Upregulation of miR-1306-5p decreases cerebral ischemia/reperfusion injury in vitro by targeting BIK

Xuelin Chen, Caixia Li, Jianghao Li, Luoping Sheng, Xianglu Liu
Bioscience, Biotechnology, and Biochemistry 2019 August 28, : 1-8
MiR-1306-5p is involved in the progression of acute heart failure, but its role in ischemic stroke remains unclear. Here, SH-SY5Y cells were exposed to oxygen-glucose deprivation (OGD) for 4, 8, and 12 h, respectively, and then reoxygenation for 12 h to construct OGD/R induced cell injury model. Cell viability, cell death, and cell apoptosis were assessed with CCK-8 assay, LDH assay, flow cytometry, and caspase-3 activity assay. The target gene of miR-1306-5p was confirmed by luciferase reporter assay. We found miR-1306-5p expression was significantly down-regulated in OGD/R-induced SH-SY5Y cell model. Moreover, miR-1306-5p protected SH-SY5Y cell against OGD/R-induced injury. Mechanistically, Bcl2-interacting killer (BIK) was the direct target gene of miR-1306-5p. Furthermore, BIK knockdown mimicked, while overexpression reversed the protective effects of miR-1306-5p against OGD/R induced injury. Our findings thus provide an experimental basis miR-1306-5p targeting BIK-based therapy for cerebral I/R injury.

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