HtrA2/Omi is Involved in 6-OHDA-Induced Endoplasmic Reticulum Stress in SH-SY5Y Cells
HtrA2/Omi is Involved in 6-OHDA-Induced Endoplasmic Reticulum Stress in SH-SY5Y Cells
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HtrA2/Omi 参与 SH-SY5Y 细胞中 6-OHDA 诱导的内质网应激
DOI：
10.1007/s12031-011-9694-0
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发表时间：
2012-05-01
影响因子：
3.1
通讯作者：
Xu, Pingyi
中科院分区：
文献类型：
--
作者：
Luo, Feifei;Wei, Lei;Xu, Pingyi
内质网（ER）应激已被证明与包括帕金森病（PD）在内的神经退行性疾病的发病机制有关。HtrA 2/Omi通过参与蛋白质质量控制，参与ER应激。然而，关于PD中HtrA 2/Omi与ER应激的关系知之甚少。在此，我们探索了HtrA 2/Omi与PD细胞模型中ER应激的关联，发现在6-OHDA处理的SH-SY 5 Y细胞中，HtrA 2/Omi的表达水平随着ER应激诱导而降低。此外，用siRNA沉默HtrA 2/Omi的内源性表达导致聚集的ER应激和细胞死亡。综上所述，我们的研究结果表明，HtrA 2/Omi可能通过调节ER应激相关蛋白在6-OHDA诱导的细胞死亡中发挥保护作用。这项研究提供了一些线索，为什么HtrA 2/Omi突变导致一些PD患者的易感性更高。
Endoplasmic reticulum (ER) stress has been shown to be associated with the pathogenesis of neurodegenerative disorders including Parkinson's disease (PD). HtrA2/Omi, from its participation in protein quality control, is involved in ER stress. However, little is known about the relationship between HtrA2/Omi and ER stress in PD. Here, we explored the association of HtrA2/Omi and ER stress in a cell model of PD and found that the expression level of HtrA2/Omi decreased with ER stress induction in 6-OHDA-treated SH-SY5Y cells. Furthermore, silencing endogenous expression of HtrA2/Omi with siRNA resulted in aggregated ER stress and cell death. Taken together, our results show that HtrA2/Omi may exert a protective function in 6-OHDA-induced cell death by regulating ER stress-related proteins. This research offers some clues as why mutations in HtrA2/Omi lead to higher susceptibility in some PD patients.