité grâce à leurs marqueurs de surface, qui permettent de mutualiser la caractérisation des cellules et la possibilité de trier des cellules vivantes. Le premier objectif de ce travail a été de décrire la variabilité des CSM entre et au sein d’échantillons venant de moelle osseuse de donneurs d’âges différents. Le deuxième objectif a été de développer une méthode de tri pour séparer les CSM selon leur expression de CD146 et de comparer les cellules triées. La troisième partie du travail a eu pour objectif de mieux connaître les marqueurs de surface des CSM sénescentes. Les résultats de cytométrie en flux sur les CSM sont soumis à de fortes fluctuations, mais certaines régularités ont pu être mises en évidence. Un ensemble de marqueurs de surface a pu être associé avec l’âge des donneurs : CD146, CD71, CD105, CD44. De plus, des liens entre l’expression de CD146, CD140b et CD71 ont été observés avec la capacité de prolifération des CSM. Des CSM de moelle osseuse provenant de donneurs d’âges différents et à différentes étapes de culture ont pu être triées avec succès selon leur expression de CD146 par une méthode immunomagnétique. Le comportement des CSM triées était encore hétérogène mais il a pu être observé que les CSM exprimant plus fortement CD146 avaient plus souvent de meilleures capacités de différentiation et de migration et étaient moins sénescentes que les cellules exprimant plus faiblement CD146. Une étude protéomique a montré que la plupart des protéines de surface détectées avaient tendance à être moins représentées sur les cellules sénescentes à l’exception de CD157. Les CSM à différentes étapes de culture jusqu’à la sénescence réplicative ont ensuite été suivies par cytométrie en flux. Cette dernière étude a révélé d’importantes fluctuations entre les différents passages, soulignant la difficulté associée à l’utilisation de ces marqueurs. Les marqueurs CD146, CD71, CD140b et CD157 méritent d’être suivis pour le contrôle qualité des CSM provenant de moelle osseuse
Mesenchymal Stromal / Stem Cells (MSC) hold great potential and are currently the most used in clinical trials with cell-based treatments. MSC quality and therapeutic effectiveness are influenced by in vitro expansion but also by other factors such as donor parameters. To ameliorate the success rate of MSC therapies, this study focused on MSC heterogeneity. To put together cell characterization and ways to act when facing cell heterogeneity, this work was oriented toward the study of surface markers that can be monitored on living cells, and can serve to sort them. The first objective was to describe initial MSC surface markers variability between and within different bone marrow MSC samples from donors of different ages. The second objective was to develop a sorting method to separate MSC according to CD146 expression and compare the sorted cells. The third objective was to widen MSC surface markers knowledge by focusing on senescent MSC. Surface markers of early passage and replicative senescent cells were compared with proteomics and flow cytometry. Flow cytometry results on MSC were shown to be submitted to strong fluctuations. However, some regularities were strong enough to stand out. A group of surface markers were found to be associated with donor age: CD146, CD71, CD105, CD44. CD146, CD140b and CD71 were also correlated with proliferation rate. CD146 expression had the particularity to be relatively stable in culture and turned out to be the most heterogeneously expressed when looking at cell population within the samples. Cultivated MSC from bone marrow coming from donor of different ages and at different culture steps were sorted successfully according to CD146 expression with immunomagnetic method. MSC behavior remained heterogeneous after sort but it could still be observed that most CD146high cells had more often better differentiation and migration capacities and were less senescent than their CD146low counterpart. Proteomics study showed that almost all surface proteins expression tended to decrease on replicative senescent MSC, except one marker that increased: CD157. MSC at different stages of culture until replicative senescence were then studied by flow cytometry. This study revealed strong fluctuation in marker expression between different passages, highlighting again the variability of MSC behavior and the difficulty to predict it. CD146, CD71, CD140b, CD157 and SSC deserve to be followed for MSC quality control

Chakraborti, Subhendu. "Structural enzymology of human senescence marker protein 30 (SMP30) insights into the gluconolactonase mechanism and role of metal ions /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 201 p, 2009. http://proquest.umi.com/pqdweb?did=1891590551&sid=1&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Maggiorani, Damien. "Caractérisation de la sénescence des cardiomyocytes et identification de marqueurs associés." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30320/document.

