Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosisReport as inadecuate




Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosis - Download this document for free, or read online. Document in PDF available to download.

Science China Life Sciences

, Volume 57, Issue 2, pp 171–180

First Online: 22 January 2014Received: 29 July 2013Accepted: 11 October 2013DOI: 10.1007-s11427-014-4607-4

Cite this article as: Wang, L., Hu, X., Zhu, W. et al. Sci. China Life Sci. 2014 57: 171. doi:10.1007-s11427-014-4607-4

Abstract

Autophagy is the basic catabolic progress involved in cell degradation of unnecessary or dysfunctional cellular components. It has been proven that autophagy could be utilized for cell survival under stresses. Hypoxic-preconditioning HPC could reduce apoptosis induced by ischemia and hypoxia-serum deprivation H-SD in bone marrow-derived mesenchymal stem cells BMSCs. Previous studies have shown that both leptin signaling and autophagy activation were involved in the protection against apoptosis induced by various stress, including ischemia-reperfusion. However, it has never been fully understood how leptin was involved in the protective effects conferred by autophagy. In the present study, we demonstrated that HPC can induce autophagy in BMSCs by increased LC3-II-LC3-I ratio and autophagosome formation. Interestingly, similar effects were also observed when BMSCs were pretreated with rapamycin. The beneficial effects offered by HPC were absent when BMSCs were incubated with autophagy inhibitor, 3-methyladenine 3-MA. In addition, down-regulated leptin expression by leptin-shRNA also attenuated HPC-induced autophagy in BMSCs, which in turn was associated with increased apoptosis after exposed to sustained H-SD. Furthermore, increased AMP-activated protein kinase phosphorylation and decreased mammalian target of rapamycin phosphorylation that were observed in HPC-treated BMSCs can also be attenuated by down-regulation of leptin expression. Our data suggests that leptin has impact on HPC-induced autophagy in BMSCs which confers protection against apoptosis under H-SD, possibly through modulating both AMPK and mTOR pathway.

KeywordsBMSCs autophagy hypoxic-preconditioning leptin apoptosis This article is published with open access at link.springer.com

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Author: LiHan Wang - XinYang Hu - Wei Zhu - Zhi Jiang - Yu Zhou - PanPan Chen - JianAn Wang

Source: https://link.springer.com/



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