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11	NFATc1 in cardiac valve development and EPDC invasion Combs, Michelle D. 19 April 2011 (has links) No description available. Developmental Biology NFATc1 valve development epicardium Cathepsin K coronary vessels fibrous matrix
12	CDH18 is a fetal epicardial biomarker regulating differentiation towards vascular smooth muscle cells / CDH18は血管平滑筋細胞への分化を制御する胎児心外膜バイオマーカーである Junghof, Julia 23 March 2022 (has links) 京都大学 / 新制・課程博士 / 博士(医科学) / 甲第23815号 / 医科博第136号 / 新制\|\|医科\|\|9(附属図書館) / 京都大学大学院医学研究科医科学専攻 / (主査)教授山下潤, 教授遊佐宏介, 教授伊藤貴浩 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM epicardium hiPSC-derived epicardial cells epicardial development CDH18 WT1 EPDCs EMT SMC CF epicardial activation 491
13	Regeneration of Cryoinjury Induced Necrotic Heart Lesions in Zebrafish Is Associated with Epicardial Activation and Cardiomyocyte Proliferation Weidinger, Gilbert, Schnabel, Kristin, Wu, Chi-Chung, Kurth, Thomas 07 January 2016 (has links) (PDF) In mammals, myocardial cell death due to infarction results in scar formation and little regenerative response. In contrast, zebrafish have a high capacity to regenerate the heart after surgical resection of myocardial tissue. However, whether zebrafish can also regenerate lesions caused by cell death has not been tested. Here, we present a simple method for induction of necrotic lesions in the adult zebrafish heart based on cryoinjury. Despite widespread tissue death and loss of cardiomyocytes caused by these lesions, zebrafish display a robust regenerative response, which results in substantial clearing of the necrotic tissue and little scar formation. The cellular mechanisms underlying regeneration appear to be similar to those activated in response to ventricular resection. In particular, the epicardium activates a developmental gene program, proliferates and covers the lesion. Concomitantly, mature uninjured cardiomyocytes become proliferative and invade the lesion. Our injury model will be a useful tool to study the molecular mechanisms of natural heart regeneration in response to necrotic cell death. Herz Zebrafisch TU Dresden Publikationsfonds Heart Heart regeneration Zebrafish Surgical resection Myocardium Cardiac ventricles Epicardium Regeneration Technical University Dresden Publication funds ddc:610 rvk:XA 10000
14	Rôle de la voie de signalisation du récepteur -1 des prokinéticines dans la fonction cardiaque et rénale : implication des cellules progénitrices / Role of prokineticin receptor 1 signaling pathways in heart and kidney function : implication of progenitor cells Boulberdaa, Mounia 13 September 2012 (has links) [...]Mon projet de Doctorat a donc visé à : 1. déterminer le rôle de la voie de signalisation PKR1 in vivo ; 2. la perte de la voie de signalisation PKR1 provenant de l’épicarde induit des dysfonctions cardiaques et rénales ; 3. mettre en évidence le rôle de PKR1 dans l’activation et la différentiation des cellules progénitrices.[...] / [...]My specific aim are the following : 1. To determine the role of PKR1 signaling pathways in vivo ; 2. To show that the inactivation of PKR1 specifically in epicardium can induce cardiac and renal disorders ; 3. To determine the role of PKR1 in activation and differentiation of progenitor cells.[...] Cardiomyopathie Pathologie rénale Communication cellulaire Angiogenèse Thérapie cellulaire Epicardin (Tcf21, capsuline, POD1) Cellules progénitrices RCPG PKR1 Epicardium Activation cells Differenciation cells 572.8 616.1 616.6
15	Regeneration of Cryoinjury Induced Necrotic Heart Lesions in Zebrafish Is Associated with Epicardial Activation and Cardiomyocyte Proliferation Weidinger, Gilbert, Schnabel, Kristin, Wu, Chi-Chung, Kurth, Thomas 07 January 2016 (has links) In mammals, myocardial cell death due to infarction results in scar formation and little regenerative response. In contrast, zebrafish have a high capacity to regenerate the heart after surgical resection of myocardial tissue. However, whether zebrafish can also regenerate lesions caused by cell death has not been tested. Here, we present a simple method for induction of necrotic lesions in the adult zebrafish heart based on cryoinjury. Despite widespread tissue death and loss of cardiomyocytes caused by these lesions, zebrafish display a robust regenerative response, which results in substantial clearing of the necrotic tissue and little scar formation. The cellular mechanisms underlying regeneration appear to be similar to those activated in response to ventricular resection. In particular, the epicardium activates a developmental gene program, proliferates and covers the lesion. Concomitantly, mature uninjured cardiomyocytes become proliferative and invade the lesion. Our injury model will be a useful tool to study the molecular mechanisms of natural heart regeneration in response to necrotic cell death. info:eu-repo/classification/ddc/610 ddc:610

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