1,25-Dyhydroxyvitamin D3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy

Title
1,25-Dyhydroxyvitamin D3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy
Authors
장우영김희주이환Kwang Deog JoMoon Kyu LeeSun Hong Song양현옥
Keywords
Calcitriol; Parkinson's disease; Autophagy; Neuroprotection
Issue Date
2014-08
Publisher
Biochemical and biophysical research communications
Citation
VOL 451, NO 1, 142-147
Abstract
Background and objectives Dysregulation of the autophagy pathway has been suggested as an important mechanism in the pathogenesis of Parkinson’s disease (PD). Therefore, modulation of autophagy may be a novel strategy for the treatment of PD. Recently, an active form of vitamin D3 has been reported to have neuroprotective properties. Therefore, we investigated the protective, autophagy-modulating effects of 1,25-dyhydroxyvitamin D3 (calcitriol) in an in vitro model of Parkinson’s disease. Methods An in vitro model of Parkinson’s disease, the rotenone-induced neurotoxicity model in SH-SY5Y cells was adapted. We measured cell viability using an MTT assay, Annexin V/propidium iodide assay, and intracellular reactive oxygen species levels and analyzed autophagy-associated intracellular signaling proteins by Western blotting. Results Rotenone treatment of SH-SY5Y cells reduced their viability. This treatment also increased reactive oxygen species levels and decreased levels of intracellular signaling proteins associated with cell survival; simultaneous exposure to calcitriol significantly reversed these effects. Additionally, calcitriol increased levels of autophagy markers, including LC3, beclin-1, and AMPK. Rotenone inhibited autophagy, as indicated by decreased beclin-1 levels and increased mTOR levels, and this effect was reversed by calcitriol treatment. Discussion Calcitriol protects against rotenone-induced neurotoxicity in SH-SY5Y cells by enhancing autophagy signaling pathways such as those involving LC3 and beclin-1. These neuroprotective effects of calcitriol against rotenone-induced dopaminergic neurotoxicity provide an experimental basis for its clinical use in the treatment of PD.
URI
http://pubs.kist.re.kr/handle/201004/50200
ISSN
0006291X
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