PSI诱导PC12细胞帕金森病模型中ERp29蛋白表达

Expression of ERp29 in model of Parkinson's disease of PC12 cells induced by proteasome inhibitor

目的:探讨泛素-蛋白酶体系统(UPS)功能障碍诱发帕金森病(PD)细胞模型的作用机制,为深入研究PD的发病机制提供理论依据。方法:建立PSI诱导的PC12细胞模型,实验组、对照组分别加入PSI和DMSO(终浓度为10μmol.L-1)孵育36 h后提取蛋白,应用荧光差异凝胶电泳(DIGE)系统获得差异蛋白点,运用基质辅助激光解吸/电离飞行时间质谱仪(MALDI-TOF Pro MS)鉴定出差异蛋白。结果:实验组与对照组比较,在36 h可见细胞内嗜酸性类Lewy小体形成及细胞凋亡(细胞核呈固缩状或碎裂状),凋亡百分率为25.53%。实验组内质网蛋白ERp29与对照组比较表达量显著降低,差异有显著性(P<0.01)。结论:内质网应激(ERS)在UPS功能障碍引起PD的病理变化过程中起重要作用。

Objective To investigate the pathogenetic mechanism of ubiquitin-proteasome dysfunction in a model of Parkinson＇ s disease （PD）, which can provide the theoretical basis for PD. Methods After establishment of PD model induced by PSI in PC12 cells, proteins of untreated （DMSO） and PSI-treated PC12 ceils were extracted 36 h after incubation, and then the maps of the extracted proteins were established by DIGE system. The altered protein spots were identified with MALDI-TOF Pro MS and database searching. Results Thirty-six treatment of PC12 cells with PSI induced the appearance of cytoplasmic Lewy body-like eosinophilic inclusions and apoptosis. The percentage of apoptotic cells was 25.53%. ERp29 were identified by MALDI-TOF Pro MS. The expression of ERp29 decreased in treatment group, compared with normal group （P〈0. 01）. Conclusion Endoplasmic reticulum stress （ERS） may play an important role in the pathogenesis of ubiquitin-proteasome system dysfunction induced PD.