Your browser doesn't support javascript.
loading
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.
Ji, Qiong; Gao, Jianbo; Zheng, Yan; Liu, Xueli; Zhou, Qiangqiang; Shi, Canxia; Yao, Meng; Chen, Xia.
Afiliación
  • Ji Q; Department of Pharmacology, College of Basic Medical Science, Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Gao J; Department of Neonatology, Frist Hospital of Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Zheng Y; Department of Pediatrics Neurology, Frist Hospital of Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Liu X; Cadre's Ward of Frist Hospital of Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Zhou Q; Department of Pharmacology, College of Basic Medical Science, Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Shi C; Department of Pharmacology, College of Basic Medical Science, Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Yao M; Department of Pharmacology, College of Basic Medical Science, Jilin University, Changchun, Jilin, 130021, People's Republic of China.
  • Chen X; Department of Pharmacology, College of Basic Medical Science, Jilin University, Changchun, Jilin, 130021, People's Republic of China.
J Biochem Mol Toxicol ; 31(7)2017 Jul.
Article en En | MEDLINE | ID: mdl-28245071
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.
Asunto(s)
Palabras clave

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Transducción de Señal / MicroARNs / Hemo-Oxigenasa 1 / Factor 2 Relacionado con NF-E2 / Modelos Neurológicos / Neuronas Tipo de estudio: Prognostic_studies Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2017 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Transducción de Señal / MicroARNs / Hemo-Oxigenasa 1 / Factor 2 Relacionado con NF-E2 / Modelos Neurológicos / Neuronas Tipo de estudio: Prognostic_studies Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2017 Tipo del documento: Article