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Text
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URL Address
<a href="http://doi.org/10.1152/ajpheart.00731.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00731.2011</a>
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Pages
H1410-H1422
Issue
7
Volume
302
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Title
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Biphasic Modulation Of The Mitochondrial Electron Transport Chain In Myocardial Ischemia And Reperfusion
Publisher
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American Journal of Physiology-Heart and Circulatory Physiology
Date
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2012
2012-04
Subject
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Cardiovascular System & Cardiology; cytochrome-c-oxidase; energy-metabolism; injury; nadh dehydrogenase; oxidative modification; oxygen-free-radicals; Physiology; postischemic myocardium; protein biosynthesis; rat-heart mitochondria; reactive oxygen species; transfer complex-i; translational control
Creator
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Lee H L; Chen C L; Yeh S T; Zweier J L; Chen Y R
Description
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Lee HL, Chen CL, Yeh ST, Zweier JL, Chen YR. Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion. Am J Physiol Heart Circ Physiol 302: H1410-H1422, 2012. First published January 20, 2012; doi: 10.1152/ajpheart.00731.2011.-Mitochondrial electron transport chain (ETC) is the major source of reactive oxygen species during myocardial ischemia-reperfusion (I/R) injury. Ischemic defect and reperfusion-induced injury to ETC are critical in the disease pathogenesis of postischemic heart. The properties of ETC were investigated in an isolated heart model of global I/R. Rat hearts were subjected to ischemia for 30 min followed by reperfusion for 1 h. Studies of mitochondrial function indicated a biphasic modulation of electron transfer activity (ETA) and ETC protein expression during I/R. Analysis of ETAs in the isolated mitochondria indicated that complexes I, II, III, and IV activities were diminished after 30 min of ischemia but increased upon restoration of flow. Immunoblotting analysis and ultrastructural analysis with transmission electron microscopy further revealed marked downregulation of ETC in the ischemic heart and then upregulation of ETC upon reperfusion. No significant difference in the mRNA expression level of ETC was detected between ischemic and postischemic hearts. However, reperfusion-induced ETC biosynthesis in myocardium can be inhibited by cycloheximide, indicating the involvement of translational control. Immunoblotting analysis of tissue homogenates revealed a similar profile in peroxisome proliferator-activated receptor-gamma coactivator-1 alpha expression, suggesting its essential role as an upstream regulator in controlling ETC biosynthesis during I/R. Significant impairment caused by ischemic and postischemic injury was observed in the complexes I-III. Analysis of NADH ferricyanide reductase activity indicated that injury of flavoprotein subcomplex accounts for 50% decline of intact complex I activity from ischemic heart. Taken together, our findings provide a new insight into the molecular mechanism of I/R-induced mitochondrial dysfunction.
Identifier
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<a href="http://doi.org/10.1152/ajpheart.00731.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00731.2011</a>
Format
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Journal Article or Conference Abstract Publication
2012
American Journal of Physiology-Heart and Circulatory Physiology
Cardiovascular System & Cardiology
Chen C L
Chen Y R
cytochrome-c-oxidase
energy-metabolism
Injury
Journal Article or Conference Abstract Publication
Lee H L
nadh dehydrogenase
oxidative modification
oxygen-free-radicals
Physiology
postischemic myocardium
Protein Biosynthesis
rat-heart mitochondria
reactive oxygen species
transfer complex-i
translational control
Yeh S T
Zweier J L