Research reportThe effect of miR-30d on apoptosis and autophagy in cultured astrocytes under oxygen-glucose deprivation

- MiR-30d inhibited Beclin1 expression in primary astrocytes.
- MiR-30d antagomirs enhanced autophagy and suppressed apoptosis in OGD astrocytes.
- Beclin1 siRNAs inhibited autophagy and promoted apoptosis in OGD astrocytes.
- Beclin1 siRNAs reversed the role of miR-30d antagomirs on autophagy and apoptosis.

MiR-30d has been demonstrated to regulate autophagy in human cancer cells. However, the role of miR-30d in astrocytes exposed to hypoxia-ischemia is not clear. In this study, we established model of oxygen and glucose deprivation (OGD) with rat primary astrocytes and evaluated the role of miR-30d in the cross-talk between autophagy and apoptosis in astrocytes after OGD. We found that miR-30d inhibited Beclin1 expression in astrocytes. Inhibition of miR-30d by antagomir significantly increased cell autophagy but decreased cell apoptosis in astrocytes exposed to OGD. Knockdown of Beclin1 reversed the upregulation of autophagy and downregulation of apoptosis induced by miR-30d inhibition in astrocytes subjected to OGD. These results strongly indicated that miR-30d played critical roles in the cross-talk between autophagy and apoptosis of astrocytes subjected to OGD by targeting Beclin1. MiR-30d is a novel target to attenuate cell injury under hypoxia-ischemia condition.