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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.
Pełny tekst źródłaAgeing 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
Nelson, Brandon John. "MicroRNA analysis of human embryonic stem cell derived cardiomyocytes and neonatal rat ventricular cardiomyocytes". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p1447322.
Pełny tekst źródłaTitle from first page of PDF file (viewed January 15, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 45-48).
Bond, Richard. "Cellular electrophysiology of rat pulmonary vein cardiomyocytes : a comparative study with left atrial cardiomyocytes". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685358.
Pełny tekst źródłaFijnvandraat, Arnoldus Cornelis. "Embryonic stem cell-derived cardiomyocytes". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/68354.
Pełny tekst źródłaRisto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.
Pełny tekst źródłaDe, Marco Margot. "BAG3 role in cardiomyocytes physiopathology". Doctoral thesis, Universita degli studi di Salerno, 2013. http://hdl.handle.net/10556/896.
Pełny tekst źródłaThe anti-apoptotic protein BAG3 is expressed at high levels in skeletal and cardiac muscle in vivo. Our group recently focused its interest on BAG3 role in myocardiocyte proliferation, survival and response to stressful stimuli. We found that BAG3 is upregulated during the differentiation of cardiomyoblasts. Our results prompted us to verify whether bag3 silencing could affect the differentiation state of cardiocytes and we found that bag3 silencing resulted in highly reducing the levels of myogenin. Furthermore, we analyzed BAG3 expression and localization following cell exposure to oxidative stress. In particular, we found that epinephrine in vitro increases BAG3 expression in adult human cardiomyocytes. We evaluated whether BAG3 could be involved in the Tako-tsubo cardiomyopathy (or stress cardiomyopathy) pathogenesis that is characterized by left ventricular dysfunction, with symptoms that can mimic an acute coronary syndrome. The absence of significant cardiovascular risk factors in patients affected by stress cardiomyopathy suggested that it might be associated with a possible genetic etiology. Therefore, we sequenced bag3 gene to check for polymorphisms in 29 patients and 1043 healthy donors. Three polymorphism were highly represented among patients (R71Q, C151R, P407L). We also showed for the first time that BAG3 protein is released from stressed cardiomyocytes and is found in chronic heart failure (HF) patients’ sera. Since anti-BAG3 antibodies are also present in patients’ sera, we developed an ELISA test for their specific detection. In serum samples from chronic HF patients, we found significantly higher values of anti-BAG3 antibodies respect to samples from healthy donors. The presence of anti-BAG3 antibodies in chronic HF patients’ sera and the availability of an ELISA test for their detection can contribute a novel tool for diagnostic and prognostic evaluations. [edited by author]
X n.s.
Driesen, Ronald Bertie Mario Antonio. "Adaptive remodeling of cardiomyocytes under stress". [Maastricht] : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=11068.
Pełny tekst źródłaKemeny, Naomi. "Alendronate affects calcium dynamics in cardiomyocytes". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40684.
Pełny tekst źródłaAlendronate est efficace dans le traitement de l’ostéoporose. Alendronate a récemment été associe avec une risque élevé de fibrillation auriculaire sérieux. On a examine les effets d’Alendronate sur la de calcium cytosolique ([Ca2+]i) dans les cellules musculaires cardiaques. Les cellules musculaires cardiaques HL-1 étaient chargés avec Fura-2 et examinés par microspectrofluorimetrie. Alendronate (10-8, 10-7, 10-6 M) ont provoqués des oscillations de [Ca2+]i fugaces et haute fréquences à 10-8 M Alendronate (61 ± 10 mHz) comparé aux concentrations plus hautes (42 ± 4 mHz). Dans les cellules traits avec 10-6 M ALN, la réponse à l’application de caféine était avec délai, et a manifesté un diminution dans la rythme et amplitude d’augmentation de [Ca2+]i. L’exposition a l’ALN à long terme (48 h) ont provoqué un délai des élévations de calcium transitoires, et un diminution du rythme d’augmentation de [Ca2+]i suites par les oscillations de [Ca2+]i, caractérisés par un augmentation de fréquences avec 10-8 M Alendronate (54 ± 8 mHz) compare aux concentrations plus hautes (35 ± 5 mHz). Le changement des dynamiques de calcium étaient accompagnés par les changements considérables dans l’expression d’ATPase (SERCA2a), calsequestrin et calreticulin du réticulum sarcoendoplasmique.
Bowers, Keith Cyril. "Pathophysiology of ATP in single cardiomyocytes". Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316576.
Pełny tekst źródłaBowman, Peter Ronald Thomas. "Regulation of glucose transport in cardiomyocytes". Thesis, University of Glasgow, 2019. http://theses.gla.ac.uk/41002/.
