AIMS: To explore the role and underlying mechanism of miR-124 in stroke. METHODS: miR-124 expression was determined by real-time PCR. The effect of miR-124 on infarct area was assessed in middle cerebral artery occlusion (MCAO) mice. The influence of miR-124 on oxygen and glucose deprivation (OGD) induced neuron apoptosis and death was examined by immunofluorescence. The effect of miR-124 on apoptosis-related proteins was determined by Western blot. RESULTS: The level of miR-124 is significantly increased in ischemic penumbra as compared with that in nonischemic area of MACO mice. Brain tissue of stroke-prone spontaneously hypertensive rats (SHR-SP) also showed higher level of miR-124 as compared with that of spontaneously hypertensive rats (SHR). Consistently, OGD treatment obviously increased miR-124 level in primary neurons. In vivo, miR-124 overexpression significantly decreased, while miR-124 knockdown significantly increased, the infarct area of MCAO mice. In vitro, gain or loss of miR-124 function resulted in reduced or increased neuron apoptosis and death induced by OGD, and increased or reduced antiapoptosis protein, Bcl-2 and Bcl-xl, respectively. CONCLUSIONS: miR-124 plays a neurons-protective role via apoptosis-inhibiting pathway in ischemic stroke.
AIMS: To explore the role and underlying mechanism of miR-124 in stroke. METHODS: miR-124 expression was determined by real-time PCR. The effect of miR-124 on infarct area was assessed in middle cerebral artery occlusion (MCAO) mice. The influence of miR-124 on oxygen and glucose deprivation (OGD) induced neuron apoptosis and death was examined by immunofluorescence. The effect of miR-124 on apoptosis-related proteins was determined by Western blot. RESULTS: The level of miR-124 is significantly increased in ischemic penumbra as compared with that in nonischemic area of MACO mice. Brain tissue of stroke-prone spontaneously hypertensiverats (SHR-SP) also showed higher level of miR-124 as compared with that of spontaneously hypertensiverats (SHR). Consistently, OGD treatment obviously increased miR-124 level in primary neurons. In vivo, miR-124 overexpression significantly decreased, while miR-124 knockdown significantly increased, the infarct area of MCAOmice. In vitro, gain or loss of miR-124 function resulted in reduced or increased neuron apoptosis and death induced by OGD, and increased or reduced antiapoptosis protein, Bcl-2 and Bcl-xl, respectively. CONCLUSIONS: miR-124 plays a neurons-protective role via apoptosis-inhibiting pathway in ischemic stroke.