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Role of p53 in the cellular response following oleic acid accumulation in Chang liver cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, Eun-Jung | - |
dc.contributor.author | Lee, Ah Young | - |
dc.contributor.author | Chang, Seung-Hee | - |
dc.contributor.author | Yu, Kyeong-Nam | - |
dc.contributor.author | Kim, Jae-Ho | - |
dc.contributor.author | Cho, Myung-Haing | - |
dc.date.accessioned | 2021-01-31T08:51:16Z | - |
dc.date.available | 2021-01-31T08:51:16Z | - |
dc.date.created | 2020-07-15 | - |
dc.date.issued | 2014-01 | - |
dc.identifier.citation | Toxicology Letters, Vol.224 No.1, pp.114-120 | - |
dc.identifier.issn | 0378-4274 | - |
dc.identifier.other | 106882 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172529 | - |
dc.description.abstract | Abnormal accumulation of fatty acids triggers the harmful cellular response called lipotoxicity. In this study, we investigated the cellular response following accumulation of oleic acid (OA), a monounsaturated fatty acid, in human Chang liver cells. OA droplets were distributed freely in the cytoplasm and/or degraded within lysosomes. OA exposure increased ATP production and concomitantly dilated mitochondria. At 24 h after OA exposure, cell viability decreased slightly and was coupled with a reduction in mitochondrial Ca2+ concentration, the alteration in cell viability was also associated with the generation of reactive oxygen species and changes in the cell cycle. Moreover, OA treatment increased the expression of autophagy- and apoptotic cell death-related proteins in a dose-dependent manner. Furthermore, we investigated the role of p53, a tumor suppressor protein, in the cellular response elicited by OA accumulation. OA-induced changes in cell viability and ATP production were rescued to control levels when cells were pretreated with pifithrin-alpha (PTA), a p53 inhibitor. By contrast, the expressions of LC3-II and perilipin, proteins required for lipophagy, were down-regulated by PTA pretreatment. Taken together, our results suggest that p53 plays a key role in the cellular response elicited by OA accumulation in Chang liver cells. (C) 2013 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | 영어 | - |
dc.publisher | Elsevier BV | - |
dc.title | Role of p53 in the cellular response following oleic acid accumulation in Chang liver cells | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 조명행 | - |
dc.identifier.doi | 10.1016/j.toxlet.2013.09.018 | - |
dc.citation.journaltitle | Toxicology Letters | - |
dc.identifier.wosid | 000327887100015 | - |
dc.identifier.scopusid | 2-s2.0-84887511490 | - |
dc.citation.endpage | 120 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 114 | - |
dc.citation.volume | 224 | - |
dc.identifier.sci | 000327887100015 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Cho, Myung-Haing | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | SATURATED FATTY-ACIDS | - |
dc.subject.keywordPlus | LIPID-METABOLISM | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
dc.subject.keywordPlus | LIPOTOXICITY | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | PATHWAYS | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | NANOPARTICLES | - |
dc.subject.keywordPlus | MITOCHONDRIA | - |
dc.subject.keywordAuthor | Oleic acid | - |
dc.subject.keywordAuthor | Autophagy | - |
dc.subject.keywordAuthor | p53 | - |
dc.subject.keywordAuthor | Lipophagy | - |
dc.subject.keywordAuthor | ATP | - |
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