Pełny tekst źródłaMcDougal, Anthony Drew. "Modeling oxygen requirements in ischemic cardiomyocytes". Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/100105.
Pełny tekst źródłaCataloged from PDF version of thesis.
Includes bibliographical references (pages 36-40).
Ischemic heart disease remains a leading cause of death globally and in the US. The most common ischemic event is a heart attack, where one or more arteries are obstructed and the cardiac muscle is deprived of oxygen. Although removing the blockage and allowing reperfusion can prevent death, at the same time it can cause significant damage through "reperfusion injury." To date, there are limited methods to predict the viability of the myocardial muscle cell (myocyte) and its quantitative conditions during ischemia. Here, we explore the viability of heart cells using a model for cellular metabolism. We use this model to predict conditions that will sustain viable concentrations of adenosine triphosphate (ATP) and compare these conditions to baseline energy consumption rates. Glycolytic metabolism is modeled using a system of coupled ordinary differential equations that describe the individual metabolic reactions that occur within the cardiac myocyte and its surrounding tissue. Over 200 conditions were simulated to characterize a range of reduced oxygen levels and ATP consumption rates. These conditions were organized according to their steady-state level of [ATP], and reveal a distinct transition region between low levels of ATP that are sustainable and depleted ATP levels that lead to cell death. Our simulations and analysis illustrate how very low concentrations of oxygen in the extracellular tissue allow the cells to perform essential survival functions. The model contains 58 of the molecular species within the cell, so that the conditions of the cell at the time of reperfusion can be predicted. We find the oxygen level required for viability increases roughly linearly with the ATP consumption rate, and is smaller than one would have expected based on previous results. An external tissue level 02 concentration of around 0.007 mM is sufficient to sustain cardiomyocyte viability in the absence of beating. This level of oxygen could be achieved through collateral circulation. This model of ischemia will also provide future investigations of the reperfusion process to proceed from a known metabolic and molecular state of the cardiomyocytes preceding re-oxygenation.
by Anthony Drew McDougal.
S.M.
Giraldo, Ramirez Diego Alejandro. "Regulation of ATF3 expression in cardiomyocytes". Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/1300.
Pełny tekst źródłaMarshall, Andrew Keith. "Signalling through Rho GTPases in cardiomyocytes". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6962.
Pełny tekst źródłaCavalli, Amy Lynn. "Characterization of sphingolipid receptors in cardiomyocytes /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3071179.
Pełny tekst źródłaEllis, Charlotte Elizabeth. "Subcellular effects of pavetamine on rat cardiomyocytes". Thesis, University of Pretoria, 2010. http://hdl.handle.net/2263/26785.
Pełny tekst źródłaThesis (PhD)--University of Pretoria, 2010.
Paraclinical Sciences
unrestricted
Kovacs, Yoann. "Rôle de la protéine découplante mitochondriale Ucp2 dans la régulation du métabolisme et de la maturation des cardiomyocytes néonataux". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS391.pdf.
Pełny tekst źródłaDuring development, the heart relies mainly on glycolysis for ATP production. At birth, exposure to atmospheric O2 levels and nutritional switch towards the fatty acid-rich maternal milk triggers a metabolic remodeling towards mitochondrial oxidative phosphorylation. Cardiomyocytes then rely on oxidative metabolism, particularly β-oxidation. The remodeling is concomitant with transcriptional changes allowing increasing mitochondrial biogenesis and maturation of the contractile machinery, thus optimizing energy production and heart contractile function. The augmentation of mitochondrial metabolic activity participates in the signaling ensuring the emergence of mature phenotypes, including cardiomyocyte cell-cycle arrest and transition to hypertrophy. Thus, in a long-term therapeutic view, a better understanding of mitochondrial signaling during maturation appears critical to improve cardiomyocyte in vitro models relevancy as well as to stimulate their proliferation in the adult in order to sustain heart regeneration. My PhD project is focused on the mitochondrial uncoupling protein 2 (Ucp2), specifically expressed in the neonatal heart, and its role during cardiomyocyte maturation. Ucp2 is a carrier located on the inner mitochondrial membrane, where it exerts 2 functions. (1) It regulates mitochondrial reactive oxygen species production and (2) it is involved in cell fuel preferences via Krebs metabolite export from the matrix to the cytosol. We have shown that Ucp2 deletion in neonatal mouse heart induces defective cardiomyocyte maturation. Indeed, Ucp2-/- cardiomyocytes display inability to induce the post-natal transcriptional program, including impaired mitochondrial biogenesis, absence of β-oxidation and defective contractility. Metabolic activity analysis revealed that Ucp2 mutant -heart poorly relies on pyruvate or fatty acids for ATP production. Instead, it shows metabolic dependency to glutamine through the GABA shunt. This is associated to unbalanced Krebs intermediates relative abundance, in particular α-ketoglutarate and succinate. These metabolites are important regulators of TET enzymes activity which activate gene expression and participate in neonatal cardiomyocyte metabolic and contractile maturation. These results demonstrate that Ucp2 plays a critical role in regulating metabolic activity of neonatal cardiomyocytes, and unravel a new type of mitochondrial signaling initiating postnatal heart maturation
Ponzielli, Romina. "Etude du contrôle génétique de la morphogenèse du tube cardiaque chez la Drosophile". Aix-Marseille 2, 2002. http://www.theses.fr/2002AIX22073.
