TITLE

TRPC1 protects dopaminergic SH-SY5Y cells from MPP+, salsolinol, and N-methyl-(R)-salsolinol-induced cytotoxicity

AUTHOR(S)
Arshad, Abida; Chen, Xuechai; Cong, Zhenzhen; Qing, Hong; Deng, Yulin
PUB. DATE
January 2014
SOURCE
Acta Biochimica et Biophysica Sinica;Jan2014, Vol. 46 Issue 1, p22
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
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-diphenyltetrazolium bromide) assays, DAPI (4′,6-diamidino-2-phenylindole), 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. Immunocytochemistry 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.
ACCESSION #
93398774

 

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