Expression of uncoupling protein 3 in mitochondria protects against stress-induced myocardial injury: a proteomic study

Expression of uncoupling protein 3 in mitochondria protects against stress-induced myocardial injury: a proteomic study
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线粒体中解偶联蛋白 3 的表达可预防应激诱导的心肌损伤:一项蛋白质组学研究

DOI:
10.1007/s12192-010-0185-y
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发表时间:
2010-04
影响因子:
3.8
通讯作者:
--
中科院分区:
生物学3区
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--
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应激在心血管疾病的发生发展中起重要作用已被证实,但其机制和分子基础尚不清楚。本研究建立了束缚应激致大鼠心肌损伤模型。为了筛选与应激性心肌损伤相关的蛋白质,采用基于双向凝胶电泳法和质谱仪的蛋白质组学技术。在我们的结果中,发现有10个蛋白质发生了改变。束缚应激后,心肌肌球蛋白重链、2-氧戊二酸脱氢酶复合体的二氢硫辛胺琥珀酰基转移酶组分、线粒体乙醛脱氢酶、H+转运型三磷酸腺苷合成酶、白蛋白和载脂蛋白A-I前体等8种蛋白的表达增加。解偶联蛋白3(UCP3)和线粒体乌头酸酶表达降低。大部分蛋白质与能量代谢有关。进一步研究表明,UCP3可能参与了束缚应激诱导的心肌细胞反应。
It has been confirmed that stress plays an important role in the induction and development of cardiovascular diseases, but its mechanism and molecular basis remain unknown. In the present study, a myocardial injury model induced by restraint stress was established in rat. To screen for the related proteins involved in stress-induced myocardial injury, proteomic techniques based on 2-DE and mass spectrometry were used. In our results, ten proteins were found to be altered. The expression of eight of these proteins was increased after restraint stress, including cardiac myosin heavy chain, dihydrolipoamide succinyltransferase component of 2-oxoglutarate dehydrogenase complex, mitochondrial aldehyde dehydrogenase, H+-transporting ATP synthase, albumin, and apolipoprotein A-I precursor. The expression of uncoupling protein 3 (UCP3) and mitochondrial aconitase was decreased. Most of the proteins were related to energy metabolism. Further research indicated that UCP3 may mediate the myocardial cell response induced by restraint stress.
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发表时间: 2005-12-27
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