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Le vieillissement de l'organisme prédispose à de nombreuses pathologies chroniques telles que l'insuffisance cardiaque (IC). Des études récentes ont montré que l'accumulation de cellules sénescentes dans les organes au cours du vieillissement est associée à l'apparition de ces pathologies. La sénescence cellulaire a initialement été décrite comme un arrêt stable du cycle cellulaire permettant de limiter la prolifération des cellules dont l'ADN est endommagé. Ce processus s'accompagne de profondes modifications de la fonction cellulaire, avec notamment l'acquisition d'un phénotype sécrétoire associé à la sénescence. La sénescence peut être induite par un raccourcissement des télomères ou par l'exposition à des signaux de stress, tels que le stress oxydant ou l'irradiation, qui entrainent l'activation de la réponse cellulaire aux dommages de l'ADN et l'expression des gènes suppresseurs de tumeurs (p16INK4a, p21CIP1, p53). Ces inhibiteurs du cycle cellulaire sont classiquement utilisés comme marqueur de sénescence car leur expression augmente de manière ubiquitaire au cours du vieillissement. Toutefois, ces marqueurs ne sont pas spécifiques du tissu concerné et un des objectifs de ma thèse a été d'identifier de nouveaux marqueurs de sénescence tissu-spécifiques qui pourraient caractériser un vieillissement cardiaque pathologique. Le vieillissement cardiaque se caractérise par une hypertrophie des cardiomyocytes, une sensibilité accrue au stress et une prédisposition à l'IC. Les cardiomyocytes étant des cellules post-mitotiques, les mécanismes de sénescence mis en jeu, les marqueurs associés et leur rôle potentiel dans l'IC demeurent à l'heure actuelle peu caractérisés. Au cours de ce travail de thèse nous avons donc entrepris : 1) d'étudier le rôle des télomères et des dysfonctions mitochondriales dans l'induction de la sénescence du cardiomyocyte et 2) d'identifier des marqueurs spécifiques. Nous avons tout d'abord montré que les cardiomyocytes de souris âgées expriment les marqueurs classiques de la sénescence comme p16INK4a, p53 et p21CIP1. Concernant les mécanismes inducteurs, nous avons étudié l'implication des dommages télomériques (telomere associated foci, TAF). Au cours du vieillissement, nous avons observé une augmentation du nombre de TAFs par cardiomyocytes en association avec l'hypertrophie. De plus, l'induction de TAFs in vitro est suffisante à l'activation de la voie de sénescence p53/p21CIP1 et l'hypertrophie dans une lignée de cardiomyoblastes H9c2. La formation des TAFs est augmentée chez des souris avec une dysfonction mitochondriale et est associée à l'activation des voies p53/p21CIP1. Par ailleurs, les cardiomyocytes âgés présentent une dérégulation des gènes impliqués dans la biologie mitochondriale pouvant rendre compte de l'augmentation des TAFs. Par l'analyse haut débit du transcriptome (RNAseq) nous avons identifié six nouveaux gènes qui sont surexprimés dans les cardiomyocytes sénescents (Prom2, Kcnk1, Pah, Edn3, Gdf15, Tgfb2). La comparaison d'expression de ces gènes dans le cœur avec d'autres tissus et avec le stroma cardiaque lors vieillissement a permis de confirmer la spécificité d'expression de ces marqueurs au niveau des cardiomyocytes. Nous avons validé cette signature dans deux modèles in vitro de sénescence induite par le stress et démontré que l'expression de certains de ces marqueurs est dépendante de la voie p53. De plus, l'expression de Prom2 est associée à l'hypertrophie des cardiomyocytes. En conclusion, nous avons démontré, qu'avec le vieillissement, les cardiomyocytes présentent un programme de sénescence associé à une dysfonction mitochondriale et une augmentation des TAFs. Cette sénescence se caractérise par l'activation des voies classiques de sénescence (p16INK4, p53/p21CIP1), une hypertrophie et l'acquisition d'une signature spécifique. Ces marqueurs offrent de nouvelles perspectives dans la compréhension de la sénescence cardiaque et dans son implication potentielle dans l'IC
