MicroRNA-29b alleviates oxygen and glucose deprivation/reperfusion-induced injury via inhibition of the p53‑dependent apoptosis pathway in N2a neuroblastoma cells
- Lei Cao
- Yu Zhang
- Shuai Zhang
- Tian‑Peng Jiang
- Li Chen
- Jing Liu
- Shi Zhou
Published online on: October 31, 2017
Copyright: © Cao et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Cerebral ischemic injury causes severe brain damage and remains one of the leading causes of morbidity and mortality worldwide. Members of the microRNA‑29 (miR‑29) family are involved in regulating the process of ischemia and may be developed as biomarkers to diagnose and treat cerebral ischemia. The role of miR‑29b in cerebral ischemia injury remains poorly understood. The purpose of the present study was to investigate whether miR‑29b overexpression suppressed cerebral ischemic injury and to explore its underlying mechanism of action. The results demonstrated that levels of miR‑29b in N2a neuroblastoma cells decreased following oxygen and glucose deprivation/reperfusion (OGD/R) treatment. Transfection with miR‑29b mimics significantly increased cell viability, decreased lactate dehydrogenase (LDH) leakage, inhibited apoptosis by decreasing morphological changes occurring in the nuclei and reduced caspase‑3 activity in OGD/R‑treated N2a cells. Conversely, miR‑29b inhibitors enhanced OGD/R‑induced cytotoxicity and apoptosis. In addition, the miR‑29b mimics blocked the increase in Bax and p53 expression and decreased Bcl‑2 expression in OGD/R‑treated N2a cells, whereas miR‑29b inhibitors exacerbated the changes in the expression of these apoptosis‑associated proteins caused by OGD/R. p53 knockdown using p53 small interfering RNA decreased cell viability and increased LDH leakage, reversing the improvements that the miR‑29b mimics induced in damaged cells. Taken together, the results of the present study demonstrated that miR‑29b attenuates ischemic injury by negatively regulating the p53‑dependent apoptosis pathway and may therefore be a novel potential therapeutic target for treating ischemic stroke.