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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Abbreviations
- ROS:
-
reactive oxygen species
- NE:
-
norepinephrine
- MEM:
-
minimum essential medium
- PTP:
-
permeability transition pore
- 2-DE:
-
two-dimensional gel electrophoresis
- UCP3:
-
uncoupling protein 3
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Acknowledgment
This work was supported in part by grants from the National Natural Science Foundation of China (No. 30770843, No. 30430590).
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Xinxing Wang and Jingbo Gong contributed equally to this work.
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Wang, X., Gong, J., Liu, X. et al. Expression of uncoupling protein 3 in mitochondria protects against stress-induced myocardial injury: a proteomic study. Cell Stress and Chaperones 15, 771–779 (2010). https://doi.org/10.1007/s12192-010-0185-y
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DOI: https://doi.org/10.1007/s12192-010-0185-y