Ageing of the organism is associated with several chronic pathologies such as heart failure (HF). Recent studies have demonstrated the link between the accumulation of senescent cells during ageing and age-associated diseases. Cellular senescence, originally defined as a stable cell cycle arrest, acts as a tumorigenic repressor by limiting the proliferation of DNA damaged cells. Despite this protective effect, senescence is characterized by deep remodeling of cell biology which drives functional disorders, such as the acquisition of a senescence-associated secretory phenotype (SASP). Senescence can be induced by telomeric attrition and by exposition to cellular stress signals such as oxidative stress or irradiation, which induce telomeric damage, activation of the DNA Damage Response (DDR) and increased expression of antitumoral genes (p16INK4a, p21CIP1, p53). These genes are classically used as markers of senescence because their expression increases in several tissues during ageing but they are not tissue-specific. Therefore, At the cardiac level, ageing is characterized by cardiomyocytes hypertrophy, increased sensitivity to stress and highest risk of developing HF. Cardiomyocytes are post- mitotic cells and the senescence inductor mechanisms, specifics markers and their role in HF remains poorly understood. This thesis project is articulated around two aims, 1/ studying the role of telomeric damages and mitochondrial dysfunction in triggering cardiomyocyte senescence and 2/ identification of specifics markers. Fisrtly, we shown that aged cardiomyocytes overexpress classic markers of senescence such as p16INK4a, p53 et p21CIP1. Concerning the inductors mechanisms, we studied the implication of telomeric damages (telomere associated foci, TAF). During ageing, we found an increased number of TAFs per cardiomyocytes and their association with hypertrophy. Moreover, TAF- induction in cardiac H9c2 in vitro activated the p53/p21 pathway and induced senescence. These data confirmed the role of TAFs in cardiomyocyte senescence induction. Furthermore, aged cardiomyocytes exhibit a global alteration of genes involved in mitochondrial biology, oxidative stress and metabolism in aged cardiomyocytes that could play a prominent role in TAF accumulation with ageing. In a second part of the study, by using a next generation sequencing method (RNA-seq) we identified 6 new genes highly expressed in senescent cardiomyocytes (Prom2, Kcnk1, Pah, Edn3, Gdf15 and Tgfb2). Expression comparison with other senescent organs and cardiac stromal cells confirmed these new genes as cardiomyocyte specific. Thanks to an in vitro approach, we validate this signature by using different models of stress-induced senescence in cardiac H9c2 cells and demonstrated the implication of the p53 in the regulation of some of these genes. Moreover, Prom2 expression is associated with cardiomyocytes hypertrophy. In conclusion, we demonstrated that, with ageing, cardiomyocytes display a senescence phenotype associated with mitochondrial dysfunction and TAFs. This process is characterized by classic markers (p16INK4, p53/p21CIP1), hypertrophy and new identified signature. These new markers offer innovative perspectives in the understanding and the identification of the cardiac senescence and their potential deleterious role in heart failure