Pełny tekst źródłaBlandin, Camille. "Rôle de la protéine d'échafaudage CASK dans le remodelage adaptatif et pathologique, chez le rongeur et l'Homme". Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS503.
Pełny tekst źródłaThe intercalated disc is the molecular entity that connects two adjacent cardiomyocytes at their terminal ends, both electrically and mechanically, via specific protein complexes. The organization of the disc, which ensures the cohesion of myocardial cells during contraction and relaxation cycles, is a hallmark of the maturity and functionality of the cardiomyocyte. Disorganization of the disc is a common feature of many cardiac pathologies, both inherited and acquired. Understanding the molecular processes involved in the organization of this membrane domain, and its disorganization in the pathological context, is a very active field of research. In this context, we have identified a lateral membrane protein, CASK, which controls the organization of intercalated disc proteins by regulating their anterograde trafficking. In in vitro models (neonatal rat cardiomyocytes or cardiomyocytes derived from induced human pluripotent stem cells), invalidation of CASK promotes the organization and stability of disc proteins. Invalidation of CASK in rodents also promotes disc protein organization and leads to improved cardiac performance. In human arrhythmogenic right ventricular cardiomyopathy (ARVC), a pathological condition associated with loss of cohesion between cardiomyocytes due to altered desmosome-type mechanical contacts, CASK expression is increased. In vitro, in a human cell model of ARVC, CASK invalidation restores the integrity of desmosomal contacts. Taken together, our results suggest that CASK is a major regulator of intracellular trafficking, addressing and organization of intercalated disc proteins
Lau, Siu-ling. "Characterization of adenosine transport in rat cardiomyocytes, H9c2 /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31494894.
Pełny tekst źródłaKane, Émilie. "Protein-protein regulation of calsequestrin expression in cardiomyocytes". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107782.
Pełny tekst źródłaLa maladie du coeur est la cause principale de mortalité chez les femmes et les hommes en Occident. L'arrêt cardiac est souvent associé à des anomalies en control de calcium intracellulaire. Le facteur de transcription Egr-1 est connu pour son contrôle négatif de l'expression de calsequestrine (CSQ2), une protéine réservoir de calcium. Un manque de CSQ2 impacte les quantités de calcium disponible pour un bon fonctionnement cardiaque. Ici nous avons examiné l'hypothèse que les protéines liées à Egr-1 et que ses modifications post-translationelles. Egr-1 et Sp1 sont en compétition pour le promoteur de CSQ2 mais sont aussi liés l'un à l'autre. En fait, ensemble ils forment un complexe avec le facteur de transcription universel YBX-1. Ce complexe a été identifié en vivo et en vitro par co-immunoprécipitations. Considérant que la formation de ce complexe ainsi que l'expression de CSQ2 peuvent être affectés par l'acétylation, des inhibiteurs d'acétyltransferase d'histone (ATH) et de déacétylase d'histone (DACH) ont été respectivement utilisés pour réduire et augmenter l'acétylation en cellules. Nous avons trouvés que la formation du complexe Egr-1: Sp1: YBX-1 qui est possiblement responsable de l'expression de CSQ2 n'est pas affecté par les changements en acétylation. Par contre, des changements ont été aperçus dans l'expression de CSQ2 quand l'acétylation a été modifiée par ATH ou par DACH. Nous croyons que l'acétylation impacte l'expression de CSQ2 mais pas par entremise du complexe Egr-1 : Sp1 : YBX-1 malgré l'acétylation de la protéine Egr-1 elle-même.
Kilborn, Michael John. "Postnatal changes in electrophysiological properties of rat cardiomyocytes". Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292673.
Pełny tekst źródłaLau, Siu-ling, i 劉少玲. "Characterization of adenosine transport in rat cardiomyocytes, H9c2". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010237.
