TRPC1 protects dopaminergic SH-SY5Y cells from MPP+, salsolinol,and N-methyl-(R)-salsolinol-induced cytotoxicity |
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作者姓名: | Abida Arshad Xuechai Chen Zhenzhen Cong Hong Qing Yulin Deng |
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作者单位: | [1]Cell Biology Laboratory, School of Life Science, Beijing Institute of Technology, Beijing 100081, China [2]Beijing Environmental and Virus Cancer Key Laboratory, College of Life Science and Bioengineering, Beijing University of Technology, Beijing 100124, China |
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基金项目: | The authors thank the support from the National Natural Science Foundation of China (20435020), and partial support from the Ministry of Industry and Information of China (A2220060002). |
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摘 要: | Neurotoxins and alterations in Ca2+ homeostasis have been associated with Parkinson's disease (PD), but the role of store-operated Ca2+ entry channels is not well understood. Previous studies have shown the neurotoxicity of salsolinol and 1-methyl-4-phenylpyridinium ion on SH-SY5Y cells and cytoprotection induced by transient receptor potential protein 1 (TRPC1). In the present study, N-methyl-(R)-salsolinol was tested for its cellular toxicity and effects on TRPC1 expression. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-dipbenyl- tetrazolium bromide) assays, DAPI (4',6-diamidino-2-pheny- lindole), fluorescein isothiocyanate-Annexin-V/propidium iodide, western blot analysis, and JC-1 labeling revealed that the three indicated drugs could induce caspase-dependent, mitochondrial-mediated apoptosis. Exposure of SH-SY5Y cells to the indicated drugs resulted in a significant decrease in thapsigargin-mediated Ca2+ influx and TRPC1 expression. Immnnocytochemistry experiments revealed that neurotoxins treatment induced TRPC1 translocation to the cytoplasm. Taken together, our results indicate that treatment with neurotoxins may alter Ca2+ homeostasis and induce mitochondrial-mediated caspase-dependent cytotoxicity, an important characteristic of PD.
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关 键 词: | SH-SY5Y细胞 细胞毒性 N-甲基 猪毛菜 诱导 MPP 多巴胺 异硫氰酸荧光素 |
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