Dotou-Huetz, Mazzarine. "Towards selective bifunctional senolytic compounds : design, mechanistic studies and proof of concept." Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS652.pdf.

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Le vieillissement s'accompagne d'un déclin des propriétés régénératrices de la plupart des tissus, et l’accumulation de cellules sénescentes au cours de l’âge est associée à ce déclin. La sénescence est une réponse cellulaire dû au raccourcissement des télomères ou à l’exposition aux stress provoquant une accumulation de dommages à l’ADN et / ou un stress oxydant. Cette réponse cellulaire est caractérisée par un arrêt irréversible du cycle cellulaire, une augmentation de l’activité β-galactosidase associée à la sénescence ainsi que la sécrétion du Senescence-Associated Secretory Phenotype ou SASP composé de cytokines, chimiokines, facteurs de croissance et protéases. La composition de ce SASP et par conséquent son rôle, dépendent du type cellulaire et de la nature du stress inducteur de sénescence et contribue aux effets délétères des cellules sénescentes. Parmi les tissus affectés, les muscles du squelette représentent un paradigme pour explorer les stratégies régénératives. Grâce à une population de cellules souches musculaires qui peuvent s'activer, proliférer et se différencier pour former de nouvelles myofibres, le muscle possède une remarquable capacité de régénération après blessure. Au cours du vieillissement et dans certaines dystrophies musculaires, ce potentiel s’épuise en raison de l'entrée progressive des cellules souches musculaires en sénescence. Le développement d’une sénotherapie basée sur l’utilisation de composés sénolytiques, capables d'éliminer les cellules sénescentes constitue donc une stratégie prometteuse. Cependant, les composés actuellement disponibles se caractérisent par un manque de spécificité. Ce travail de thèse a consisté à concevoir, synthétiser et évaluer pour la première fois deux nouveaux types de composés bifonctionnels innovants avec une sélectivité optimisée en ciblant la DPP4, protéase membranaire surexprimée sur la surface des cellules sénescentes. Le premier composé est la conjugaison entre le sénolytique puissant et un ligand de haute affinité de la DPP4 permettant un adressage moléculaire. La seconde est caractérisée, en plus, par un linker immolable, sensible à l’activité β-galactosidase associée à la sénescence permettant la libération spécifique du sénolytique au sein des cellules sénescentes. Les évaluations de ces composés ont été réalisé sur différentes lignées rendues sénescentes par différents stress et comparés à des sénolytiques et sénormorphiques de référence. En conclusion, les molécules bifonctionnelles développées au cours de cette thèse possèdent un pouvoir sénolytique similaire à la Piperlongumine, agent sénolytique utilisé pour la conception avec une sélectivité améliorée vis-à-vis des cellules non-sénescentes comparative aux sénolytiques de référence, Quercetin et Dasatinib par exemple. L’étude du mode d’action de la Piperlongumine a également été étudié, en particulier de l’état métabolique quelques cibles intracellulaires. Nos données constituent ainsi une excellente base pour développer un nouveau format de sénomodulateurs avec une sélectivité améliorée à des fins de régénération musculaire
Ageing is accompanied by a decline in the regenerative properties of most tissues, and the accumulation of senescent cells as we age is associated with this decline. Senescence is a cellular response due to telomere shortening or exposure to stresses causing an accumulation of DNA damage and/or oxidative stress. This cellular response is characterized by an irreversible cell cycle arrest, an increase in the β-galactosidase activity associated with senescence and the secretion of the Senescence-Associated Secretory Phenotype or SASP composed of cytokines, chemokines, growth factors and proteases. The composition of this SASP, and therefore its role, depends on the cell type and the nature of the senescence-inducing stress, and contributes to the deleterious effects of senescent cells. Among the tissues affected, skeletal muscle represents a paradigm for exploring regenerative strategies. Thanks to a population of muscle stem cells that can activate, proliferate and differentiate to form new myofibers, muscle has remarkable capacity for regeneration after injury. During the ageing process and muscular dystrophies, this potential is depleted as muscle stem cells gradually enter senescence. The development of senotherapy based on the use of senolytic compounds capable of eliminating senescent cells is therefore a promising strategy. However, the compounds currently available lack specificity. This thesis involved designing, synthesizing and evaluating for the first time two new types of innovative bifunctional compounds with optimized selectivity targeting DPP4, a membrane protease overexpressed on the surface of senescent cells. The first compound is characterized by a conjugation between a potent senolytic and a high-affinity ligand for DPP4, enabling molecular addressing. The second is additionally characterized by an immolative linker, sensitive to the senescence associated β-galactosidase activity, enabling specific release of the senolytic within senescent cells. These constructs were evaluated on different cell lines rendered senescent by various stresses and compared with reference senolytics and senormorphics. In conclusion, the bifunctional molecules developed during this thesis have a senolytic power similar to that of Piperlongumine, the parent senolytic agent used for design purposes, with improved selectivity towards non-senescent cells compared with reference senolytics such as Quercetin and Dasatinib. The mode of action of Piperlongumine was also studied in particular metabolism disruption, and intracellular targets. Hence, our data constitute an excellent basis to develop a new format of senomodulators with improved selectivity for muscle regeneration strategy purposes

Morcinek, Kerstin [Verfasser]. "Brainstem of the P301L tau transgenic pR5 model : pattern of tau hyperphosphorylation and neurotransmitter markers in senescent mice / Kerstin Morcinek." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1037403789/34.

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Vijayalakshmi, Kolluru. "Physiological and genetic analyses of post-anthesis heat tolerance in winter wheat (Triticum aestivum L.)." Diss., Manhattan, Kan. : Kansas State University, 2007. http://hdl.handle.net/2097/300.

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Labarthe, Laura. "Immunothérapie et infection VIH-1 : étude préclinique dans un modèle de souris humanisée pour le système immunitaire Frontline Science: Exhaustion and senescence marker profiles on human T cells in BRGSF-A2 humanized mice resemble those in human samples Pharmacokinetics and tissue distribution of Tenofovir, Emtricitabine and Dolutegravir in a murine model humanized for the immune system Combination of immunotherapies and ART during chronic HIV infection: Blocking type I interferon signaling reduces PD-Ll expression on T cells in BRGSFA2 humanized mice." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASQ005.