Pełny tekst źródłaPaïta, Lucille. "Caractérisation du canal cationique TRPV1 dans les cardiomyocytes". Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1329/document.
Pełny tekst źródłaAcute myocardial infarction (MI), a leading cause of morbidity and mortality worldwide, is the irreversible death of heart muscle secondary to ischemia. This ischemia, i.e. oxygen and nutrients deprivation, triggers a reticular stress disrupting the Ca2+ balance of the cardiac cell. Several Ca2+ pumps and channels located at the sarcolemma or at the reticulum membrane are key players in this maintenance of Ca2+ homeostasis. Among them, we find passive leak channels, such as TRPs and little is known about their precise role in MI.TRPV1 represents a non-selective cation channel that is activated by capsaicin, pH and noxious heat. In skeletal muscle, we previously demonstrated that TRPV1 is located in the longitudinal part of the SR and respond to pharmacological and physiological activations (Lotteau et al., 2013). We questioned here whether TRPV1 might have a similar role in heart physiology. Biochemical analysis and intracellular Ca2+ measurements were performed on cardiomyocytes from wild-type and TRPV1-KO mice. Our in vitro results show that: (i) TRPV1 is expressed in cardiac cells; (ii) an increase in intracellular calcium concentration ([Ca2+]i) is elicited under TRPV1 activation; (iii) TRPV1 could be a direct target of isoflurane. In parallel, our in vivo results indicate that a pharmacological preconditioning by isoflurane decrease the infarct size, probably though activation of TRPV1. According to the fact that TRPV1 activity can be modulated by a lot of pharmacological molecules, TRPV1 may serve as therapeutic target to reduce the infarct size. Most of published data have already evidenced this TRPV1 cardioprotective role in the peripheral heart system. The aim of the present work is to describe how TRPV1 channels behave in adult cardiomyocytes
Kranzhöfer, David K. [Verfasser], Lutz [Akademischer Betreuer] Hein i Christian [Akademischer Betreuer] Flotho. "DNA demethylation in cardiomyocytes during development and maturation". Freiburg : Universität, 2021. http://d-nb.info/1226091261/34.
Pełny tekst źródłaKanaan, Georges. "Mitochondrial Dysfunction: From Mouse Myotubes to Human Cardiomyocytes". Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37582.
Pełny tekst źródłaHurst, MaryKathryn. "VEGF-R1 AGONISTS PROTECT CARDIOMYOCYTES AGAINST OXIDATIVE STRESS". Master's thesis, Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/239774.
Pełny tekst źródłaM.S.
VEGF-R1 Agonists protect Cardiomyocytes against Oxidative Stress Background: Selective agonists of the vascular endothelial growth factor receptor 1 (VEGFR-1) display cytoprotective and anti-apoptotic effects in the failing heart. Since a major determinant of myocardial damage in heart failure is oxidative stress, we tested the hypothesis that VEGFR-1 mediates anti-oxidant mechanisms. Methods: Freshly prepared cardiac tissue slices were obtained from dogs with pacing-induced heart failure that had been previously transduced with the VEGFR-1 selective ligand VEGF-B. Dihydroetidium (DHE) fluorescence was used to monitor the production of reactive oxygen species. In addition, cultured rat neonatal cardiomyocytes were tested with two major mediators causing oxidative stress in the failing heart, namely angiotensin II (10-8 M for 24 hours) and norepinephrine (50 µM for 24 hours). The experiments were performed in the absence or in the presence of the VEGFR-1 agonists VEGF-B and PlGF or of the mixed VEGFR-1 and VEGFR-2 agonist VEGF-A or of the selective VEGFR-2 agonist VEGF-E. Mitochondrial superoxide and cytosolic hydrogen peroxide were measured, respectively, as MitoSox and DCF fluorescence intensity. Results: In fresh cardiac tissue slices, DHE fluorescence indicated that superoxide production was significantly reduced in VEGF-B treated hearts compared to control failing hearts. In cultured cardiomyocytes, VEGF-B and PlGF, but not VEGF-A or VEGF-E, prevented mitochondrial superoxide and cytosolic hydrogen peroxide overproduction in response to angiotensin II or norepinephrine. These findings were consistent with the induction of mitochondrial superoxide dismutase and glutathione peroxidase-1 overexpression in VEGF-B-treated cells. Conclusions: VEGF-R1 activation can reduce oxidative stress both in vivo and in vitro. Our results provide insights in the cardioprotective mechanisms activated by VEGF-B gene therapy in the failing heart.
Temple University--Theses
Jeziorowska, Dorota. "Analyse des voies de régulation de la cardiogenèse et de la différenciation cardiomyocytaire". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066631/document.
