Micro‐RNA‐30a regulates ischemia‐induced cell death by targeting heat shock protein HSPA5 in primary cultured cortical neurons and mouse brain after stroke

• DOI: 10.1002/jnr.23637
• Publication Date: 2015-08-24T18:06:35Z
• Authors: Peng Wang; Nan Zhang; Jia Liang; Jiefei Li; Song Han; Junfa Li
• Keywords: Brain ischemia

Micro-RNAs (miRs) have emerged as key gene regulators in many diseases, including stroke. We recently reported that miR-30a protects N2A cells against ischemic injury, part through enhancing beclin 1-mediated autophagy. The present study explores further the involvement of ischemia-induced apoptosis and its possible mechanisms primary cortical neurons stroked mouse brain. demonstrate level is significantly decreased after 1-hr oxygen-glucose deprivation (OGD)/24-hr reoxygenation. Overexpression aggravated OGD-induced neuronal cell death, whereas inhibition attenuated necrosis determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-di-phenyl-2H-tetrazolium bromide, lactate dehydrogenase, TUNEL, cleaved caspase-3. amount HSPA5 protein, which predicted to be a putative target TargetScan, could reduced pre-miR-30a, it was increased anti-miR-30a. Furthermore, luciferase reporter assay confirmed directly binds 3'-UTR sites hspa5 gene. injury regulated OGD-treated siRNA. also observed an interaction caspase-12 coimmunoprecipitation speculate might involved endoplasmic reticulum stress-induced apoptosis. In vivo, brain infarction focal ischemia-stroked mice. Downregulation prevent neural upregulating protein expression, ER one underlying HSPA5-mediated neuroprotection.