Upregulation of miR-130b protects against cerebral ischemic injury by targeting water channel protein aquaporin 4 (AQP4).

Altered microRNA regulation has been implicated in the pathogenesis of various disorders, including cerebral ischemia/reperfusion injury (I/RI). However, the regulatory mechanism of miR-130b in cerebral ischemia injury has not been reported. In this study, we explored the role of miR-130b in cerebral ischemia injury and investigated its potential mechanism. Levels of miR-130b were quantified by real-time PCR, and the protein level of AQP4 was detected by Western blotting. Cell apoptosis was detected by flow cytometry. In vitro, miR-130b levels in astrocytes were found significantly downregulated after OGD. Overexpression of miR-130b by miR-130b mimic decreased LDH release and apoptosis, but promoted cell health of astrocytes with OGD, thus playing a protective role in astrocyte I/RI. The level of miR-130b was also downregulated in ischemic tissues in MCAO model compared with the sham group, and the expression of miR-130b was gradually downregulated over time after reperfusion. AQP4 was upregulated both in two models, and as the reperfusion went on, AQP4 expression gradually upregulated. Our results indicated knockdown of AQP4 could ameliorate astrocyte injury induced by OGD. Finally, we found that miR-130b regulated astrocyte expression of AQP4, and rescue experiments further proved the protective role of miR-130b was mediated by AQP4 downregulation. Our study demonstrated that miR-130b might exert a neuroprotective effect following cerebral I/RI by regulating AQP4 expression at the post-transcriptional level. Therefore, miR-130b may be a potential therapeutic target for stroke treatment.
Competing Interests: None.