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Malgré l’apport du traitement antirétroviral (ART), l’infection chronique par le virus de l’immunodéficience humaine de type 1 (VIH-1) reste associée à des défauts immunitaires. En association au traitement ART, des immunothérapies pourraient notamment permettre d’agir sur l’inflammation à bas bruit et/ou l’épuisement. La mise en place d’un modèle préclinique est nécessaire pour évaluer l’efficacité de stratégies ciblant la voie PD1/PD-L1. Nous avons utilisé le modèle de souris humanisée pour le système immunitaire (HIS) Balb/c Rag2KO IL2rγcKO SirpαNOD Flk2KO HLA-A2HHD (BRGSF-A2). Nous avons confirmé le développement physiologique du compartiment T humain dans ce modèle, et montré des profils d’épuisement (PD1, TIGIT) et de sénescence (CD57) similaires à ceux observés chez l’homme. Nous avons ensuite développé un modèle HIS d’infection contrôlée par trithérapie et évalué l’impact de thérapies ciblant la voie PD1/PD-L1. Dans un modèle d’interruption du traitement ART, nous n’avons pas observé d’effets majeurs d’un blocage αPD1 préalable à l’arrêt du traitement ART. Ce résultat pourrait être lié à l’absence de modification de l’expression de PD1 à la surface des lymphocytes T (LT) au cours de l’infection ou du traitement ART. A l’inverse, nous avons observé une modification des proportions de LT PD-L1⁺ en phase aiguë et durant le traitement ART. L’ajout du traitement αJAK accentuait la diminution de la proportion de LT PD-L1⁺ déjà observée sous ART.Cibler la voie IFN-I permettrait à la fois de moduler l’inflammation et l’épuisement et constituerait un nouveau levier pour améliorer la qualité des réponses dans le contexte de l’infection VIH-1 contrôlée
Despite the success of antiretroviral treatment (ART), chronic infection with human immunodeficiency virus type 1 (HIV-1) associates with various immune defects. The combination of immunotherapies with ART may be a promising strategy to modulate low-grade inflammation, and/or exhaustion. The development of a preclinical model is required to evaluate the efficacy of therapies targeting the PD1-PDL1 pathway. In this work, we used the Balb/c Rag2KO IL2rγcKO SirpαNOD Flk2KO HLA-A2HHD (BRGSF-A2) humanized immune system (HIS) mouse model.We confirmed the physiological development of the human T cell compartment in this model, and observed similar exhaustion (PD1, TIGIT) and senescence (CD57) profiles on T cells in HIS mice, as those observed in humans. We next developed an HIS model of controlled infection induced by tritherapy and evaluated the impact of therapies targeting the PD1/PD-L1 pathway. In a model of ART interruption, we did not observe any major effects of αPD1 blockage induced prior to ART treatment interruption. This result may be related to the absence of modulation of PD1 expression on T cells during infection or ART treatment. On the contrary, we observed changes in the proportion of PD-L1⁺ T cells in the acute phase of the infection, and also during ART treatment. The addition of αJAK reinforced the reduction in the proportion of PD-L1⁺ T cells, already observed upon ART treatment.Targeting the IFN-I signaling pathway appears to modulate both inflammation and exhaustion. It may represent a valuable strategy to improve immune responses during chronic controlled HIV-1 infection

Книги з теми "Senescence markers":

Tollefsbol, Trygve O. Biological Aging: Methods and Protocols. Humana Press, 2014.

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Tollefsbol, Trygve O. Biological Aging: Methods and Protocols. Humana Press, 2017.

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Ferraro, Kenneth F. Causality. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190665340.003.0002.

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Gerontologists are often skeptical of age as a presumed cause of the aging process. Although age is an indispensable marker of life experiences, it is a rather crude indicator of the many factors that actually shape the aging experience, including senescence. To address the multiple meanings associated with age, some gerontologists have advanced concepts such as biological age or functional age. These are useful concepts, isolating one domain or facet of aging, but even these concepts must be applied with a skepticism for age effects. Gullible gerontology ensues when well-meaning persons accept age as an explanatory variable and disregard or minimize other factors or processes that are associated with age differences. Gerontologists prioritize longitudinal research designs and urge caution when one attempts to generalize from age differences. Concepts such as terminal drop and the age-period-cohort are used to illustrate this axiom.

Частини книг з теми "Senescence markers":

Carnero, Amancio. "Markers of Cellular Senescence." In Methods in Molecular Biology, 63–81. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-239-1_4.

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Zhao, Liming, Yan Xia, Xiao-Yuan Wu, Jos H. M. Schippers, and Hai-Chun Jing. "Phenotypic Analysis and Molecular Markers of Leaf Senescence." In Methods in Molecular Biology, 35–48. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7672-0_3.

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Storer, Mekayla, and William M. Keyes. "Detection of Senescence Markers During Mammalian Embryonic Development." In Methods in Molecular Biology, 199–210. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_19.

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Xia, Xiuying. "Phenotypic Analysis and Molecular Markers of Plant Nodule Senescence." In Methods in Molecular Biology, 65–80. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7672-0_5.

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Fan, Dorothy N. Y., and Clemens A. Schmitt. "Detecting Markers of Therapy-Induced Senescence in Cancer Cells." In Methods in Molecular Biology, 41–52. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_4.

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Jose, Shyam Sushama, Kamila Bendickova, and Jan Fric. "High-Throughput Screening of Senescence Markers in Hematopoietic Stem Cells Derived from Induced Pluripotent Stem Cells." In Methods in Molecular Biology, 121–30. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7792-5_10.

