Expression of uncoupling protein 3 in mitochondria protects against stress-induced myocardial injury: a proteomic study |
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Authors: | Xinxing Wang Jingbo Gong Xiaohua Liu Rui Zhan Ruirui Kong Yun Zhao Di Wan Xue Leng Ming Chen Lingjia Qian |
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Institution: | (1) Key Laboratory of Stress Medicine, Tianjing Institute of Hygiene and Environmental Medicine, 1 Dali Road, Heping District, Tianjing, 300050, China;(2) Department of Stress Medicine, Institute of Health & Environmental Medicine, No.1 DaLi Road, Tianjin, 300050, China |
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Abstract: | 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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Keywords: | Myocardial injury Mitochondria Proteomic Restraint stress UCP3 |
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