Overexpression of mitochondrial peroxiredoxin-3 prevents left ventricular remodeling and failure after myocardial infarction in mice
Overexpression of mitochondrial peroxiredoxin-3 prevents left ventricular remodeling and failure after myocardial infarction in mice
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DOI：
10.1161/circulationaha.105.582239
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发表时间：
2006-04-11
期刊：
影响因子：
37.8
通讯作者：
Tsutsui, H
中科院分区：
文献类型：
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作者：
Matsushima, S;Ide, T;Tsutsui, H
线粒体氧化应激和损伤在心肌梗死（MI）后左心室（LV）重构和衰竭的发生和发展中起主要作用。我们假设，过表达的线粒体抗氧化剂，过氧化物酶-3（Prx-3），可以减弱这种有害的processing.Methods和Results-We创建MI在12至16周龄，雄性Prx-3转基因小鼠（TG+MI，n=37）和非转基因野生型小鼠（WT+MI，n=39）结扎左冠状动脉。TG小鼠心脏中的Prx-3蛋白水平比WT小鼠高1.8倍，其他抗氧化酶没有显着变化。MI后4周，TG+MI小鼠左室线粒体中硫代巴比妥酸反应物质显著低于WT+MI小鼠（平均值± SEM，1.5 ± 0.2 vs 2.2 ± 0.2 nmol/mg蛋白;各n=8，P
Background-Mitochondrial oxidative stress and damage play major roles in the development and progression of left ventricular (LV) remodeling and failure after myocardial infarction (MI). We hypothesized that overexpression of the mitochondrial antioxidant, peroxiredoxin-3 (Prx-3), could attenuate this deleterious process.Methods and Results-We created MI in 12- to 16-week-old, male Prx-3-transgenic mice (TG+MI, n=37) and nontransgenic wild-type mice (WT+MI, n=39) by ligating the left coronary artery. Prx-3 protein levels were 1.8 times higher in the hearts from TG than WT mice, with no significant changes in other antioxidant enzymes. At 4 weeks after MI, LV thiobarbituric acid-reactive substances in the mitochondria were significantly lower in TG+MI than in WT+MI mice (mean +/- SEM, 1.5 +/- 0.2 vs 2.2 +/- 0.2 nmol/mg protein; n=8 each, P