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Fletcher, David, and Murray G. Efford. "Effect of Senescence on Estimation of Survival Probability When Age Is Unknown." In Modeling Demographic Processes In Marked Populations, 1037–53. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-78151-8_47.

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Althubiti, Mohammad, and Salvador Macip. "Detection of Senescent Cells by Extracellular Markers Using a Flow Cytometry-Based Approach." In Methods in Molecular Biology, 147–53. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_14.

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Bala, Jyoti, Anupam J. Das, and Hoshang Unwalla. "Senescence-Associated Markers." In Senescence Signalling and Control in Plants, 273–81. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-813187-9.00017-2.

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Cross, Heide S., and Enikö Kallay. "Induction of differentiation of human intestinal cells in vitro." In Cell Growth, Differentiation and Senescence, 241–62. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780199637690.003.0012.

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Abstract The intestinal epithelium is, in principle, a valuable tissue for the study of cell differentiation, as it is spatially organized around its proliferative units, the crypt (small intestine) or the basal section of the crypt (large intestine). The progeny of clonal undifferentiated proliferating cells express eventually at least four very different phenotypes (1), e.g. enterocytes, mucin-producing goblet cells, endocrine cells, and Paneth cells. The determinants of this phenotypic commitment are largely unknown. During the orderly upward migration of cells from crypt to villus along the crypt length in the colon, the temporal sequence of differentiative events can be well defined. However, this situation unfortunately cannot be recreated in intestinal culture systems, probably because of the absence of supportive tissues, and the inability to recapitulate this complex dynamic process with continuous cell proliferation and cell loss within a few days. Thus, in vitro studies of differentiation markers in normal intestinal cells are difficult to perform.

Тези доповідей конференцій з теми "Senescence markers":

Baker, J., P. S. Fenwick, L. E. Donnelly, and P. J. Barnes. "Elevated Levels of Cellular Senescence and Senescence-Associated Secretory Phenotype Markers in COPD Small Airway Epithelial Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4014.

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Kim, Eun Kyung, Seung-Ick Cha, Aaron Schroeder, Jasleen Kukreja, Kirk D. Jones, Jeffrey A. Golden, Michael A. Matthay, Harold R. Collard, David J. Erle, and Paul J. Wolters. "Alveolar Epithelial Cells Express Markers Of Senescence In Lungs From Patients With Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5281.

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Rojas, Mauricio, Nina Morse, Tracy Tabib, John Sembrat, Kristina Buschur, Humberto Trejo, Tamara Cruz, et al. "Identification of Cell Populations with Increase Expression of Markers of Cell Senescence in Explanted IPF Lungs." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3714.

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Wrench, C. L., J. R. Baker, P. S. Fenwick, L. E. Donnelly, and P. J. Barnes. "Senescence and Fibrotic Markers Are Induced by Oxidative Stress in Small Airway Fibroblasts from COPD Patients." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2834.

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Bouamar, Hakim, Larry Broome, Xiang Gu, Alia Nazarullah, Andrew Brenner, Virginia Kaklamani, Ismail Jatoi, and Lu-Zhe Sun. "Abstract PS14-17: Rapamycin inhibits stem cell function and diminishes inflammation and senescence markers in human mammary gland." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps14-17.

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Lim, Kah Suan, Eli E. Bar, Eric H. Raabe, Deepali Jain, and Charles G. Eberhart. "Abstract 3459: Expression of oncogene-induced senescence markers in pilocytic astrocytomaIs associated with younger age and longer survival." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3459.

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Lee, Joyce, Janet La, Sara Aziz, Robert Brownell, Kirk Jones, Gary Green, Brett Elicker, et al. "Molecular Markers of Telomere Dysfunction and Senescence are Common Findings in the Usual Interstitial Pneumonia Pattern of Lung Fibrosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa5362.

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Wyman, A. E., A. J. Dabo, W. Ezegbunam, I. Garcia-Arcos, N. Baumlin-Schmid, M. A. Salathe, P. Geraghty, and R. F. Foronjy. "Downregulation of the RNA Binding Protein HuR Correlates with Enhanced Expression of Senescence Markers in COPD Bronchial Epithelial Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3771.

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Webster, Marie R., Mai Xu, Kathryn Kinzler, Amanpreet Kaur, Jessica Appleton, Michael P. O'Connell, Katie Marchbank, et al. "Abstract B27: Wnt5A-expressing melanoma cells show classical markers of senescence following radiation and therapeutic stress, but retain the ability to metastasize and proliferate at distant sites." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-b27.

