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.
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Acknowledgments
This work was supported by “863” project (2007AA02Z460), “973” project (2010AB973Z531) from the Ministry of Science and Technology of the People’s Republic of China, a grant from Nature Science Foundation of China (81071032), and a grant supported by key project (ZDXM080214) from Hainan provincial Science and Technology Department.
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Feifei Luo, Lei Wei, Congcong Sun, and Xiaowu Chen contributed equally to this work.
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Luo, F., Wei, L., Sun, C. et al. HtrA2/Omi is Involved in 6-OHDA-Induced Endoplasmic Reticulum Stress in SH-SY5Y Cells. J Mol Neurosci 47, 120–127 (2012). https://doi.org/10.1007/s12031-011-9694-0
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DOI: https://doi.org/10.1007/s12031-011-9694-0