Trx2/ASK1信号通路介导天疱疮诱导的线粒体损伤及机制

Trx2/ASK1 signaling pathway mediates mitochondrial injury induced by Pemphigus vulgaris

目的研究Trx2/ASK1信号通路在天疱疮诱导线粒体损伤的调控机制。方法在重庆医科大学附属第一医院收集天疱疮(PV)和健康血清样本,PV及健康患者血清培养的HACAT细胞,Western blot检测凋亡相关蛋白Bax和Bcl-2蛋白表达;流式细胞术检测天疱疮患者血清培养对细胞凋亡率的影响;ELISA实验检测天疱疮患者血清培养对HACAT细胞中SOD2蛋白表达水平的影响;Western blot检测天疱疮患者血清培养对Trx2/ASK1信号通路的影响;使用Trx2过表达质粒转染细胞,检测天疱疮患者血清对细胞内线粒体损伤标志物SOD2表达的影响。结果天疱疮患者血清诱导线粒体损伤,下调Trx2蛋白表达,促进ASK1磷酸化,进而促进角质形成细胞凋亡,且这一过程通过Trx2/ASK1信号通路调控。结论 Trx2/ASK1信号通路调控线粒体损伤诱导天疱疮发生。

Objective To investigate the regulatory mechanism of Trx2/ASK1 signaling pathway in pemphigus vulgaris(PV)-induced mitochondrial injury. Methods The serum samples of PV patients and healthy were collected in the first affiliated hospital of Chongqing medical university. The expression of apoptosis-related protein Bax and Bcl-2 in HACAT cells was detected by Western blot;the apoptosis rate was detected by flow cytometry, the expression of SOD2 protein in HACAT cells was detected by ELISA. The expression of Trx2/ASK1 signal pathway and intracellular mitochondrial damage marker SOD2 were detected by Western blot. Results Serum of pemphigus vulgaris patients induced mitochondrial injury, down-regulated Trx2 protein expression level, promoted ASK1 phosphorylation and keratinocyte apoptosis, which is regulated by Trx2/ASK1 signaling pathway. Conclusion Trx2/ASK1 signaling pathway regulates mitochondrial injury and induces pemphigus vulgaris.