miR-142-3p suppresses apoptosis in spinal cord-injured rats

Abstract

AbstractIntroductionSpinal cord injury (SCI) leads to abnormal expression of miRs, leading to secondary responses such as oxidative stress, inflammation and apoptosis. In the present work, we screened the miRs involved and the associated pathway.MethodsIn a rat model of SCI, the microarray analysis for expression of miRs at various time points post-SCI was done. The locomotor analysis was done by Basso, Beattie and Bresnahan score, and Cresyl violet staining was done for lesion volume and TUNEL assay was done for apoptosis in neuronal cells. The expression of apoptotic proteins was done by the western blot study.ResultsIt was evidenced that the expression of the number of miRs was altered on the 14th day post-SCI, and miR-142-3p was found to be the most significantly suppressed miR. The results suggested that overexpression of miR-142-3p by its agomir-attenuated functional recovery decreased lesion size and apoptosis of neuronal cells in rats subjected to SCI. The luciferase assay indicated that miR-142-3p blocked the levels of Bax, which is a significant activator of the mitochondrial apoptotic pathway (MAP) via targeting the 3′UTR region of BV-2 cells, and in addition, pc-DNA-Bax restored Bax and inhibited the correcting role of miR-142-3p in hydrogen peroxide-treated BV-2 cells. The findings suggested that miR-142-3p may inhibit the MAP by inhibiting the expression of cleaved-caspase-3/-9 and Bax in SCI rats.ConclusionThis study concludes that miR-142-3p may attenuate the functional recovery and decrease apoptosis in neuronal cells via inhibiting the MAP in the spinal cord-injured rats, confirming miR-142-3p as a potential therapeutic target in treating SCI.