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Author Notes:
Correspondence: Ling Wei, 101 Woodruff Circle, Department of Anesthesiology, Emory University, School of Medicine, Atlanta, GA 30322; Email: lwei7@emory.edu.
Subjects:
Research Funding:
This work was supported by NIH grants NS 045810 (LW), NS062097 (LW), NS 058710 (LW), NS057255 (SPY) and the American Heart Association Established Investigator Award (LW).
It was also supported by the NIH grant NS055077 to the ENNCF (Emory Neurology-NINDS Core Facility).
Keywords:
- Apelin-13
- Bone marrow mesenchymal stem cells
- Serum deprivation
- Apoptosis
Protective effect of apelin on cultured rat bone marrow mesenchymal stem cells against apoptosis
Abstract:
Bone marrow-derived mesenchymal stem cells (BMSCs) have shown great promise for ischemic tissue repair. However, poor viability of transplanted BMSCs within ischemic tissues has limited their therapeutic potential. Apelin, an endogenous peptide, whose level is elevated following ischemia, has been shown to enhance survival of cardiomyocytes and neuronal cells during ischemia. We hypothesized that apelin-13 protects BMSCs from apoptotic death. In this paper we determined the potential mechanism of apelin-13 effects using cultured BMSCs from adult rats. Apoptosis was induced by the specific apoptotic insult serum deprivation (SD) for up to 36 hrs. Apoptotic cell death was measured using immunostaining and Western blotting in the presence and absence of apelin-13 (0.1 to 5.0 nM) co-applied during SD exposure. SD-induced apoptosis was significantly reduced by apelin-13 in a concentration-dependent manner. SD-induced mitochondrial depolarization, cytochrome c release, and caspase-3 activation were largely prevented by apelin-13. The apelin-13 anti-apoptotic effects were blocked by inhibiting the MAPK/ERK1/2 and PI3K/Akt signaling pathways. Taken together, our findings indicate that apelin-13 is a survival factor for BMSCs and its anti-apoptotic property may prove to be of therapeutic significance in terms of exploiting BMSC-based transplantation therapy.
Copyright information:
© 2012 Elsevier B.V. All rights reserved.
This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).