Pełny tekst źródłaThe general objective of this work was centered on the use of human induced pluripotent cells in modeling and therapeutic evaluation of cardiac pathologies. Since their discovery in 2006, the iPSC provide an opportunity for the development of human cellular models and specific patients for the study of pathophysiological mechanisms, evaluation of pharmacological responses and the generation redifférenciées cells (cardiomyocytes here) for applications cellular therapeutic. In this work we demonstrated that the quantity but also the final quality of cardiomyocytes derived from iPSC depends on the spatial and pharmacological conditions used during the various stages of differentiation. The use of a monolayer differentiation protocol with simultaneous and transient blocking of all Wnt pathways (canonical and noncanonical) allows to obtain a higher maturation of the sarcomere, an essential step for modeling sarcomeropathies IPSC differentiation into cardiomyocytes can also be obtained by targeted molecular approach to specifically activate cardiogenic program. This is achieved through the use of a mutated Cas9 protein and coupled with transactivator system. This allows simultaneous targeting of 3 key cardiogenesis transcription factors (Gata4, MEF2C and Tbx5). This molecular approach is enhanced by the combination with a pharmacological stimulation targeting the Wnt pathway. Beyond modeling of monogenic cardiac disease, cardiomyocytes derived from iPSC can reproduce more complex and multigenic diseases
Anwar, Attia. "Functional role of NFAT in ventricular cardiomyocytes of rat". Giessen VVB Laufersweiler, 2006. http://geb.uni-giessen.de/geb/volltexte/2006/3817/index.html.
Pełny tekst źródłaPotter, Ryan Wayne. "Protamine alters sodium and potassium currents in isolated cardiomyocytes /". Title page and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09SB/09sbp868.pdf.
Pełny tekst źródłaHuang, Brandon Pei Han. "The regulation of protein synthesis in adult rat cardiomyocytes". Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/976.
Pełny tekst źródłaSchulson, Meredith Nicole. "The structure of excitation-contraction coupling in atrial cardiomyocytes". Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3981.
Pełny tekst źródłaChan, Sai Yen Victor, i 陳世欽. "Effect of homocysteine on nitric oxide production in cardiomyocytes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970321.
Pełny tekst źródłaPlamondon, Philippe. "La MAP kinase p38γ influence la structure des cardiomyocytes". Mémoire, Université de Sherbrooke, 2014. http://savoirs.usherbrooke.ca/handle/11143/5307.
Pełny tekst źródłaMiller, Stewart L. W. "A study of excitation contraction coupling in rabbit cardiomyocytes". Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404445.
Pełny tekst źródłaBettencourt, Carvalho Dias Monica. "Plasticity of the differentiated state in adult newt cardiomyocytes". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274931.
Pełny tekst źródłaSusaeta, Isidro Allue. "Rigor, cytosolic ATP and pH in metabolically poisoned cardiomyocytes". Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262588.
Pełny tekst źródłaMotion, J. P. Michael (Joseph Patrick Michael Motion Champana). "Mechanically-induced intercellular remodeling of cardiomyocytes by magnetic micromanipulation". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37202.
Pełny tekst źródłaIncludes bibliographical references (leaves 68-72).
Gap junctions are responsible for providing and maintaining a pathway for intercellular communication. This is critical in the heart where gap junctions are responsible for maintaining electrical impulse propagation. Connexin43 (Cx43) is the most abundant gap junction in the heart, and studies have shown that spatial heterogeneity of Cx43 may promote electrical instability and anisotropic conduction pathways that may cause cardiac arrhythmias. Structural and electrical remodeling of gap junctions have been linked to increases in stresses in conditions such as hypertrophy. Understanding how local mechanical forces influence the remodeling of gap junctions can provide insight into arrhythmias and reentry circuits. In this work, I describe a system for exerting local mechanical forces on cardiomyocytes to study gap junction remodeling and I show that cell-to-cell movement and subsequent remodeling of Cx43 can occur. The system consisted of patterned linear strands on polyacrylamide gels and mechanical stimulation using magnetic micromanipulation. Cardiomyocytes were patterned on polyacrylamide gel using 25pm and 50pm microchannels. Mechanical stimulation was induced in sections with high densities of magnetic beads.
(cont.) With a maximal input current of 1.5A, the system generated 1.5nN at 100pm distance from the magnetic trap, and this was sufficient to induce cell-to-cell movement. Cell-to-cell movement was measured to be 0.032±0.03pm/min, three times faster than the average cell-to-cell movement under no applied force. Remodeling of Cx43 was also shown using Cx43-YFP transfected cells while a local force induced cell-to-cell movement. Changes in both the distribution and expression of the protein were seen throughout time as the linear strand was pulled by the magnetic force. We conclude that this system can induce remodeling of Cx43 by an applied local force. This work establishes a system to allow to quantification of applied mechanical loads and resultant Cx43 remodeling.
by J.P. Michael Motion.
