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Enhanced engraftment, proliferation, and therapeutic potential in heart using optimized human iPSC-derived cardiomyocytes / 至適化したiPS細胞由来心筋細胞による、細胞移植後の生着、増殖、治療効果の評価Funakoshi, Shunsuke 23 March 2016 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第19595号 / 医博第4102号 / 新制||医||1014(附属図書館) / 32631 / 京都大学大学院医学研究科医学専攻 / (主査)教授 山下 潤, 教授 瀬原 淳子, 教授 前川 平 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Characterization of TRP Ion Channels in Cardiac MuscleAndrei, Spencer R. 22 June 2017 (has links)
No description available.
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MicroRNA Mediated Proliferation of Adult Cardiomyocytes to Regenerate Ischemic MyocardiumPandey, Raghav 15 December 2017 (has links)
No description available.
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Ligantes de miócitos cardíacos para a glicoproteína de 85kda. (tc-85) de Trypanosoma cruzi / Ligand cardiac myocytes to 85 kda glycoprotein. (CT-85) of Trypanosoma cruziSá Junior, Paulo Luiz de 28 September 2005 (has links)
O Trypanosoma cruzi expressa um grupo de glicoprotcinas de superfície, denominadas Tc-85, que pertencem à superfumília gêmca das gp85/traus-sialidases. Nosso laboratório clonou e caracterizou um membro da fumília Tc85 (Tc85-11), cuja região carboxila tenninal (clone Tc85-1) adere em laminina e em células de mamífero. Usando peptídeos sintéticos, correspondendo em seqüência à Tc85-1, caracterizou-se o motivo mais conservado da superfamilia gênica das gp85/trans-sialidases (VTVxNVFLYNR), o qual não adere em laminina. Esse motivo foi chamado peptídeo J. Por cromatografia de extratos de membrana de cardiomiócitos em coluna de afmidade contendo peptídeo J, foi isolada uma molécula de 30kDa identificada como sendo a subunidade β3 da Na+, K+ ATPase. A porção extracelular da subunidade β3 da Na+, K+ ATPase foi clonada e a interação in vitro desta proteína com peptídeo J foi observada. Deste modo, é sugerido aqui que a subunidade β3 da Na+, K+ ATPase pode ter um papel importante na interação do parasita com a célula hospedeira. / Abstract not available.
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Rôles des cardiofibroblastes dans la protection des cardiomyocytes au cours de l'ischémie-reperfusion / Role of cardiac fibroblasts in cardiomyocyte protection during ischemia reperfusionAbrial, Maryline 07 November 2013 (has links)
Les cardiofibroblastes (CF) possèdent des rôles clés dans la régulation de la structure et du fonctionnement myocardique. Leurs implications physiopathologiques, notamment dans le remodelage et la fibrose, ont été largement décrites dans les maladies cardiovasculaires chroniques. Cependant, leurs rôles au cours de la phase aigüe d'ischémie-reperfusion (l/R) restent encore à élucider. Nous avons donc émis l'hypothèse que les CF pouvaient participer à la protection des cardiomyocytes (CM) face aux lésions d'l/R. Le but de ce travail a donc consisté en l'exploration et l'identification des mécanismes de cette protection. Un modèle cellulaire de CM et CF de rats nouveau-nés in vitro et un modèle d'l/R in vivo chez la souris ont été utilisés. Nos résultats montrent que la présence des CF, en co-culture avec les CM, augmente de façon paracrine leur viabilité, face aux lésions d'l/R. Cette action paracrine a été confirmée par l'utilisation du sécrétome de CF hypoxiques capable, à lui seul, d'augmenter la viabilité des CM. Ces résultats ont été corroborés par des expériences d'l/R in vivo, dans lesquelles les souris traitées avec le sécrétome de CF présentent une diminution de la taille d'infarctus. De plus, nous avons montré que TlMP-1, un facteur fortement détecté dans le sécrétome de CF, est capable de diminuer à la fois la mortalité cellulaire in vitro des CM et la taille de l'infarctus in vivo. L'utilisation d'inhibiteurs pharmacologiques nous a permis de mettre en évidence que cette protection paracrine était médiée en partie par l'activation des voies de signalisation Pl3K/Akt et ERK1/2. En conclusion cette étude démontre pour la première fois que les CF participent, de façon paracrine, à la protection des CM au cours la phase aigüe d'ischémie reperfusion. TlMP-1 semble être un des facteurs clé de cette cardioprotection par les CF. En parallèle de ce travail, plusieurs études collaboratives ont été réalisées, sur une cible majeure d'investigation dans la cardioprotection : le pore de transition de perméabilité mitochondriale et notamment sa régulation par le complexe l de la chaîne respiratoire et les échanges calciques, ainsi que son implication dans la défaillance multi-organe face à l'arrêt cardiaque / Roles of cardiac fibroblasts (CF) in the regulation of myocardial structure and function have been emphasized in the last decade. Their implications in pathophysiological aspects of chronic heart diseases such as myocardial remodelling and fibrosis is now well established. However their contribution to the acute phase of ischemia reperfusion injury still