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Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a(mi R-27a),which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1,an important transcription factor for regulating the oxidative stress response.miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a.Results showed increased hippocampal neuronal viability and decreased caspase-3 expression.The luciferase reporter gene system demonstrated that mi R-27 a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression,suggesting that FOXO1 was the target gene for mi R-27 a.These findings confirm that mi R-27 a 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.
Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a (mi R-27a), which regulates sensitivity of cortical neurons to apoptosis. We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1, an important transcription factor for regulating the oxidative stress response. miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a. Results showed increased hippocampal neuronal viability and decreased human caspase-3 expression. The luciferase reporter gene system suggesting that mi R-27 a directly binded to FOXO1 3 ’UTR in hippocampal neurons and inhibited FOXO1 expression, suggesting that FOXO1 was the target gene for mi R-27 a. The findings identify that mi R-27 a 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.