Abstract
Long non-coding RNA (LncRNA) H19 plays an important role on the biological functions of endogenous neural stem/progenitor cells (NSPCs). Our study aimed to explore the functions of H19 in NSPCs induced by oxygen-glucose deprivation/reperfusion (OGD/R) in vitro and the underlying mechanisms. In this study, our results showed that knockdown of H19 significantly inhibited NSPCs proliferation. Additionally, the apoptosis of NSPCs after ODG/R injury was notably promoted by H19 knockdown. Cell cycle arrest was induced in NSPCs at G0/G1 phase after OGD/R, while knockdown of H19 decreased the percentage of cells at G2/S phase. The results of immunofluorescence analysis revealed that H19 knockdown reduced the staining intensity of Ki-67 and DCX. Furthermore, H19 knockdown enhanced the expression of p53, Bax and Cleaved Caspase-3, while Bcl-2 expression was decreased. Silencing of H19 suppressed the NSPCs proliferation, cell cycle progression and differentiation, whereas cell apoptosis was promoted. Upregulation of H19 abolished OGD/R-induced NSPCs apoptosis, while cell proliferation and differentiation were promoted. Furthermore, the effects of overexpressed H19 on NSPCs proliferation, differentiation and apoptosis were abrogated by the upregulation of p53. In summary, overexpressed H19 resulted in the inactivation of p53, which promoted NSPCs proliferation, differentiation, and inhibited cell apoptosis. These findings suggested that H19 could promote cell proliferation and differentiation after OGD/R through suppressing the p53 signaling.
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