Abstract
Neural stem/progenitor cells (NSPCs) are self-renewing, multipotent cells and remain in the human brain throughout an individual's lifetime. NSPCs are activated by brain damage and contribute towards repair and motor function recovery in the central nervous system (CNS). It was previously reported that miR-29 was involved in regulating proliferation, differentiation and survival in hepatocellular carcinoma, and osteoblast and mantle cell lymphoma; however, the effects of miR-29 on NSPCs remain unclear. In the present study, it was demonstrated via Cell Counting Kit-8 assays that overexpression of miR-29 promoted the viability of NPSCs, and downregulated the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) protein. Additionally, treatment with a PTEN-specific inhibitor (VO-OHpic trihydrate) abolished the effects of the miR-29 inhibitor on PTEN expression, as determined via western blotting. Flow cytometry and 5-bromo-2-deoxyuridine (BrdU) staining revealed that overexpression of miR-29 further promoted the proliferation of NSPCs; however, knocking down miR-29 inhibited cell proliferation. VO-OHpic trihydrate reversed the effects of miR-29 knockdown on cell proliferation. Furthermore, it was observed that overexpression of miR-29 increased the phosphorylation levels of AKT. Collectively, the results indicated that overexpression of miR-29 promoted the proliferation of cultured rat NSPCs and decreased the expression of PTEN protein, and that the activation of Akt may be a potential underlying mechanism. The present findings may provide novel insight for the development of strategies for stem cell-mediated treatment of CNS diseases.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.