Expression of miR-210 mediated by adeno-associated virus performed neuroprotective effects on a rat model of acute spinal cord injury.

Acute spinal cord injuries (ASCI) are common neural disorders in traumatology medicine. MicroRNA-210 (miR-210) plays a crucial role in cell survival, endothelial cell migration and cell regeneration. This paper is aim to validate the pathophysiological function of miR-210 on ASCI. We built a rat model of ASCI and utilized an adeno-associated virus (rAAV)-expressing miR-210 for stable over-expression of miR-210. We tested in vivo miR-210 gain of function on ASCI by microinjected rAAV-miR-210 into the rat spinal cord. We further screened the targeting genes of miR-210 by PCR array and detected related signal proteins by Western Blot and qPCR. Over-expression of miR-210 protected neurons while neurologic function scores were improved. We further identified less TUNEL-positive cells, few features of apoptosis under electron microscopy, decreased activities of caspase-3 and 8 and increased vessel count in the spinal cord from rAAV-miR-210 group. We also found rAAV-miR-210 promoted expression of angiogenesis and metastasis-related protein (VEGF and Glut1) and regulated serum levels of inflammation-related cytokines. PCR screen array showed PTP1B, target of miR-210, was significantly down-regulated and Akt phosphorylation was significantly increased in rAAV-miR-210 group. The current data suggest that over-expression of miR-210 may target PTP1B and plays a neuroprotective role on rats after ASCI.