Department of Spine Surgery, The Second Affiliated Hospital of Nantong University, Haier Lane North Road No. 6, Nantong, Jiangsu, 226001, China.
J Mol Neurosci. 2017 Sep;63(1):91-99. doi: 10.1007/s12031-017-0961-6. Epub 2017 Aug 8.
Vimentin, among the family of the intermediate filament, plays as the organizer of some critical proteins involved in migration, attachment, and cell signaling. In this study, the role of vimentin in chronic constriction injury (CCI) was investigated. Western blot revealed increased protein level of vimentin following CCI, peaking at 7 days. Double immunofluorescent staining showed that vimentin was mostly co-localized with astrocytes, not with neurons or microglia. In vitro, sensory neuronal injury stimulated astrocytes to produce more pro-inflammation cytokines, p-ERK (phosphorylated extracellular signal-regulated protein kinase), and vimentin. However, vimentin knockdown by siRNA (small interfering RNA) reversed the upregulation of p-ERK and vimentin expression and reduced the release of pro-inflammatory cytokines. Overall, stimulated astrocytes might release pro-inflammatory cytokines to promote the development of neuropathic pain via vimentin/ERK signaling.
波形蛋白属于中间丝家族,作为参与迁移、黏附以及细胞信号传导的一些关键蛋白的组织者。本研究旨在探究波形蛋白在慢性压迫性损伤(CCI)中的作用。Western blot 显示 CCI 后波形蛋白的蛋白水平增加,在第 7 天达到峰值。双重免疫荧光染色显示,波形蛋白主要与星形胶质细胞共定位,而不是与神经元或小胶质细胞共定位。在体外,感觉神经元损伤刺激星形胶质细胞产生更多的促炎细胞因子、p-ERK(磷酸化细胞外信号调节蛋白激酶)和波形蛋白。然而,通过 siRNA(小干扰 RNA)敲低波形蛋白逆转了 p-ERK 和波形蛋白表达的上调,并减少了促炎细胞因子的释放。总的来说,受刺激的星形胶质细胞可能会释放促炎细胞因子,通过波形蛋白/ERK 信号通路促进神经病理性疼痛的发展。