Apelin-13 inhibits methylglyoxal-induced unfolded protein responses and endothelial dysfunction via regulating ampk pathway
DC Field | Value | Language |
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dc.contributor.author | Kim S. | - |
dc.contributor.author | Kim S. | - |
dc.contributor.author | Hwang A.-R. | - |
dc.contributor.author | Choi H.C. | - |
dc.contributor.author | Lee J.-Y. | - |
dc.contributor.author | Woo C.-H. | - |
dc.date.available | 2020-07-13T05:20:30Z | - |
dc.date.issued | 2020-06 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/41800 | - |
dc.description.abstract | It has been suggested that methylglyoxal (MGO), a glycolytic metabolite, has more detrimental effects on endothelial dysfunction than glucose itself. Recent reports showed that high glucose and MGO induced endoplasmic reticulum (ER) stress and myocyte apoptosis in ischemic heart disease was inhibited by apelin. The goal of the study is to investigate the molecular mechanism by which MGO induces endothelial dysfunction via the regulation of ER stress in endothelial cells, and to examine whether apelin-13, a cytoprotective polypeptide ligand, protects MGO-induced aortic endothelial dysfunction. MGO-induced ER stress and apoptosis were determined by immunoblotting and MTT assay in HUVECs. Aortic endothelial dysfunction was addressed by en face immunostaining and acetylcholine-induced vasodilation analysis with aortic rings from mice treated with MGO in the presence or absence of apelin ex vivo. TUDCA, an inhibitor of ER stress, inhibited MGO-induced apoptosis and reduction of cell viability, suggesting that MGO signaling to endothelial apoptosis is mediated via ER stress, which leads to activation of unfolded protein responses (UPR). In addition, MGO-induced UPR and aortic endothelial dysfunction were significantly diminished by apelin-13. Finally, this study showed that apelin-13 protects MGO-induced UPR and endothelial apoptosis through the AMPK pathway. Apelin-13 reduces MGO-induced UPR and endothelial dysfunction via regulating the AMPK activating pathway, suggesting the therapeutic potential of apelin-13 in diabetic cardiovascular complications. © 2020 by the authors. Licensee MDPI, Basel, Switzerland. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | MDPI AG | - |
dc.title | Apelin-13 inhibits methylglyoxal-induced unfolded protein responses and endothelial dysfunction via regulating ampk pathway | - |
dc.type | Article | - |
dc.identifier.doi | 10.3390/ijms21114069 | - |
dc.identifier.bibliographicCitation | International Journal of Molecular Sciences, v.21, no.11, pp 1 - 13 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000543400300331 | - |
dc.identifier.scopusid | 2-s2.0-85086083802 | - |
dc.citation.endPage | 13 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 1 | - |
dc.citation.title | International Journal of Molecular Sciences | - |
dc.citation.volume | 21 | - |
dc.type.docType | Article | - |
dc.publisher.location | 스위스 | - |
dc.subject.keywordAuthor | AMPK | - |
dc.subject.keywordAuthor | Apelin | - |
dc.subject.keywordAuthor | Endothelial dysfunction | - |
dc.subject.keywordAuthor | Methylglyoxal | - |
dc.subject.keywordAuthor | UPR unfolded protein response | - |
dc.subject.keywordPlus | acetylcholine | - |
dc.subject.keywordPlus | apelin | - |
dc.subject.keywordPlus | apelin 13 | - |
dc.subject.keywordPlus | methylglyoxal | - |
dc.subject.keywordPlus | reactive oxygen metabolite | - |
dc.subject.keywordPlus | unclassified drug | - |
dc.subject.keywordPlus | AMPK signaling | - |
dc.subject.keywordPlus | animal experiment | - |
dc.subject.keywordPlus | animal model | - |
dc.subject.keywordPlus | apoptosis | - |
dc.subject.keywordPlus | Article | - |
dc.subject.keywordPlus | Aviadenovirus | - |
dc.subject.keywordPlus | cardiovascular disease | - |
dc.subject.keywordPlus | cell protection | - |
dc.subject.keywordPlus | cell viability | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | endoplasmic reticulum stress | - |
dc.subject.keywordPlus | endothelial dysfunction | - |
dc.subject.keywordPlus | human | - |
dc.subject.keywordPlus | human cell | - |
dc.subject.keywordPlus | immunoblotting | - |
dc.subject.keywordPlus | male | - |
dc.subject.keywordPlus | mouse | - |
dc.subject.keywordPlus | MTT assay | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | protein expression | - |
dc.subject.keywordPlus | unfolded protein response | - |
dc.subject.keywordPlus | vasodilatation | - |
dc.subject.keywordPlus | Western blotting | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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