Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (7): 1147-1152.doi: 10.4103/1673-5374.156983

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Loss of microRNA-124 expression in neurons in the peri-lesion area in mice with spinal cord injury

Yu Zhao 1, Hui Zhang 1, Dan Zhang 2, Cai-yong Yu 3, Xiang-hui Zhao 3, Fang-fang Liu 3, Gan-lan Bian 3, Gong Ju 3, Jian Wang 3   

  1. 1 Department of Anatomy, Hebei North University, Zhangjiakou, Hebei Province, China
    2 Department of Stomatology, the First Hospital of Zhangjiakou, Zhangjiakou, Hebei Province, China
    3 Institute of Neurosciences, the Fourth Military Medical University, Xi’an, Shaanxi Province, China
  • Received:2015-06-02 Online:2015-07-24 Published:2015-07-24
  • Contact: Gong Ju or Jian Wang, jugong@fmmu.edu.cn or jwangfm@163.com.
  • Supported by:

    This work was supported by the National Natural Science Foundation of China, No. 81371364.

Abstract:

MicroRNA-124 (miR-124) is abundantly expressed in neurons in the mammalian central nervous system, and plays critical roles in the regulation of gene expression during embryonic neurogenesis and postnatal neural differentiation. However, the expression profile of miR-124 after spinal cord injury and the underlying regulatory mechanisms are not well understood. In the present study, we examined the expression of miR-124 in mouse brain and spinal cord after spinal cord injury using in situ hybridization. Furthermore, the expression of miR-124 was examined with quantitative RT-PCR at 1, 3 and 7 days after spinal cord injury. The miR-124 expression in neurons at the site of injury was evaluated by in situ hybridization combined with NeuN immunohistochemical staining. The miR-124 was mainly expressed in neurons throughout the brain and spinal cord. The expression of miR-124 in neurons significantly decreased within 7 days after spinal cord injury. Some of the neurons in the peri-lesion area were NeuN+/miR-124−. Moreover, the neurons distal to the peri-lesion site were NeuN+/miR-124+. These findings indicate that miR-124 expression in neurons is reduced after spinal cord injury, and may reflect the severity of spinal cord injury.

Key words: nerve regeneration, spinal cord injury, microRNA, spinal cord, in situ hybridization, immunohistochemistry, digoxin, NeuN protein, brain, neural plasticity, repair, apoptosis, NSFC grants, neural regeneration