title: Protective mechanisms of microRNA-27a against oxygen-glucose deprivation-induced injuries in hippocampal neurons.
abstract: Hypoxic injuries during fetal distress have been shown to cause reduced expression of microRNA-27a (miR-27a), which regulates sensitivity of cortical neurons to apoptosis. We hypothesized that miR-27a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1, an important transcription factor for regulating the oxidative stress response. miR-27a mimic was transfected into hippocampal neurons to overexpress miR-27a. Results showed increased hippocampal neuronal viability and decreased caspase-3 expression. The luciferase reporter gene system demonstrated that miR-27a directly binded to FOXO1 3'UTR in hippocampal neurons and inhibited FOXO1 expression, suggesting that FOXO1 was the target gene for miR-27a. These findings confirm that miR-27a protects hippocampal neurons against oxygen-glucose deprivation-induced injuries. The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.
authors.affiliation: Department of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
authors.forename: Qun
authors.identifier: 0000-0002-4540-1348
authors.initials: Q
authors.lastname: Cai
authors.affiliation: Department of Emergency, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Medical College of Nantong University, Nantong, Jiangsu Province, China.
authors.forename: Wen-Jie
authors.initials: WJ
authors.lastname: Yang
authors.affiliation: Department of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
authors.forename: Xing
authors.initials: X
authors.lastname: Fen
keywords: FOXO1; apoptosis; brain injury; caspase 3; cell survival; hippocampal neurons; hypoxic-ischemic; luciferase reporter gene system; miR-27a; nerve regeneration; neural regeneration; neuroprotection; oxygen-glucose deprivation