Administration of antagomir-223 inhibits apoptosis, promotes angiogenesis and functional recovery in rats with spinal cord injury.

MicroRNAs (miRNAs) are recently described as a class of short non-coding RNAs, which play important roles in post-transcriptional gene regulation and involved in many physiological and pathological processes. MicroRNA-223 (miR-223) has been showed highly elevated in the injured spinal cord. However, the potential role and underlying mechanisms of miR-223 in spinal cord injury (SCI) were incompletely understood. In the present study, we observed the persistent high levels of miR-223 in the injured spinal cord at different time points (1, 3, 7, and 14 days) after SCI. Besides, inhibiting miR-223 by intrathecally injection with antagomir-223 significantly improved recovery in hindlimb motor function and attenuated cell apoptosis in spinal cord-injured rats. Additionally, antagomir-223 treatment markedly decreased the pro-apoptotic protein levels, including Bax and cleaved caspase-3, up-regulated the anti-apoptotic Bcl-2 protein level, as well as the expression of GluR2. Moreover, inhibition of miR-223 promoted angiogenesis, as evidenced by the increased CD31 expression and microvascular density. Taken together, our results indicate that inhibition of miR-223 with antagomir-223 exerts protective role in functional recovery, angiogenesis, and anti-apoptosis during SCI. Thereby, miR-223 may be a promising target of therapy for SCI.