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Cardiac ischemic preconditioning prevents dystrophin proteolysis by MMP-2 inhibition
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作者 MANUEL RODRIGUEZ BRUNO BUCHHOLZ +7 位作者 VERONICA D'ANNUNZIO MARTÍN DONATO GERMAN E.GONZALEZ maria ailin goyeneche TAMARA MAZO VIRGINIA PEREZ LUCIANA WILENSKY RICARDO J.GELPI 《BIOCELL》 SCIE 2016年第1期43-46,共4页
Dystrophin is a membrane-associated protein responsible for structural stability of the sarcolem-ma in cardiac myocytes and is very sensitive to ischemic damage.The goal of our study was to determine if ischemic preco... Dystrophin is a membrane-associated protein responsible for structural stability of the sarcolem-ma in cardiac myocytes and is very sensitive to ischemic damage.The goal of our study was to determine if ischemic preconditioning could prevent dystrophin breakdown through inhibition of matrix metalloprotein-ase-2(MMP-2)activity.Isolated rabbit hearts were subjected to global ischemia with or without reperfusion in order to evaluate if dystrophin is preserved by ischemic preconditioning through MMP-2 inhibition.Ischemic preconditioning significantly reduced the infarct size induced by 30 min of ischemia and 180 min of reperfusion.Importantly,it also diminished dystrophin proteolysis and attenuated MMP-2 activity after 30 min ischemia.Thus,our study shows a novel protective role of ischemic preconditioning as a mechanism of preservation of plasma membrane integrity by inhibiting MMP-2 activation. 展开更多
关键词 ISCHEMIA/REPERFUSION MMPS membrane associated proteins RABBIT
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