Syringaresinol causes vasorelaxation by elevating nitric oxide production through the phosphorylation and dimerization of endothelial nitric oxide synthase

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dc.contributor.authorB H Chung-
dc.contributor.authorS Kim-
dc.contributor.authorJ D Kim-
dc.contributor.authorJung Joon Lee-
dc.contributor.authorY Y Baek-
dc.contributor.authorD Jeoung-
dc.contributor.authorH Lee-
dc.contributor.authorJ Choe-
dc.contributor.authorK S Ha-
dc.contributor.authorM H Won-
dc.contributor.authorY G Kwon-
dc.contributor.authorY M Kim-
dc.date.accessioned2017-04-19T09:29:43Z-
dc.date.available2017-04-19T09:29:43Z-
dc.date.issued2012-
dc.identifier.issnI000-0028-
dc.identifier.uri10.3858/emm.2012.44.3.014ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10696-
dc.description.abstractNitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in vascular functions, including vasorelaxation. We here investigated the pharmacological effect of the natural product syringaresinol on vascular relaxation and eNOS-mediated NO production as well as its underlying biochemical mechanism in endothelial cells. Treatment of aortic rings from wild type, but not eNOS -/- mice, with syringaresinol induced endothelium-dependent relaxation, which was abolished by addition of the NOS inhibitor N G-monomethyl-L-arginine. Treatment of human endothelial cells and mouse aortic rings with syringaresinol increased NO production, which was correlated with eNOS phosphorylation via the activation of Akt and AMP kinase (AMPK) as well as elevation of intracellular Ca 2+ levels. A phospholipase C (PLC) inhibitor blocked the increases in intracellular Ca 2+ levels, AMPK-dependent eNOS phosphorylation, and NO production, but not Akt activation, in syringaresinol- treated endothelial cells. Syringaresinol-induced AMPK activation was inhibited by co-treatment with PLC inhibitor, Ca 2+ chelator, calmodulin antagonist, and CaMKKβ siRNA. This compound also increased eNOS dimerization, which was inhibited by a PLC inhibitor and a Ca 2+-chelator. The chemicals that inhibit eNOS phosphorylation and dimerization attenuated vasorelaxation and cGMP production. These results suggest that syringaresinol induces vasorelaxation by enhancing NO production in endothelial cells via two distinct mechanisms, phosphatidylinositol 3-kinase/Akt- and PLC/Ca 2+/CaMKKβ-dependent eNOS phosphorylation and Ca 2+-dependent eNOS dimerization.-
dc.publisherSpringer-Nature Pub Group-
dc.titleSyringaresinol causes vasorelaxation by elevating nitric oxide production through the phosphorylation and dimerization of endothelial nitric oxide synthase-
dc.title.alternativeSyringaresinol causes vasorelaxation by elevating nitric oxide production through the phosphorylation and dimerization of endothelial nitric oxide synthase-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number3-
dc.citation.endPage201-
dc.citation.startPage191-
dc.citation.volume44-
dc.contributor.affiliatedAuthorJung Joon Lee-
dc.contributor.alternativeName정병희-
dc.contributor.alternativeName김수곤-
dc.contributor.alternativeName김종대-
dc.contributor.alternativeName이정준-
dc.contributor.alternativeName백이용-
dc.contributor.alternativeName정두일-
dc.contributor.alternativeName이한수-
dc.contributor.alternativeName채종선-
dc.contributor.alternativeName하권수-
dc.contributor.alternativeName원무호-
dc.contributor.alternativeName권영근-
dc.contributor.alternativeName김영명-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 44, no. 3, pp. 191-201-
dc.identifier.doi10.3858/emm.2012.44.3.014-
dc.subject.keywordNitric oxide synthase type III-
dc.subject.keywordPhosphorylation-
dc.subject.keywordProtein multimerization-
dc.subject.keywordSyringaresinol-
dc.subject.keywordType C phospholipases-
dc.subject.keywordVasodilation-
dc.subject.localNitric oxide synthase type III-
dc.subject.localPhosphorylation-
dc.subject.localphosphorylation-
dc.subject.localProtein multimerization-
dc.subject.localsyringaresinol-
dc.subject.localSyringaresinol-
dc.subject.localType C phospholipases-
dc.subject.localVasodilation-
dc.description.journalClassY-
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