M.Eng.
Humphrey, Peter Saah. "Signal transduction mechanisms for stem cell differentation into cardiomyocytes". Thesis, University of Hertfordshire, 2009. http://hdl.handle.net/2299/3760.
Pełny tekst źródłaKolker, Ljudmila. "Differentation and maturation of pluripotent stem cell-derived cardiomyocytes". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/26149.
Pełny tekst źródłaEmond-Boisjoly, Marc-Alexandre. "Rôle de la protéine DUSP5 dans l’autophagie des cardiomyocytes". Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8908.
Pełny tekst źródłaAbstract: Autophagy is a process essential to the maintenance of cellular homeostasis. It helps degrade and recycle whole organelles and nonfunctional cytoplasmic components. In addition, the adaptative up regulation of autophagy in stress condition promotes cell survival. In cardiomyocytes basal autophagy is essential to the renewal of, among others, mitochondria and proteins forming sarcomeres. In addition, stresses such as ischemic heart or nutrient deficiency induce an increase in protective autophagy. In extreme conditions, it has been suggested that autophagy may exacerbate cardiac disease causing the death of cardiomyocytes. Considering the importance of this process in cardiac pathophysiology, identify ing safety mechanisms regulating autophagy in cardiomyocytes has been the subject of intense research. To this end, activation of mitogen-activated protein kinase (MAPK) has been demonstrated to regulate, with other signaling pathways, autophagy and cardiomyocyte apoptosis. It is therefore likely that Dual-Specificity Phosphatases (DUSPs), key enzymes that control the activity of MAPKs, also participate in the regulation of autophagy. To test this hypothesis, we have induced autophagy in isolated cardiomyocytes of newborn rats in culture. Analysis of autophagy markers by immunoblotting demonstrated that the activation of MAPKs ERK1/2 and p38 correlates with autophagic activity in cardiomyocytes. Under these conditions, the decrease in expression of the majority of mRNAs encoding different DUSPs found in cardiomyocytes contrast sharply with the increase mRNA expression of Dusp5. Furthermore, we demonstrated by again of function study that sustained activation of p38 by overexpression of a constitutively active MKK6 mutant stimulates autophagy in cardiomyocytes. Surprisingly, the loss of p38 function obtained by overexpression of a dominant negative p38 mutant does not affect the autophagic response in our in vitro model, but increases the lipidation of autophagosomes marker LC3. Our results suggest that DUSPs can regulate, through their actions on MAPKs, important stages of autophagy in cardiomyocytes.
Góes, Maria Elisa Almeida. "Kinin B2-Receptor in human iPSC differentiation into cardiomyocytes". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24092018-144907/.
Pełny tekst źródłaDoenças cardiovasculares são responsáveis por quase um terço de todas as mortes globais anualmente, e por isto o sistema cardiovascular é amplamente estudado. Cardiomiócitos derivados a partir de células-tronco pluripotentes induzidas humanas (hiPSCCM) emergiram como uma promissora tecnologia para modelagem de doenças cardíacas e terapia personalizada. No entanto, desafios acerca de sua maturação funcional e molecular ainda são enfrentados. Além disso, protocolos de diferenciação geralmente levam à obtenção de populações heterogêneas contendo células com fenótipos similares aos de cardiomiócitos nodais, atriais e ventriculares sendo, portanto, inapropriadas para fins terapêuticos. A bradicinina (BK) é um peptídio vasoativo que exerce importantes papeis fisiológicos no sistema cardiovascular, além de ter sido previamente descrita como importante para a diferenciação neuronal, de queratinócitos e de músculo esquelético. Este projeto foi realizado em colaboração com a empresa PluriCell Biotech, uma startup especializada na produção e diferenciação de hiPSC-CM, e buscou (1) caracterizar a expressão gênica e proteíca de marcadores moleculares de maturação e de especificação de subtipos cardíacos durante a diferenciação; (2) avaliar a funcionalidade elétrica de hiPSC-CM por meio da caracterização de seus potenciais de ação (PAs) e (3) Investigar se o progresso da diferenciação de hiPSCCM é regulado por bradicinina por meio do receptor B2 (B2R). Nossos resultados validaram o modelo que propõe um switch na expressão das isoformas funcionais de troponina I esquelética (ssTnI) e cardíaca (cTnI), durante o desenvolvimento e diferenciação celular, pelo menos parcialmente. Além disso, tempo prolongado em cultura resultou em maiores níveis de expressão do marcador ventricular MLC2v, assim como maiores frequências de PAs com morfologias similares a de cardiomiócitos ventriculares. Análise eletrofisiológica de hiPSCCM revelam a existência de uma população mista contendo PAs correspondentes aos subtipos nodais, atriais e ventriculares, assim como pronunciada automaticidade e outros atributos típicos de cardiomiócitos imaturos, como baixa amplitude e devagar velocidade de despolarização. Estes resultados são coerentes com os de outros grupos que ainda não foram totalmente bem-sucedidos em diferenciar células cardíacas maduras similares acardiomiócitos nativos a partir de células-troncos pluripotentes. Após mostrar