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Mallakin, Ali, Kazushi Inoue, and Martin Guthold. "In-Situ Quantitative Analysis of Tumor Suppressor Protein (hDMP1) Using a Nanomechanical Cantilever Beam." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-84503.

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This study is focused on testing “immuno-sensors” of micro-cantilever beams for the purpose of future design of high-throughout bioassays. We currently study the aberrant expression, deletion and mutation of hDMP1 (Human DMP1) in human lung cancer. Lung cancer is the leading cause of cancer deaths among men and women in North America. There are four major histological subtypes of human lung cancer: small-cell carcinoma (SCC), adenocarcinoma (AC), squamous cell carcinoma (SCC), and large-cell carcinoma (LCC). The hDMP1 locus is localized on chromosome 7q21, a region frequently deleted as part of the 7q-minus and monosomy 7 abnormalities of acute myeloid leukemia and myelodysplastic syndrome. Recent data demonstrate the critical role of Dmp1 in Ras-Raf-Arf signaling and cellular senescence. In order to study the interactions of hDMP1 gene product and selected tumor markers with BioMEMS devices, protein coating (Antibody) conduct on cantilevers with silicon nitride (SiNx) surfaces. Silicon nitride surface has the potential to provide a good interface for BioMEMS devices, due to enhanced adherence of substances on this surface. The cantilever biosensors coated with hDMP1 antibody were used for the detection of hDMP1 antigen, which is known to be a tumor suppressor protein. Results revealed that the changes in nano-mechanical forces provided sufficient differential torque to bend the cantilever beam upon injection of the antigen. Theoretical models have been developed for the prediction of the vibrational responses of atomic force microscope (AFM) cantilevers before and after antigen/antibody interaction. Exposure of the proteins to micro-cantilever (MC) resulted in un-reversible large stress. Static deflection of micro-cantilever appeared as a result of the surface stresses that are induced by changes upon antibody-antigen interaction. This indicated that the micro-cantilever approach is useful for detecting proteins and tumor markers, and this system is applicable as a model to design miniaturized biosensor systems. We also applied gene micro-array to identify unknown targets for hDMP1 and extend our observation of the complicated process of carcinogenesis.

Звіти організацій з теми "Senescence markers":

Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .

Dubcovsky, Jorge, Tzion Fahima, Ann Blechl, and Phillip San Miguel. Validation of a candidate gene for increased grain protein content in wheat. United States Department of Agriculture, January 2007. http://dx.doi.org/10.32747/2007.7695857.bard.

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High Grain Protein Content (GPC) of wheat is important for improved nutritional value and industrial quality. However, selection for this trait is limited by our poor understanding of the genes involved in the accumulation of protein in the grain. A gene with a large effect on GPC was detected on the short arm of chromosome 6B in a Triticum turgidum ssp. dicoccoides accession from Israel (DIC, hereafter). During the previous BARD project we constructed a half-million clones Bacterial Artificial Chromosome (BAC) library of tetraploid wheat including the high GPC allele from DIC and mapped the GPC-B1 locus within a 0.3-cM interval. Our long-term goal is to provide a better understanding of the genes controlling grain protein content in wheat. The specific objectives of the current project were to: (1) complete the positional cloning of the GPC-B1 candidate gene; (2) characterize the allelic variation and (3) expression profile of the candidate gene; and (4) validate this gene by using a transgenic RNAi approach to reduce the GPC transcript levels. To achieve these goals we constructed a 245-kb physical map of the GPC-B1 region. Tetraploid and hexaploid wheat lines carrying this 245-kb DIC segment showed delayed senescence and increased GPC and grain micronutrients. The complete sequencing of this region revealed five genes. A high-resolution genetic map, based on approximately 9,000 gametes and new molecular markers enabled us to delimit the GPC-B1 locus to a 7.4-kb region. Complete linkage of the 7.4-kb region with earlier senescence and increase in GPC, Zn, and Fe concentrations in the grain suggested that GPC-B1 is a single gene with multiple pleiotropic effects. The annotation of this 7.4-kb region identified a single gene, encoding a NAC transcription factor, designated as NAM-B1. Allelic variation studies demonstrated that the ancestral wild wheat allele encodes a functional NAC transcription factor whereas modern wheat varieties carry a non-functional NAM-B1 allele. Quantitative PCR showed that transcript levels for the multiple NAMhomologues were low in flag leaves prior to anthesis, after which their levels increased significantly towards grain maturity. Reduction in RNA levels of the multiple NAMhomologues by RNA interference delayed senescence by over three weeks and reduced wheat grain protein, Zn, and Fe content by over 30%. In the transgenic RNAi plants, residual N, Zn and Fe in the dry leaves was significantly higher than in the control plants, confirming a more efficient nutrient remobilization in the presence of higher levels of GPC. The multiple pleiotropic effects of NAM genes suggest a central role for these genes as transcriptional regulators of multiple processes during leaf senescence, including nutrient remobilization to the developing grain. The cloning of GPC-B1 provides a direct link between the regulation of senescence and nutrient remobilization and an entry point to characterize the genes regulating these two processes. This may contribute to their more efficient manipulation in crops and translate into food with enhanced nutritional value. The characterization of the GPC-B1 gene will have a significant impact on wheat production in many regions of the world and will open the door for the identification of additional genes involved in the accumulation of protein in the grain.

