myocardial overexpression of mecr, a gene of mitochondrial fas ii leads to cardiac dysfunction in mouse心肌mecr的过度表达,基因的线粒体fas ii导致小鼠的心脏功能障碍.pdfVIP
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myocardial overexpression of mecr, a gene of mitochondrial fas ii leads to cardiac dysfunction in mouse心肌mecr的过度表达,基因的线粒体fas ii导致小鼠的心脏功能障碍
Myocardial Overexpression of Mecr, a Gene of
Mitochondrial FAS II Leads to Cardiac Dysfunction in
Mouse
1 2 3 4 1
Zhijun Chen , Hanna Leskinen , Erkki Liimatta , Raija T. Sormunen , Ilkka J. Miinalainen , Ilmo E.
3 1
Hassinen , J. Kalervo Hiltunen *
1 Biocenter Oulu and Department of Biochemistry, University of Oulu, Oulu, Finland, 2 Biocenter Oulu and Department of Pharmacology and Toxicology, University of
Oulu, Oulu, Finland, 3 Department of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland, 4 Biocenter Oulu and Department of Pathology,
University of Oulu, 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), which catalyzes the NADPH-dependent reduction of trans-2-enoyl thioesters, generating saturated
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
remained an enigma. To study the in vivo function of the mitochondrial FAS in mammals, with special reference to Mecr, we
generated mice overexpressing Mecr under control of the mouse metallothionein-1 promoter. These Mecr transgenic mice
developed cardiac abnormalities as demonstrated by echocardiography in vivo, heart perfusion ex vivo, and electron
microscopy in situ. Moreover, the Mecr transgenic mice showed decreased performance
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