神经病理性疼痛
个人识别码1
伤害
医学
周围神经损伤
背根神经节
神经损伤
基因敲除
麻醉
药理学
化学
生物
内科学
细胞生物学
背
解剖
受体
细胞凋亡
生物化学
坐骨神经
磷酸化
丝氨酸
作者
Yun Zou,Yumeng Cao,Yuqi Liu,Xinyi Zhang,Jinbao Li,Yang Xiong
标识
DOI:10.1016/j.neulet.2019.134375
摘要
Neuropathic pain induced by peripheral nerve injury is a complex and chronic state that is accompanied by poor quality of life. However, whether PIM1 (proviral integration site 1) contributes to the development of nociceptive hypersensitivity induced by nerve injury remains unknown. The present study was designed to investigate the effects of PIM1 on spinal nerve ligation (SNL) induced pain hypersensitivity. Here, we found that PIM1 positive neurons in the dorsal root ganglion (DRG) were colocalized with nociceptive neuronal markers CGRP, IB4 and substance P and were upregulated after SNL surgery. Knockdown PIM1 in the DRG by AAV5-shPIM1 alleviated SNL-induced pain hypersensitivity. In neuroblastoma cells (neuro-2a), PIM1 regulated the expression of CXCR4 phosphorylated at ser339 (pCXCR4) as well as the CXCL12/CXCR4 pathway. In the DRG tissues, we found that PIM1 was co-expressed with CXCR4, and knockdown of PIM1 attenuated pCXCR4 (ser339) protein expression but had little effect on total CXCR4 protein expression after SNL surgery. These findings suggest that PIM1 contributes to nerve injury-induced nociceptive hypersensitivity. Based on these findings and the characteristics of PIM1, we speculate that PIM1 might be a viable therapeutic target for the treatment of neuropathic pain in the near future.
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