Arun, Peethambaran, Vineela Aleti, Neil S. Jensen, Veeraswamy Manne, Moonsuk Choi, and Nageswararao Chilukuri. Overexpression of Human Senescence Marker Protein 30 in Mice Fails to Offer Protection Against Challenge with Organophosphorus Compounds. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada555371.

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Grumet, Rebecca, Rafael Perl-Treves, and Jack Staub. Ethylene Mediated Regulation of Cucumis Reproduction - from Sex Expression to Fruit Set. United States Department of Agriculture, February 2010. http://dx.doi.org/10.32747/2010.7696533.bard.

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Reproductive development is a critical determinant of agricultural yield. For species with unisexual flowers, floral secualdifferentation adds additional complexity, that can influenec productivity. The hormone ethylene has long, been known to play a primary role in sex determination in the Cucumis species cucumber (C. sativus) and melon (C. melo). Our objectives were to: (1) Determine critical sites of ethylene production and perception for sex determination; (2) Identify additional ethylene related genes associated with sex expression; and (3) Examine the role of environment ami prior fruit set on sex expression, pistillate flower maturation, and fruit set. We made progress in each of these areas. (1) Transgenic melon produced with the Arabidopsis dominant negative ethylene perception mutant gene, etrl-1, under the control of floral primordia targeted promoters [AP3 (petal and stamen) and CRC (carpel and nectary)], showed that ethylene perception by the stamen primordia, rather than carpel primordia, is critical for carpel development at the time of sex determination. Transgenic melons also were produced with the ethylene production enzyme gene. ACS, encoding l-aminocyclopropane-lcarboylate synthase, fused to the AP3 or CRC promoters. Consistent with the etr1-1 results, CRC::ACS did not increase femaleness; however, AP3::ACS reduced or eliminated male flower production. The effects of AP3:ACS were stronger than those of 35S::ACS plants, demonstratin g the importance of targeted expression, while avoiding disadvantages of constitutive ethylene production. (2) Linkage analysis coupled with SNP discovery was per formed on ethylene and floral development genes in cucumber populations segregating for the three major sex genes. A break-through towards cloning the cucumber M gene occurred when the melon andromonoecious gene (a), an ACS gene, was cloned in 2008. Both cucumber M and melon a suppress stamen development in pistillate flowers. We hypothesized that cucumber M could be orthologous to melon a, and found that mutations in CsACS2 co-segregated perfectly with the M gene. We also sought to identify miRNA molecules associated with sex determination. miRNA159, whose target in Arabidopsis is GAMYB[a transcription factor gene mediating response to10 gibberellin (GA)], was more highly expressed in young female buds than male. Since GA promotes maleness in cucumber, a micro RNA that counteracts GAMYB could promote femaleness. miRNA157, which in other plants targets transcription factors involved in flower development , was expressed in young male buds and mature flower anthers. (3) Gene expression profiling showed that ethylene-, senescence-, stress- and ubiquitin-related genes were up-regulated in senescing and inhibited fruits, while those undergoing successful fruit set up-regulated photosynthesis, respiration and metabolic genes. Melon plants can change sex expression in response to environmental conditions, leading to changes in yield potential. Unique melon lines with varying sex expression were developed and evaluated in the field in Hancock, Wisconsin . Environmental changes during the growing season influenced sex expression in highly inbred melon lines. Collectively these results are of significance for understanding regulation of sex expression. The fact that both cucumber sex loci identified so far (F and M) encode isoforms of the same ethylene synthesis enzyme, underscores the importance of ethylene as the main sex determining hormone in cucumber. The targeting studies give insight into developmental switch points and suggest a means to develop lines with earlier carpel-bearing flower production and fruit set. These results are of significance for understanding regulation of sex expression to facilitate shorter growing seasons and earlier time to market. Field results provide information for development of management strategies for commercial production of melon cultivars with different sex expression characteristics during fruit production.