Suppr超能文献

HtrA2/Omi 参与了 6-OHDA 诱导的 SH-SY5Y 细胞内质网应激。

HtrA2/Omi is involved in 6-OHDA-induced endoplasmic reticulum stress in SH-SY5Y cells.

机构信息

Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, People's Republic of China.

出版信息

J Mol Neurosci. 2012 May;47(1):120-7. doi: 10.1007/s12031-011-9694-0. Epub 2012 Jan 13.

Abstract

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.

摘要

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。HtrA2/Omi 通过参与蛋白质质量控制而与 ER 应激有关。然而,关于 HtrA2/Omi 与 PD 中的 ER 应激之间的关系知之甚少。在这里,我们在 PD 的细胞模型中探讨了 HtrA2/Omi 与 ER 应激之间的关联,发现 HtrA2/Omi 的表达水平随着 6-OHDA 处理的 SH-SY5Y 细胞中 ER 应激的诱导而降低。此外,用 siRNA 沉默 HtrA2/Omi 的内源性表达会导致聚集的 ER 应激和细胞死亡。总之,我们的研究结果表明,HtrA2/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,说明为什么 HtrA2/Omi 的突变会导致一些 PD 患者更高的易感性。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验