Rac-Induced Left Ventricular Dilation in Thyroxin-Treated ZmRacD Transgenic Mice Role of Cardiomyocyte Apoptosis and Myocardial Fibrosis 英文参考文献.docVIP

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Rac-Induced Left Ventricular Dilation in Thyroxin-Treated ZmRacD Transgenic Mice Role of Cardiomyocyte Apoptosis and Myocardial Fibrosis 英文参考文献.doc

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Rac-Induced Left Ventricular Dilation in Thyroxin-Treated ZmRacD Transgenic Mice Role of Cardiomyocyte Apoptosis and Myocardial Fibrosis 英文参考文献

Rac-InducedLeftVentricularDilationinThyroxin-Treated ZmRacDTransgenicMice:RoleofCardiomyocyte ApoptosisandMyocardialFibrosis MohammadT.Elnakish1,2,MohamedD.H.Hassona1,MazinA.Alhaj1,LeniMoldovan3, PaulM.L.Janssen2,MahmoodKhan4,HamdyH.Hassanain1* 1Department of Anesthesiology, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America, 2Department of Physiology and Cell Biology, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America, 3Department 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, 4Department of Internal Medicine, and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus,Ohio,UnitedStatesofAmerica Abstract Thepathwaysinducingthecriticaltransitionfromcompensatedhypertrophytocardiacdilationandfailureremainpoorly understood.ThegoalofourstudyistodeterminetheroleofRac-inducedsignalinginthistransitionprocess.Ourprevious resultsshowedthatThyroxin(T4)treatmentresultedinincreasedmyocardialRacexpressioninwild-typemiceandahigher levelofexpressioninZeamaizeRacD(ZmRacD)transgenicmice.OurcurrentresultsshowedthatT4treatmentinduced physiologiccardiachypertrophyinwild-typemice,asdemonstratedbyechocardiographyandhistopathologyanalyses.This was associated with significant increases in myocardial Rac-GTP, superoxide and ERK1/2 activities. Conversely, echocardiography and histopathology analyses showed that T4 treatment induced dilated cardiomyopathy along with compensatory cardiac hypertrophy in ZmRacD mice. These were linked with further increases in myocardial Rac-GTP, superoxide and ERK1/2 activities. Additionally, there were significant increases in caspase-8 expression and caspase-3 activity. However, there was a significant decrease in p38-MAPK activity. Interestingly,