remains elusive. We hypothesized that CF may contribute to cardiomyocytes (CM) protection against ischemia reperfusion (l/R) injuries. This study was designed to investigate this protection and identify some of its mechanisms. Experiments were performed both on isolated neonatal rat CF and CM in vitro and in vivo mice model of myocardial infarction. We demonstrated that the presence of CF increases CM viability in co-cultures and that CF protect CM against l/R injuries in a paracrine manner. lt was confirmed by a similar effect of hypoxic CF secretome alone on CM viability. These findings were corroborated by in vivo experiments in which an infarct size reduction was observed in CF secretome treated mice. Furthermore, experiments with Tissue lnhibitor of Metalloproteinases-1 (TlMP-1), abundantly detected in CF secretome, was able to both decrease CM cell death and infarct size. Experiments with pharmacological inhibitors provided more evidence that this paracrine protection is partly mediated by Pl3K/Akt and ERK signalling pathways. Our data demonstrated for the first time that CF participate in cardioprotection during the acute phase of ischemia reperfusion, via a paracrine pathway, involving TlMP-1. Besides this first work, other collaborative studies have been performed, to investigate a major target in cardioprotection research : the mitochondrial permeability transition pore and its regulation by chain respiratory complex l and Ca2+ transfers and finally its implication in multiple organ failure in cardiac arrest
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Etude cellulaire et moléculaire de l'insuffisance cardiaque à fonction systolique préservée / Heart failure with preserved systolic function : Cellular and molecular pathophysiological pathwaysRouhana, Sarah 30 November 2018 (has links)
L'insuffisance cardiaque à fraction d’éjection préservée (IC/FEp) constitue un problème de santé croissant. Elle pourrait devenir la principale cause d'IC d'ici une décennie. C’est une pathologie associée à un taux élevé de morbidité et de mortalité. La prise en charge thérapeutique de l’IC/FEp reste limitée en raison de sa physiopathologie encore mal élucidée. Dans le présent travail, après avoir mis au point un modèle d’IC/FEp sur le rat adulte mâle et l’avoir caractérisé, nous avons évalué le phénotype fonctionnel et l’homéostasie calcique des cardiomyocytes. Les cœurs de ces animaux ont montré une fraction d’éjection supérieure à 50%, associée à une congestion pulmonaire, une hypertrophie concentrique avec une augmentation de la masse du ventricule gauche, une rigidité myocardique, une relaxation et un remplissage ventriculaire passif altérés et une dilatation auriculaire. Au niveau cellulaire, la contraction mesurée sur des cardiomyocytes isolés ainsi que le transitoire calcique sont augmentées. On note, de même, une surcharge en Ca2+ diastolique favorisée par une fuite à travers les canaux Ryanodine 2 et par un dysfonctionnement de l’échangeur Na+ /Ca2+ qui contribuent à générer des événements calciques spontanés. La phosphorylation du phospholamban, régulateur de l’activité de la SERCA2a, a également augmenté, laissant suggérer une compensation adaptative du cycle de Ca2+. Enfin, en présence de Ranolazine, inhibiteur du courant sodique soutenu, les évènements calciques spontanés ont été réprimés. En conclusion, le remodelage cardiaque dans l’IC/FEp semble être diffèrent de celui observé dans l’IC/FEr et ouvre la voie vers de nouveaux acteurs physiopathologiques et thérapeutiques. / Heart failure with preserved ejection fraction (HFpEF) is a growing health problem. It could become the leading cause of HF within a decade. It is a pathology associated with high morbidity and mortality. Therapeutic options are limited due to a lack of knowledge of the pathology and its evolution. In this work, we investigated the cellular phenotype and Ca2+ handling in hearts recapitulating HFpEF criteria. HFpEF was induced in a portion of male Wistar rats four weeks after abdominal aortic banding. These animals had nearly normal ejection fraction and presented elevated blood pressure, lung congestion, concentric hypertrophy, increased LV mass, wall stiffness, impaired active relaxation and passive filling of the left ventricle, enlarged left atrium, and cardiomyocyte hypertrophy. Left ventricular cell contraction was stronger and the Ca2+ transient larger. Ca2+ cycling was modified with a RyR2 mediated Ca2+ leak from the sarcoplasmic reticulum and impaired Ca2+ extrusion through the Na+ /Ca2+ (NCX), which promoted an increase in diastolic Ca2+ and spontaneous Ca2+ waves. PLN phosphorylation which promotes SERCA2a activity, was increased, suggesting an adaptive compensation of Ca2+ cycling. In the presence of Ranolazine, a sustained sodium current inhibitor, spontaneous Ca2+ events were suppressed. Cardiac remodeling in hearts with a HFpEF status differs from that known for HFrEF and opens the way to new pathophysiological and therapeutic actors.
