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Cited 15 times in

G protein-coupled estrogen receptor-1 is involved in the protective effect of protocatechuic aldehyde against endothelial dysfunction.

DC FieldValueLanguage
dc.contributor.author공병수-
dc.contributor.author이은직-
dc.contributor.author조윤희-
dc.date.accessioned2015-12-28T11:06:53Z-
dc.date.available2015-12-28T11:06:53Z-
dc.date.issued2014-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/138722-
dc.description.abstractProtocatechuic aldehyde (PCA), a phenolic aldehyde, has therapeutic potency against atherosclerosis. Although PCA is known to inhibit the migration and proliferation of vascular smooth muscle cells and intravascular thrombosis, the underlying mechanism remains unclear. In this study, we investigated the protective effect of PCA on endothelial cells and injured vessels in vivo in association with G protein-coupled estrogen receptor-1 (GPER-1). With PCA treatment, cAMP production was increased in HUVECs, while GPER-1 expression was increased in both HUVECs and a rat aortic explant. PCA and G1, a GPER-1 agonist, reduced H2O2 stimulated ROS production in HUVECs, whereas, G15, a GPER-1 antagonist, increased ROS production further. These elevations were inhibited by co-treatment with PCA or G1. TNFα stimulated the expression of inflammatory markers (VCAM-1, ICAM-1 and CD40), phospho-NF-κB, phospho-p38 and HIF-1α; however, co-treatment with PCA or G1 down-regulated this expression significantly. Likewise, increased expression of inflammatory markers by treatment with G15 was inhibited by co-treatment with PCA. In re-endothelization, aortic ring sprouting and neointima formation assay, rat aortas treated with PCA or G1 showed accelerated re-endothelization of the endothelium and reduced sprouting and neointima formation. However, aortas from G15-treated rats showed decelerated re-endothelization and increased sprouting and neointima formation. The effects of G15 were restored by co-treatment with PCA or G1. Also, in the endothelia of these aortas, PCA and G1 increased CD31 and GPER-1 and decreased VCAM-1 and CD40 expression. In contrast, the opposite effect was observed in G15-treated endothelium. These results suggest that GPER-1 might mediate the protective effect of PCA on the endothelium.-
dc.description.statementOfResponsibilityopen-
dc.format.extente113242-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAorta, Thoracic/drug effects*-
dc.subject.MESHAorta, Thoracic/metabolism-
dc.subject.MESHBenzaldehydes/pharmacology*-
dc.subject.MESHBenzodioxoles/pharmacology-
dc.subject.MESHCarotid Artery Injuries/drug therapy*-
dc.subject.MESHCarotid Artery Injuries/metabolism-
dc.subject.MESHCarotid Artery Injuries/pathology-
dc.subject.MESHCatechols/pharmacology*-
dc.subject.MESHCyclic AMP/metabolism-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHHuman Umbilical Vein Endothelial Cells-
dc.subject.MESHHydrogen Peroxide/pharmacology-
dc.subject.MESHMale-
dc.subject.MESHNeointima/drug therapy*-
dc.subject.MESHNeointima/etiology-
dc.subject.MESHOrgan Culture Techniques/methods-
dc.subject.MESHQuinolines/pharmacology-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHReceptors, Estrogen-
dc.subject.MESHReceptors, G-Protein-Coupled/metabolism*-
dc.titleG protein-coupled estrogen receptor-1 is involved in the protective effect of protocatechuic aldehyde against endothelial dysfunction.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorByung Soo Kong-
dc.contributor.googleauthorYoon Hee Cho-
dc.contributor.googleauthorEun Jig Lee-
dc.identifier.doi10.1371/journal.pone.0113242-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00159-
dc.contributor.localIdA03050-
dc.contributor.localIdA03878-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid25411835-
dc.contributor.alternativeNameKong, Byung Soo-
dc.contributor.alternativeNameLee, Eun Jig-
dc.contributor.alternativeNameCho, Yoon Hee-
dc.contributor.affiliatedAuthorKong, Byung Soo-
dc.contributor.affiliatedAuthorLee, Eun Jig-
dc.contributor.affiliatedAuthorCho, Yoon Hee-
dc.citation.volume9-
dc.citation.number11-
dc.citation.startPagee113242-
dc.identifier.bibliographicCitationPLOS ONE, Vol.9(11) : e113242, 2014-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
5. Research Institutes (연구소) > Institute of Endocrinology (내분비연구소) > 1. Journal Papers

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