que as hiPSCCM expressam receptores B2 funcionais e responsivos, submetemos o receptor a uma ativação crônica com BK 10µM e BK 1µM ou inibição crônica com Firazyr 5µM + BK. Apesar da modulação do B2R não ter interferido de forma negativa no rendimento da diferenciação ou na morfologia celular, análise de expressão gênica e proteica de ssTnI e cTnI e do marcador ventricular MLC2v não revelou resultados significativos em comparação aos controles não-tratados. Isto sugere que a BK não interfere na maturação e especificação de subtipos cardíacos em hiPSC-CM, apesar de não podermos ignorar o fato de que ela poderia estar desencadeando outros efeitos inexplorados. Nós recomendamos um estudo mais aprofundado acerca de quais vias de sinalização se tornam ativas após estimulação do receptor B2 em hiPSC-CM, com o objetivo de afunilar quais processos celulares poderiam ser investigados em uma próxima etapa deste estudo.
Chan, Sai-yen Victor. "Effect of homocysteine on nitric oxide production in cardiomyocytes". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23476552.
Pełny tekst źródłaSun, Haipeng. "Regulation of Cyclooxygenase Gene Expression by Glucocorticoids in Cardiomyocytes". Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/194896.
Pełny tekst źródłaAguilar, David Christopher. "GILZ: A Novel Glucocorticoid Induced Cytoprotective Protein in Cardiomyocytes". Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/228177.
Pełny tekst źródłaJahangiri, Anisa. "n-3 PUFAs and reperfusion injury in isolated cardiomyocytes". Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phj251.pdf.
Pełny tekst źródłaCohen-Aubart, Fleur. "Rôle de la protéine STIM1 sur la fonction des cellules musculaires vaculaires et cardiaques par modulation de la voie de signalisationcalcineurine-NFAT : implications physiopathologiques et pharmacologiques". Paris 6, 2012. http://www.theses.fr/2012PA066169.
Pełny tekst źródłaGonzalez, Granillo Marcela Alejandra. "La bioénergétique systémique moléculaire des cellules cardiaques : la relation structure-fonction dans la régulation du métabolisme énergétique compartmentalisé". Thesis, Grenoble, 2012. http://www.theses.fr/2012GRENV078/document.
Pełny tekst źródłaUn élément important de la régulation du métabolisme énergétique des muscles cardiaque et squelettiques est l'interaction des mitochondries avec le cytosquelette. Les mitochondries sont responsables de l'approvisionnement des cellules en énergie, elles sont capables d'ajuster leur activité fonctionnelle en fonction des conditions de stress ou d'autres aspects de la vie. Les mitochondries ont une distribution spécifique selon les tissus. Dans les cardiomyocytes de rats adultes, les mitochondries sont disposées régulièrement dans un entrelacement longitudinal au niveau des bandes A, entre les myofibrilles et dans les limites des sarcomères. En interaction avec le cytosquelette, le sarcomère et le réticulum sarcoplasmique, elles forment des complexes fonctionnels appelés unités énergétiques intracellulaires (ICEUs). Les ICEUs ont des voies spécialisées de transfert d'énergie et de régulation des feedback métaboliques entre les mitochondries et les ATPases, médiée par la CK et l'AK. La structure centrale des ICEUs est l'interactosome mitochondrial (MI) qui confient l'ATP synthasome, la chaîne respiratoire, la créatine kinase mitochondriale et VDAC, qui pourrait être régulé par les tubulines. Le rôle principal du MI est la régulation de la respiration et des flux d'énergie intracellulaires via les réseaux de phosphotransfert. La régulation des ICEUs est liée aux protéines structurales. L'association des mitochondries avec plusieurs protéines du cytosquelette, décrite par plusieurs groupes, a mis en évidence l'importance de la relation structure-fonction dans la régulation métabolique des cardiomyocytes de rats adultes. Pour fournir une meilleure compréhension de ces résultats, le présent travail étudie le mécanisme de contrôle des flux d'énergie et le rôle des relations structure-fonction dans la régulation métabolique de cardiomyocytes de rats adultes. Pour montrer ces associations complexes dans les cellules cardiaques adultes, plusieurs protéines ont été visualisées par microscopie confocale: l'α-actinine et les isoformes des β-tubulines. Pour la première fois, l'existence d'une distribution spécifique des isoformes de β-tubuline dans les cellules cardiaques adultes a été montré. Des mesures respiratoires ont été réalisées pour étudier le rôle des tubulines dans la régulation de la consommation d'oxygène. Ces résultats ont confirmé le rôle déterminant des protéines du cytosquelette -tubulines, α-actinine, plectine, desmine, et autres- pour le maintien de la forme normale des cellules cardiaques, ainsi que de l'arrangement et de la régulation mitochondrial. En outre, la dynamique mitochondriale a été étudiée in vivo et in situ par la transfection de la GFP-α-actinine, ceci permettant la mise en évidence du fait que le phénomène de fusion ne se produit pas aussi souvent qu'on ne le croit pour des cellules cardiaques adultes en bonne santé
David, Florian. "Hétérogénéité ribosomique et régulation de la traduction des ARNm des facteurs de croissance (lymph)angiogéniques dans les cardiomyocytes stressés". Thesis, Toulouse 3, 2022. http://www.theses.fr/2022TOU30054.
