MicroRNA-130b inhibits cerebral ischemia/reperfusion induced cell apoptosis via regulation of IRF1.

OBJECTIVE

Cerebral ischemia/reperfusion (CIR) frequently causes serious disabilities and correlates with certain neurological processes. Some studies have shown that microRNAs (miRNAs) exert a neuroprotective effect by modulating the inflammatory process in CIR. However, the biofunction and the mechanism of miR-130b in CIR need to be fully elucidated.

MATERIALS AND METHODS

An oxygen-glucose deprivation/reperfusion (OGD/R) model was constructed using SH-SY5Y cell line to analyze the function of miR-130b in CIR. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine the expression levels of miR-130b and IRF1. Western blot was performed to detect the protein levels of IRF1, Bax, and Bcl-2. Cell viability was determined using MTT (3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays. Dual-Luciferase reporter assay was conducted to confirm the target gene of miR-130b.

RESULTS

In this study, we found that miR-130b level was prominently decreased after treatment with OGD/R. Through gain and loss assays, we concluded that miR-130b restoration promoted cell proliferation and inhibited cell apoptosis in OGD/R-treated cells. Moreover, we also identified IRF1 as an important target of miR-130b. Additionally, IRF1 knockdown remarkably abrogated the protection mediated by miR-130b against the injuries in OGD/R-treated cells.

CONCLUSIONS

Taken together, our results suggested that miR-130b facilitated cell viability and suppressed cell apoptosis of CIR via negatively regulating of IRF1.