miR‐202 modulates the progression of neuropathic pain through targeting RAP1A

Neuropathic pain is a somatosensory disorder which is caused by disease or nerve injury that affects the nervous system. microRNAs (miRNAs) are proved to play crucial roles in the development of neuropathic pain. However, the role of miR‐202 in neuropathic pain is still unknown. Sprague‐Dawley rats were used for constructing the neuropathic pain model. The expression of miR‐202 was determined by quantitative real‐time polymerase chain reaction. Potential target gene for miR‐202 was measured using bioinformatics methods and Western blot analysis. In this study, we used rats to establish a neuropathic pain model and measured the effect of miR‐202 in neuropathic pain. We demonstrated that miR‐202 expression was downregulated in the spinal dorsal horn of bilateral sciatic nerve chronic constriction injury (bCCI) rat. However, miR‐202 expression was not changed in the dorsal root ganglion, hippocampus, and anterior cingulated cortex of bCCI rat. We identified that RAP1A was a direct target gene of miR‐202 in the PC12 cell. RAP1A expression was upregulated in the spinal dorsal horn of bCCI rat. Overexpression of miR‐202 could improve the pain threshold for bCCI rats in both hindpaws, indicating that miR‐202 overexpression could lighten the pain threshold for model rats. Moreover, RAP1A overexpression increased the pain threshold effect of miR‐202 overexpression treated bCCI rats, indicating that miR‐202 could lighten the pain threshold through inhibiting RAP1A expression. These data suggested that miR‐202 acted pivotal roles in the development of neuropathic pain partly through targeting RAP1A gene. miR‐202 expression was downregulated in the spinal dorsal horn of bilateral sciatic nerve chronic constriction injury (bCCI) rat. We identified that RAP1A was a direct target gene of miR‐202 in the PC12 cell. miR‐202 acted pivotal roles in the development of neuropathic pain partly by targeting RAP1A gene.