Pełny tekst źródłaCardiac ischemia, defined as a blood perfusion diminution in a part of the heart, subjects cells to various stresses caused by oxygen and nutrient supply diminution. If they persist, these stresses induce cell death and subsequently myocardial infarction. In order to restore tissue homeostasis as well as the vascularization of ischemic tissue, cells activate various mechanisms such as angiogenesis and lymphangiogenesis. My thesis project focused on the study of these pathways and their regulation at the translational level in cardiomyocytes subjected to different stresses. The semi-global analysis of the transcriptome and the translatome in hypoxic condition showed us that angiogenic and lymphangiogenic genes are not drastically regulated at the transcriptional level while the majority of them are induced at the translational level in murine cardiomyocytes. Among these genes, those having IRES (Internal Ribosome Entry Site) structures are recruited more efficiently into polysomes. Regulation of translation through the presence of these structures is a key mechanism in the response to hypoxia. We have identified a protein, vasohibin 1, bound to FGF1 IRES and presenting during hypoxia an ITAF (IRES Trans-Acting Factor) function. In a second part of this thesis work, we characterized the key role of a long non-coding RNA, Neat1, in the regulation of IRES-dependent translation in response to hypoxia. Neat1 is the main component of a nuclear body, the paraspeckle, which forms in response to stress. The paraspeckle is made up of Neat1 and several proteins, that interact with this long ncRNA, and are also known to exhibit ITAF function, hence the hypothesis of a role of the paraspeckle in the control of translation. Thus we have identified by depletion experiments, that Neat1, more particularly the long isoform of this ncRNA, Neat1-2, has a role of ITAF promoting the IRES-dependent translation of angiogenic and lymphangiogenic factors. Other components of the paraspeckle, p54nrb and pSPC1, regulate different subgroups of IRESs. The analysis of the interactome of p54nrb by mass spectrometry allowed to identify new nuclear and cytoplasmic partner specific of hypoxia, among them the ribosomal protein uS5 (RPS2) and nucleolin, which both present an ITAF function. These results suggest that the paraspeckle could be an assembly platform for IRESome, a complex responsible for IRES-dependent translation, and that Neat1 is a key regulator of this mechanism. The third part of my thesis concerns the identification of specialized ribosomes involved in IRES-dependent translation during stress. Analysis of the composition of polysomes of human cardiomyocytes under endoplasmic reticulum (ER) stress allowed us to discover several mitochondrial ribosomal proteins associated with the polysomes. Cellular stresses induced a switch in polysome composition, inducing an increase of the association with some mitochondrial ribosomal proteins (MRPS12 and MRPS15) while others were decreased (MRPS35 and MRPL52). The rest of the study focused on MRPS15. First, experiments with PLA (proximity ligation assay) and immunoprecipitations from cytosolic and polysomal fractions confirmed the interaction of this mitochondrial protein with the ribosome. In addition, a cytoplasmic fraction of MRPS15 increases in response to stress. [...]
Aguilar, Sanchez Cristina. "Epigenetic transitions in cardiovascular development and cell reprogramming". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28787.
Pełny tekst źródłaGhaffari, Nader. "Block of Na+ current in isolated rat cardiomyocytes by protamine /". Title page and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09SB/09sbg4111.pdf.
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