rac-induced left ventricular dilation in thyroxin-treated zmracd transgenic mice role of cardiomyocyte apoptosis and myocardial fibrosisrac-induced左心室扩张在thyroxin-treated zmracd转基因小鼠心肌细胞凋亡和心肌纤维化的作用.pdfVIP

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rac-induced left ventricular dilation in thyroxin-treated zmracd transgenic mice role of cardiomyocyte apoptosis and myocardial fibrosisrac-induced左心室扩张在thyroxin-treated zmracd转基因小鼠心肌细胞凋亡和心肌纤维化的作用.pdf

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rac-induced left ventricular dilation in thyroxin-treated zmracd transgenic mice role of cardiomyocyte apoptosis and myocardial fibrosisrac-induced左心室扩张在thyroxin-treated zmracd转基因小鼠心肌细胞凋亡和心肌纤维化的作用

Rac-Induced Left Ventricular Dilation in Thyroxin-Treated ZmRacD Transgenic Mice: Role of Cardiomyocyte Apoptosis and Myocardial Fibrosis 1,2 1 1 3 Mohammad T. Elnakish , Mohamed D. H. Hassona , Mazin A. Alhaj , Leni Moldovan , 2 4 1 Paul M. L. Janssen , Mahmood Khan , Hamdy H. Hassanain * 1 Department of Anesthesiology, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America, 2 Department of Physiology and Cell Biology, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America, 3 Department of Pulmonary, Allergy, Critical Care and Sleep Medicine, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America, 4 Department of Internal Medicine, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America Abstract The pathways inducing the critical transition from compensated hypertrophy to cardiac dilation and failure remain poorly understood. The goal of our study is to determine the role of Rac-induced signaling in this transition process. Our previous results showed that Thyroxin (T4) treatment resulted in increased myocardial Rac expression in wild-type mice and a higher level of expression in Zea maize RacD (ZmRacD) transgenic mice. Our current results showed that T4 treatment induced physiologic cardiac hypertrophy in wild-type mice, as demonstrated by echocardiography and histopathology analyses. This was associated with s