Full metadata record
DC Field | Value | Language |
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dc.contributor.author | Jang, Wooyoung | - |
dc.contributor.author | Kim, Hee Ju | - |
dc.contributor.author | Li, Huan | - |
dc.contributor.author | Jo, Kwang Deog | - |
dc.contributor.author | Lee, Moon Kyu | - |
dc.contributor.author | Song, Sun Hong | - |
dc.contributor.author | Yang, Hyun Ok | - |
dc.date.accessioned | 2024-01-20T09:03:29Z | - |
dc.date.available | 2024-01-20T09:03:29Z | - |
dc.date.created | 2021-09-02 | - |
dc.date.issued | 2014-08-15 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://pubs.kist.re.kr/handle/201004/126465 | - |
dc.description.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 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.language | English | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | VITAMIN-D-RECEPTOR | - |
dc.subject | PARKINSON-DISEASE | - |
dc.subject | ALPHA-SYNUCLEIN | - |
dc.subject | PATHOGENESIS | - |
dc.subject | NEURONS | - |
dc.subject | NEUROPROTECTION | - |
dc.subject | DEGRADATION | - |
dc.subject | PREVALENCE | - |
dc.subject | MECHANISMS | - |
dc.subject | EXPRESSION | - |
dc.title | 1,25-Dyhydroxyvitamin D-3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.bbrc.2014.07.081 | - |
dc.description.journalClass | 1 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.451, no.1, pp.142 - 147 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 451 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 142 | - |
dc.citation.endPage | 147 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.identifier.wosid | 000340864200023 | - |
dc.identifier.scopusid | 2-s2.0-84906217905 | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | VITAMIN-D-RECEPTOR | - |
dc.subject.keywordPlus | PARKINSON-DISEASE | - |
dc.subject.keywordPlus | ALPHA-SYNUCLEIN | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | NEURONS | - |
dc.subject.keywordPlus | NEUROPROTECTION | - |
dc.subject.keywordPlus | DEGRADATION | - |
dc.subject.keywordPlus | PREVALENCE | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordAuthor | Calcitriol | - |
dc.subject.keywordAuthor | Parkinson&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | Autophagy | - |
dc.subject.keywordAuthor | Neuroprotection | - |
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