| 23696417 | We also identified that miR-10a expression was significantly decreased with age by comparing the miRNA expression of hMSCs derived from young and aged individuals |
| 23696417 | Therefore, we hypothesized that the downregulation of miR-10a may be associated with the decreased differentiation capability of hMSCs from aged individuals |
| 23696417 | Lentiviral constructs were used to up- or downregulate miR-10a in young and old hMSCs |
| 23696417 | Upregulation of miR-10a resulted in increased differentiation to adipogenic, osteogenic, and chondrogenic lineages and in reduced cell senescence |
| 23696417 | Conversely, downregulation of miR-10a resulted in decreased cell differentiation and increased cell senescence |
| 23696417 | These constructs were cotransfected with the miR-10a mimic into cells |
| 23696417 | The luciferase activity was significantly repressed by the miR-10a mimic, proving the direct binding of miR-10a to the 3'-UTR of KLF4 |
| 23696417 | In conclusion, miR-10a restores the differentiation capability of aged hMSCs through repression of KLF4 |
| 23072816 | We identified 2 microRNAs, microRNA-10A* (miR-10A*), and miR-21, and their common target gene Hmga2 as critical regulators for EPC senescence |
| 23072816 | Overexpression of miR-10A* and miR-21 in young EPCs suppressed Hmga2 expression, caused EPC senescence, as evidenced by senescence-associated beta-galactosidase upregulation, decreased self-renewal potential, increased p16(Ink4a)/p19(Arf) expression, and resulted in impaired EPC angiogenesis in vitro and in vivo, resembling EPCs derived from aged mice |
| 23072816 | In contrast, suppression of miR-10A* and miR-21 in aged EPCs increased Hmga2 expression, rejuvenated EPCs, resulting in decreased senescence-associated beta-galactosidase expression, increased self-renewal potential, decreased p16(Ink4a)/p19(Arf) expression, and improved EPC angiogenesis in vitro and in vivo |
| 23072816 | CONCLUSIONS: miR-10A* and miR-21 regulate EPC senescence via suppressing Hmga2 expression and modulation of microRNAs may represent a potential therapeutic intervention in improving EPC-mediated angiogenesis and vascular repair |
