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Ischemic post-conditioning promotes mitochondrial translocation of DJ-1 and stabilizes binding to Bcl- xL to attenuate myocardial ischemic-reperfusion injury in STZ-induced diabetic rats
- Publication Year :
- 2021
- Publisher :
- Research Square Platform LLC, 2021.
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Abstract
- Background Ischemic post-conditioning (IPO) is a strategy in reducing myocardial ischemic-reperfusion (I/R) injury, but its specific molecular mechanism is incompletely understood. Deletions or mutations in the DJ-1 gene are directly linked to the cardiovascular system. DJ-1 plays a critical role in regulating mitochondrial homeostasis in response to stress through translocation of DJ-1 from the cytoplasm into the nucleus. Meanwhile, how the DJ-1 is removed in myocardial I/R injury and regulating apoptosis is needed to further verified. Given the discovery mentioned above, we hypothesize that DJ-1 translocate to mitochondria recover IPO induced cardioprotection in STZ-induced diabetic rats. To evaluate our hypothesis, we overexpressed the DJ-1 protein under high glucose condition, subjected IPO or not. And then measure the expression of DJ-1 in mitochondria and cytoplasm after myocardial I/R. Results We found that DJ-1 translocated to mitochondria combined with Bcl-xL was reduced cardiomyocyte injury and apoptosis in diabetic myocardial I/R heart. Additionally, the binding of DJ-1 and Bcl-xL is dependent on the oxidative state of DJ-1(oxidation of DJ-1 at Cys-106 is important for its protective effect). Conclusions If our hypothesis is correct, promote DJ-1 mitochondrial transfer may be critical with respect to restoring myocardial responsiveness to IPO in diabetes.
Details
- Database :
- OpenAIRE
- Accession number :
- edsair.doi...........b2b456a65d9e8b5e712b3c90028953f7