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Inhibition of microRNA‐153 protects neurons against ischemia/reperfusion injury in an oxygen–glucose deprivation and reoxygenation cellular model by regulating Nrf2/HO‐1 signaling
Author(s) -
Ji Qiong,
Gao Jianbo,
Zheng Yan,
Liu Xueli,
Zhou Qiangqiang,
Shi Canxia,
Yao Meng,
Chen Xia
Publication year - 2017
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21905
Subject(s) - neuroprotection , ischemia , reperfusion injury , oxidative stress , downregulation and upregulation , microrna , gene silencing , neuron , pharmacology , reactive oxygen species , heme oxygenase , heme , chemistry , brain ischemia , microbiology and biotechnology , biology , neuroscience , medicine , biochemistry , gene , enzyme
Abstract MicroRNAs are emerging as critical regulators in cerebral ischemia/reperfusion injury; however, their exact roles remain poorly understood. miR‐153 is reported to be a neuron‐related miRNA involved in neuroprotection. In this study, we aimed to investigate the precise role of miR‐153 in regulating neuron survival during cerebral ischemia/reperfusion injury using an oxygen–glucose deprivation and reoxygenation (OGD/R) cellular model. We found that miR‐153 was significantly upregulated in neurons subjected to OGD/R treatment. Inhibition of miR‐153 significantly attenuated OGD/R‐induced injury and oxidative stress in neurons. Nuclear factor erythroid 2‐related factor 2 (Nrf2) was identified as a target gene of miR‐153. Inhibition of miR‐153 significantly promoted the expression of Nrf2 and heme oxygenase‐1 (HO‐1). However, silencing of Nrf2 significantly blocked the protective effects of miR‐153 inhibition. Our study indicates that the inhibition of miR‐153 protects neurons against OGD/R‐induced injury by regulating Nrf2/HO‐1 signaling and suggests a potential therapeutic target for cerebral ischemia/reperfusion injury.