OBJECTIVE: To explore the role of microRNA (miR) 137 in spinal cord injury and its mechanism. MATERIALS AND METHODS: The model of spinal cord injury in mice was established to detect the recovery differences of grip strength in upper and lower limbs of mice. The expressions of miR-137 and neuronal differentiation 4 (NEUROD4) were detected at the same time. The inflammation level and the oxidative stress response after spinal cord injury were subsequently detected after overexpression of miR-137. Target genes of miR-137 were identified by bioinformatics. Finally, dual-luciferase reporter gene assay was used to identify the target genes of miR-137. RESULTS: By establishing the model of spinal cord injury in mice, the strength of upper and lower limbs recovered after 7 days of injury in mice. The expression of miR-137 in spinal cord injury was found to decrease in a time-dependent manner by quantitative Real-time polymerase chain reaction (qRT-PCR), while the expression of NEUROD4 gradually increased. Inflammation indicators and oxidative stress level were found to be significantly higher after spinal cord injury. However, the inflammation level and oxidative stress were significantly reduced after transfection of miR-137. Finally, we predicted the target gene of miR-137 through bioinformatics website and found that NEUROD4 was a potential target gene of miR-137. Using dual luciferase reporter assays, we found that NEUROD4 bound to miR-137. After overexpression of miR-137, the expression of NEUROD4 was significantly reduced. Overexpression of NEUROD4 could promote spinal cord injury inflammation and oxidative stress. After intracellular transfection of NEUROD4 and miR-137 at the same time, the inflammation level and oxidative stress of spinal cord injury decreased significantly. CONCLUSIONS: These results suggested that miR-137 promoted the recovery of spinal cord injury by degrading NEUROD4 to relieve the spinal cord inflammation and the progression of oxidative stress, thus promoting the recovery of spinal cord injury.
OBJECTIVE: To explore the role of microRNA (miR) 137 in spinal cord injury and its mechanism. MATERIALS AND METHODS: The model of spinal cord injury in mice was established to detect the recovery differences of grip strength in upper and lower limbs of mice. The expressions of miR-137 and neuronal differentiation 4 (NEUROD4) were detected at the same time. The inflammation level and the oxidative stress response after spinal cord injury were subsequently detected after overexpression of miR-137. Target genes of miR-137 were identified by bioinformatics. Finally, dual-luciferase reporter gene assay was used to identify the target genes of miR-137. RESULTS: By establishing the model of spinal cord injury in mice, the strength of upper and lower limbs recovered after 7 days of injury in mice. The expression of miR-137 in spinal cord injury was found to decrease in a time-dependent manner by quantitative Real-time polymerase chain reaction (qRT-PCR), while the expression of NEUROD4 gradually increased. Inflammation indicators and oxidative stress level were found to be significantly higher after spinal cord injury. However, the inflammation level and oxidative stress were significantly reduced after transfection of miR-137. Finally, we predicted the target gene of miR-137 through bioinformatics website and found that NEUROD4 was a potential target gene of miR-137. Using dual luciferase reporter assays, we found that NEUROD4 bound to miR-137. After overexpression of miR-137, the expression of NEUROD4 was significantly reduced. Overexpression of NEUROD4 could promote spinal cord injury inflammation and oxidative stress. After intracellular transfection of NEUROD4 and miR-137 at the same time, the inflammation level and oxidative stress of spinal cord injury decreased significantly. CONCLUSIONS: These results suggested that miR-137 promoted the recovery of spinal cord injury by degrading NEUROD4 to relieve the spinal cord inflammation and the progression of oxidative stress, thus promoting the recovery of spinal cord injury.