Myocardial Overexpression of Mecr, a Gene of Mitochondrial FAS II Leads to Cardiac Dysfunction in Mouse 英文参考文献.docVIP

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Myocardial Overexpression of Mecr, a Gene of Mitochondrial FAS II Leads to Cardiac Dysfunction in Mouse 英文参考文献.doc

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Myocardial Overexpression of Mecr, a Gene of Mitochondrial FAS II Leads to Cardiac Dysfunction in Mouse 英文参考文献

MyocardialOverexpressionofMecr,aGeneof MitochondrialFASIILeadstoCardiacDysfunctionin Mouse ZhijunChen1,HannaLeskinen2,ErkkiLiimatta3,RaijaT.Sormunen4,IlkkaJ.Miinalainen1,IlmoE. Hassinen3,J.KalervoHiltunen1* 1BiocenterOuluandDepartmentofBiochemistry,UniversityofOulu,Oulu,Finland,2BiocenterOuluandDepartmentofPharmacologyandToxicology,Universityof Oulu, Oulu, Finland, 3Department of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland, 4Biocenter Oulu and Department of Pathology, UniversityofOulu,Oulu,Finland Abstract It has been recently recognized that mammalian mitochondria contain most, if not all, of the components of fatty acid synthesis type II (FAS II). Among the components identified is 2-enoyl thioester reductase/mitochondrial enoyl-CoA reductase(Etr1/Mecr),whichcatalyzestheNADPH-dependentreductionof trans-2-enoylthioesters,generatingsaturated acyl-groups. Although the FAS type II pathway is highly conserved, its physiological role in fatty acid synthesis, which apparently occurs simultaneously with breakdown of fatty acids in the same subcellular compartment in mammals, has remainedanenigma.TostudytheinvivofunctionofthemitochondrialFASinmammals,withspecialreferencetoMecr ,we generatedmiceoverexpressingMecrundercontrolofthemousemetallothionein-1promoter.TheseMecrtransgenicmice developed cardiac abnormalities as demonstrated by echocardiography in vivo, heart perfusion ex vivo, and electron microscopyinsitu.Moreover,theMecrtransgenicmiceshoweddecreasedperformanceinenduranceexercisetesting.Our results showed a ventricular dilatation behind impaired heart function upon Mecr overexpression, concurrent with appearanceofdysmorphicmitochondria.Furthermore,thedatasuggestedthatinappropriateexpressionofgenesofFASII canresultinthedevelopmentofhereditarycardiomyopathy. Citation:ChenZ,LeskinenH,LiimattaE,SormunenRT,MiinalainenIJ,etal.(2009)MyocardialOverexpressionofMecr,aGeneofMitochondrialFASIILeadsto CardiacDysfunctioninMouse.PLoSONE4(5):e