Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 433, Issue 4, Pages 526-531Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.03.018
Keywords
Mesenchymal stem cells (MSCs); MicroRNAs; High glucose; Phosphatase and tensin homologs deleted on chromosome 10 (PTEN); Phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway; G0/G1 phase
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Funding
- National Science and Technology Support Program of Special Funds [2009BAI87B003]
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MicroRNAs regulate a host of physiological and pathological processes in mesenchymal stem cells (MSCs), although no published studies describe changes in microRNA expression or function in MSCs under in vitro hyperglycemic conditions. By using a microRNA microarray approach, we have identified that miRNA-32-5p expression is significantly reduced under hyperglycemic conditions in rat bone marrow-derived MSCs. Expression of miRNA-32-5p targets the 3'-untranslated region of the mRNA encoding phosphatase and tensin homologs deleted on chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Exposure to high glucose levels reduced miR-32-5p expression, induced PTEN expression, and inhibited activation of the PI3K/Akt signaling pathway of MSCs. Conversely, overexpression of miR-32-5p inhibited the expression of PTEN, ameliorated the inhibitory effect of high glucose levels on the PI3K/Akt signaling pathway, and promoted cell cycle progression from G0/G1 to G2/M and S phases. Our study indicates that exposure of MSCs to hyperglycemic conditions reduces miR-32-5p expression and disturbs cell cycle progression through a PTEN-mediated inhibitory effect on the PI3K/Akt signaling pathway. In summary, MiR-32-5p is a potentially important therapeutic agent for preventing MSC dysfunction under hyperglycemic conditions. (C) 2013 Elsevier Inc. All rights reserved.
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