Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells
DC Field | Value | Language |
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dc.contributor.author | Jung, Tae Woo | - |
dc.contributor.author | Hwang, Hwan-Jin | - |
dc.contributor.author | Hong, Ho Cheol | - |
dc.contributor.author | Choi, Hae Yoon | - |
dc.contributor.author | Yoo, Hye Jin | - |
dc.contributor.author | Baik, Sei Hyun | - |
dc.contributor.author | Choi, Kyung Mook | - |
dc.date.accessioned | 2021-09-05T07:37:40Z | - |
dc.date.available | 2021-09-05T07:37:40Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2014-06-25 | - |
dc.identifier.issn | 0303-7207 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/98198 | - |
dc.description.abstract | Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from omega-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD. (C) 2014 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER IRELAND LTD | - |
dc.subject | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject | LIPID MEDIATORS | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | HEPATIC STEATOSIS | - |
dc.subject | ADIPOSE-TISSUE | - |
dc.subject | INSULIN SENSITIVITY | - |
dc.subject | PROMOTE RESOLUTION | - |
dc.subject | INFLAMMATION | - |
dc.subject | CHOLESTEROL | - |
dc.subject | LIVER | - |
dc.title | Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Jung, Tae Woo | - |
dc.contributor.affiliatedAuthor | Yoo, Hye Jin | - |
dc.contributor.affiliatedAuthor | Baik, Sei Hyun | - |
dc.contributor.affiliatedAuthor | Choi, Kyung Mook | - |
dc.identifier.doi | 10.1016/j.mce.2014.04.012 | - |
dc.identifier.scopusid | 2-s2.0-84899853191 | - |
dc.identifier.wosid | 000337881900004 | - |
dc.identifier.bibliographicCitation | MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.391, no.1-2, pp.30 - 40 | - |
dc.relation.isPartOf | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.citation.title | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.citation.volume | 391 | - |
dc.citation.number | 1-2 | - |
dc.citation.startPage | 30 | - |
dc.citation.endPage | 40 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | LIPID MEDIATORS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | HEPATIC STEATOSIS | - |
dc.subject.keywordPlus | ADIPOSE-TISSUE | - |
dc.subject.keywordPlus | INSULIN SENSITIVITY | - |
dc.subject.keywordPlus | PROMOTE RESOLUTION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | CHOLESTEROL | - |
dc.subject.keywordPlus | LIVER | - |
dc.subject.keywordAuthor | Non-alcoholic fatty liver | - |
dc.subject.keywordAuthor | Resolvin D1 | - |
dc.subject.keywordAuthor | c-Jun N-terminal kinase | - |
dc.subject.keywordAuthor | Proliferator-activated receptor-gamma | - |
dc.subject.keywordAuthor | ER stress | - |
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