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Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury

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Acta Pharmacologica Sinica 2005年第9期26卷 1076-1080页

作者： yan-hui zhu xian wang~2 department of physiology and pathophysiology,basic medical college,key laboratory of molecular cardiovascular biology,ministry of education,peking university,beijing 100083,china department of physiology and pathophysiology Basic Medical College Key Laboratory of Molecular Cardiovascular Biology Ministry of Education Peking University Beijing China

Aim:To explore whether overexpression of the small heat shock protein HSP20 inrat cardiomyocytes protects against simulated ischemia/reperfusion(SI/R)***:Recombinant adenovirus expressing HSP20 was used to infect rat H9c2cardiomyocytes at high efficiency,as assessed by green fluorescent protein.H9c2cells were subjected to SI/R stress;survival was estimated through assessment oflactate dehydrogenase and cell apoptosis through caspase-3 ***:Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% andcaspase-3 activity by 58.8%.Pretreatment with the protein kinase C inhibitor Ro-31-8220(0.1 μmol/L)for 30 min before SI/R canceled the protective effect of *** selective mitochondrial K+awP channel inhibitor 5-hydroxydecanoate(100 μmol/L)had a similar ***,the non-selective K~+ATPchannel inhibitorglibenclamide(100 μmol/L)had no significant ***:These dataindicate that the protective effect of HSP20 in vitro is primarily due to reducednecrotic and apoptotic death of cardiomyocytes,possibly via the protein kinaseC/mitochondrial K~+ATP pathway.

关键词： reperfusion injury adenovirus apoptosis necrosis heat-shock proteins

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Gene transfer of heat-shock protein 20 protects against ischemia/reperfusion injury in rat hearts

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Acta Pharmacologica Sinica 2005年第10期26卷 1193-1200页

作者： yan-hui zhu, Tie-min MA, xian wang~2 department of physiology and pathophysiology, basic medical college, key laboratory of molecular cardiovascular biology, ministry of education, peking university, beijing 100083, china department of physiology and pathophysiology Basic Medical College Key Laboratory of Molecular Cardiovascular Biology Ministry of Education Peking University Beijing China

Aim: To explore whether overexpression of HSP20 in the myocardium could protect against ischemia/reperfusion injury in rats. Methods: Rat hearts were injected with vector, recombinant adenovirus encoding green fluorescent protein(***) or recombinant adenovirus encoding wild-type HSP20 (***20) in the left ventricle. Four days later, hearts were removed and expression of HSP20was measured in the left ventricle. Subsets of animals in the vector-, ***-, ***20-treated groups were subjected to 20-rain ischemia and 120-rainreperfusion. Myocardial injury was evaluated by infarct size and level of serumcardiac troponin T and creatine phosphokinase. Apoptosis of cardiomyocyteswas determined by TUNEL staining. Cardiac function was evaluated by hemodyamic indexes. Results: Infarct size and serum cardiac troponin T and creatinephosphokinase levels were significantly reduced in ***20-treated hearts compared with vector-and ***-treated hearts. The ratio of TUNEL-positivecardiomyocytes to total number of cardiomyocytes in the ***20 group wassignificantly reduced as compared with the vector and *** groups. Left ventricular end systolic pressure, and maximal rate of pressure increase (+dp/dtmax)and decrease (-dp/dtmin) values were increased significantly, while left ventricularend diastolic pressure was decreased significantly in ***20-treated heartscompared with vector- and ***-treated hearts. Conclusion: These data indicate that the cardioprotective effects of HSP20 may contribute to the reduction ofmyocardial necrosis and apoptosis in ischemia/reperfusion injury in rats.

关键词： reperfusion injury adenovirus apoptosis myocardial infarction heat-shock proteins

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