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dc.contributor.authorJang, Wooyoung-
dc.contributor.authorKim, Hee Ju-
dc.contributor.authorLi, Huan-
dc.contributor.authorJo, Kwang Deog-
dc.contributor.authorLee, Moon Kyu-
dc.contributor.authorSong, Sun Hong-
dc.contributor.authorYang, Hyun Ok-
dc.date.accessioned2024-01-20T09:03:29Z-
dc.date.available2024-01-20T09:03:29Z-
dc.date.created2021-09-02-
dc.date.issued2014-08-15-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/126465-
dc.description.abstractBackground 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 D-3 has been reported to have neuroprotective properties. Therefore, we investigated the protective, autophagy-modulating effects of 1,25-dyhydroxyvitamin D-3 (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. (C) 2014 Elsevier Inc. All rights reserved.-
dc.languageEnglish-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.subjectVITAMIN-D-RECEPTOR-
dc.subjectPARKINSON-DISEASE-
dc.subjectALPHA-SYNUCLEIN-
dc.subjectPATHOGENESIS-
dc.subjectNEURONS-
dc.subjectNEUROPROTECTION-
dc.subjectDEGRADATION-
dc.subjectPREVALENCE-
dc.subjectMECHANISMS-
dc.subjectEXPRESSION-
dc.title1,25-Dyhydroxyvitamin D-3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy-
dc.typeArticle-
dc.identifier.doi10.1016/j.bbrc.2014.07.081-
dc.description.journalClass1-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.451, no.1, pp.142 - 147-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume451-
dc.citation.number1-
dc.citation.startPage142-
dc.citation.endPage147-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000340864200023-
dc.identifier.scopusid2-s2.0-84906217905-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.type.docTypeArticle-
dc.subject.keywordPlusVITAMIN-D-RECEPTOR-
dc.subject.keywordPlusPARKINSON-DISEASE-
dc.subject.keywordPlusALPHA-SYNUCLEIN-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusNEUROPROTECTION-
dc.subject.keywordPlusDEGRADATION-
dc.subject.keywordPlusPREVALENCE-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordAuthorCalcitriol-
dc.subject.keywordAuthorParkinson&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorAutophagy-
dc.subject.keywordAuthorNeuroprotection-
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