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Engineering the Myocardial Niche in a Microscale Self-assembling Tissue-mimetic in vitro ModelThavandiran, Nimalan 23 July 2012 (has links)
Drug- and cell-based strategies for treating heart disease, including myocardial infarction, face significant roadblocks on the path to the clinic, a primary obstacle being the lack of information-rich in vitro human model systems. Conventional model systems are hampered by at least one of three fundamental limitations which include a) the lack of an in vivo-like microenvironment specifically engineered for the input cell population, b) a relatively low-throughput assays, and c) the low-content nature of output parameters. We describe an integrated computational, design, and experimental strategy for the rational design of a microfabricated high-content screening platform which we term the Cardiac MicroWire (CMW) system. Within this system, we recapitulate the basic microenvironment found in the heart, one which integrates cardiomyocytes, non-myocytes, the extracellular matrix, and dynamic electromechanical forces. Our results highlight the CMW system’s potential as a powerful discovery tool for screening small molecules and transplantable cells toward heart regeneration therapies.
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Engineering the Myocardial Niche in a Microscale Self-assembling Tissue-mimetic in vitro ModelThavandiran, Nimalan 23 July 2012 (has links)
Drug- and cell-based strategies for treating heart disease, including myocardial infarction, face significant roadblocks on the path to the clinic, a primary obstacle being the lack of information-rich in vitro human model systems. Conventional model systems are hampered by at least one of three fundamental limitations which include a) the lack of an in vivo-like microenvironment specifically engineered for the input cell population, b) a relatively low-throughput assays, and c) the low-content nature of output parameters. We describe an integrated computational, design, and experimental strategy for the rational design of a microfabricated high-content screening platform which we term the Cardiac MicroWire (CMW) system. Within this system, we recapitulate the basic microenvironment found in the heart, one which integrates cardiomyocytes, non-myocytes, the extracellular matrix, and dynamic electromechanical forces. Our results highlight the CMW system’s potential as a powerful discovery tool for screening small molecules and transplantable cells toward heart regeneration therapies.
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Ligantes de miócitos cardíacos para a glicoproteína de 85kda. (tc-85) de Trypanosoma cruzi / Ligand cardiac myocytes to 85 kda glycoprotein. (CT-85) of Trypanosoma cruziPaulo Luiz de Sá Junior 28 September 2005 (has links)
O Trypanosoma cruzi expressa um grupo de glicoprotcinas de superfície, denominadas Tc-85, que pertencem à superfumília gêmca das gp85/traus-sialidases. Nosso laboratório clonou e caracterizou um membro da fumília Tc85 (Tc85-11), cuja região carboxila tenninal (clone Tc85-1) adere em laminina e em células de mamífero. Usando peptídeos sintéticos, correspondendo em seqüência à Tc85-1, caracterizou-se o motivo mais conservado da superfamilia gênica das gp85/trans-sialidases (VTVxNVFLYNR), o qual não adere em laminina. Esse motivo foi chamado peptídeo J. Por cromatografia de extratos de membrana de cardiomiócitos em coluna de afmidade contendo peptídeo J, foi isolada uma molécula de 30kDa identificada como sendo a subunidade β3 da Na+, K+ ATPase. A porção extracelular da subunidade β3 da Na+, K+ ATPase foi clonada e a interação in vitro desta proteína com peptídeo J foi observada. Deste modo, é sugerido aqui que a subunidade β3 da Na+, K+ ATPase pode ter um papel importante na interação do parasita com a célula hospedeira. / Abstract not available.
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Commercialization of Pre-Clinical Cardiac Safety Using Stem Cell Derived Human CardiomyocytesSethia, Vinay K. 06 July 2011 (has links)
No description available.
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