MicroRNA‑381/Hes1 is a potential therapeutic target for spinal cord injury.

Abstract

The aim of the present study was to investigate whether microRNA‑381 is a potential therapeutic target for spinal cord injury (SCI) and its possible mechanism. Reverse transcription quantitative polymerase chain reaction (qPCR) for mRNA expression was used to analyze the changes of microRNA-381 expression. Cell viability and cell apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Caspase‑3 activity was measured using caspase‑3 activity kit, and western blot analysis was used to measure the protein expression of neurogenic locus notch homolog protein1 (Notch1), notch1 intracellular domain (NICD) and transcription factor HES-1 (Hes1). The data showed that microRNA‑381 expression of model SCI rats was downregulated compared with that of control rats. Overexpression of microRNA‑381 promoted cell proliferation, and inhibited apoptosis and caspase‑3 and apoptosis regulator BAX (Bax) protein expression in neurocytes. Overexpression of microRNA‑381 also increased Wnt and β‑catenin protein expression, and suppressed the protein expression of Notch1, NICD and Hes1 in neurocytes. Wnt inhibitor, Wnt‑C59 (1µmol/l), inhibited cell proliferation, promoted apoptosis and caspase‑3 and Bax protein expression, suppressed β‑catenin protein expression and induced Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Notch inhibitor, FLI‑06 (1µmol/l), promoted cell proliferation, inhibited apoptosis and caspase‑3 and Bax protein expression, and suppressed NICD and Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Thus, this study showed that overexpression of microRNA‑381 promotes cell proliferation of neurocytes in SCI via Hes1 expression, which may be a novel important mechanism for SCI in clinical applications.