MicroRNA-125b promotes the regeneration and repair of spinal cord injury through regulation of JAK/STAT pathway

J. Dai, L.-J. Xu, G.-D. Han, H.-L. Sun, G.-T. Zhu, H.-T. Jiang, G.-Y. Yu, X.-M. Tang

Department of Orthopedic, Huai’an First People’s Hospital, Huai’an, China. 13905239800@163.com

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• Orthopedics

OBJECTIVE: Spinal cord injury (SCI) is a severe trauma to the central nervous system. Long non-coding RNAs have been reported to play essential roles in spinal cord injury. This study mainly explored the role of micro-125 in the regulation of spinal cord injury by regulating STAT3.

MATERIALS AND METHODS: The stable mouse model of cervical spinal cord contusion was established by Infinite Horizon spinal cord striker, and the model mice’ motor function was analyzed. Bioinformatics databases were used to screen the target mRNAs of micro-125b. qRT-PCR was performed to detect the expression of micro-125b and its target genes in injury area of mice’ spinal cord. Western Blot and ELISA were introduced to detect the expression of inflammation and apoptosis-related proteins in each group. The recovery status of spinal cord after SCI was assessed by motor function scores and axon counts of mice in each group.

RESULTS: Micro-125b appeared to be significantly down-regulated over-time after SCI. JAK1 and STAT1, two important neuregulin proteins, were predicted to be the target genes of micro-125b, and overexpression of micro-125b induced the decrease of phosphorylated JAK1 and STAT1. Enhanced micro-125b expression also allowed axons from the injury area of spinal cord to extend into the outer periphery of the damaged area, thus improving the motor function of the injured rats. Besides, overexpression of micro-125b demonstrated significant neuronal protective effects by reducing apoptosis and inflammatory responses in neurons.

CONCLUSIONS: Our data revealed that micro-125b was down-regulated in injured spinal cord, and overexpression of micro-125b promoted the repair and regeneration following spinal cord injury through the regulation of the JAK/STAT pathway.

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