Methylglyoxal causes endothelial dysfunction: The role of endothelial nitric oxide synthase and amp-activated protein kinase

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dc.contributor.authorTurkseven S.
dc.contributor.authorErtuna E.
dc.contributor.authorYetik-Anacak G.
dc.contributor.authorYasa M.
dc.date.accessioned2019-10-26T21:30:18Z
dc.date.available2019-10-26T21:30:18Z
dc.date.issued2014
dc.departmentEge Üniversitesien_US
dc.description.abstractBackground: Methylglyoxal is a major precursor in the formation of advanced glycation end products and is associated with the pathogenesis of diabetes-related vascular complications. The aim of this study was to evaluate whether methylglyoxal induces endothelial dysfunction and to determine the contributors involved in this process. Methods: Rat thoracic aortic rings were treated for 24 h with 100 µM methylglyoxal by using an organ culture method. A cumulative dose-response curve to acetylcholine was obtained to determine endothelium-dependent relaxation. The protein levels of endothelial nitric oxide synthase (eNOS) and its phosphorylated form at the serine 1177 site [p-eNOS (Ser1177)], heat shock protein 90 (Hsp90), AMP-activated protein kinase (AMPK?) and its phosphorylated form at the threonine 172 site [p-AMPK? (Thr172)] were evaluated. Superoxide production was determined by lucigenin-chemiluminescence. Results: Treatment with 100 µM methylglyoxal for 24 h decreased acetylcholine-induced vascular relaxation. The levels of eNOS and p-eNOS (Ser1177) were reduced while no effect on Hsp90 was observed. Levels of p-AMPK? (Thr172) were significantly decreased without any change in total AMPK? protein levels. Superoxide level was not affected by methylglyoxal treatment. Conclusions: In rat aortic rings, methylglyoxal determines a reduction in endothelium-dependent relaxation. This effect seems to be mediated via a reduction in p-eNOS (Ser1177) and p-AMPK(Thr172).en_US
dc.description.sponsorship93ECZ028en_US
dc.description.sponsorshipAcknowledgments: This study was supported by a Grant of Ege University Fund for Scientific Research (93ECZ028). --en_US
dc.identifier.doi10.1515/jbcpp-2013-0095en_US
dc.identifier.endpage115en_US
dc.identifier.issn0792-6855
dc.identifier.issue1en_US
dc.identifier.pmid24127540en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage109en_US
dc.identifier.urihttps://doi.org/10.1515/jbcpp-2013-0095
dc.identifier.urihttps://hdl.handle.net/11454/17617
dc.identifier.volume25en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWalter de Gruyter GmbHen_US
dc.relation.ispartofJournal of Basic and Clinical Physiology and Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAmp-activated protein kinase (ampk?)en_US
dc.subjectEndothelium-dependent relaxationen_US
dc.subjectEnosen_US
dc.subjectMethylglyoxalen_US
dc.titleMethylglyoxal causes endothelial dysfunction: The role of endothelial nitric oxide synthase and amp-activated protein kinaseen_US
dc.typeArticleen_US

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