Journal
IUBMB LIFE
Volume 66, Issue 3, Pages 220-227Publisher
WILEY
DOI: 10.1002/iub.1259
Keywords
microRNA; mesenchymal stem cells; target gene; PI3K; miR-203
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Funding
- China Postdoctoral Science Foundation [2013M541185]
- National Natural Science Foundation of China [81270528, 81170444]
- Natural Science Foundation of Tianjin [08JCYBJC08400, 12JCZDJC25200, 11JCZDJC27800]
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As a group of heterogeneous multipotent cells, mesenchymal stem cells (MSCs) have potential in treatment of a variety of clinical diseases. However, the low survival of the transplanted MSCs reduced their therapeutic effects. In this study, we revealed that rno-miR-203 suppressed activity and colony formation and enhanced apoptosis of the rat bone marrow-derived MSCs (BM-MSCs). Using bioinformatics analysis, we found a potential miR-203 binding site within rat phosphatidylinositol 3-kinase (PI3K) 3 ' UTR, and fluorescent reporter experiments validated the direct and negative regulation of PI3K expression by miR-203 through this site. Ectopic expression of PI3K rescued BM-MSCs from depressed activity induced by miR-203, and suppression of PI3K attenuated the increased BM-MSCs activity by miR-203 inhibitor treatment. Moreover, miR-203 blocking partly protected BM-MSCs from impairment caused by low nutrition. We conclude that inhibition of endogenous miR-203 elevated PI3K expression, which may strengthen PI3K/Akt pathway and promote BM-MSCs activity and survival. (c) 2014 IUBMB Life, 66(3):220-227, 2014
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