MiR-152 promotes spinal cord injury recovery via c-jun amino terminal kinase pathway.

Abstract

The aim of this research is to explore the possible role of miR-152 in spinal cord injury and its underlying mechanism. After a mouse model of spinal cord injury (SCI) was developed, Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect the expression of miR-152 and c-jun in the mouse. In addition, the expression levels of interleukin-1b (IL-1b), interleukin-18 (IL-18) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). Subsequently, miR-152 was overexpressed and the levels of inflammation and c-jun after spinal cord injury were detected by Western blot. Furthermore, the grip strength of double forelimb, left forelimb or right forelimb of the mice was detected using a grip force test after miR-152 was overexpressed in the injured area of each group. By constructing a mouse model of spinal cord injury, we found that the expression of miR-152 in the injured area decreased with time; meanwhile, the inflammatory relative genes including IL-1b, IL18, TNF-α, and c-jun were significantly increased. However, miR-152 overexpression significantly reduced the levels of inflammation genes as well as the expression of c-jun. Besides, the strength of the forelimbs in the spinal cord injury mice was restored. MiR-152 could inhibit inflammatory responses and promote the recovery of the spinal cord injury through the c-jun N-terminal kinase pathway and it can be a target molecular for treating spinal cord injury.