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dc.contributor.author강덕희-
dc.contributor.author김달아-
dc.contributor.author류정화-
dc.date.accessioned2020-02-10T16:30:09Z-
dc.date.available2020-02-10T16:30:09Z-
dc.date.issued2019-
dc.identifier.issn0892-6638-
dc.identifier.issn1530-6860-
dc.identifier.otherOAK-26317-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/253389-
dc.description.abstractRecent data suggested a causative role of uric acid (UA) in the development of renal disease, in which endothelial dysfunction is regarded as the key mechanism. Endothelial-to-mesenchymal transition (EndoMT) and shedding of the glycocalyx are early changes of endothelial dysfunction. We investigated whether UA induced EndoMT in HUVECs and an animal model of hyperuricemia fed with 2% oxonic acid for 4 wk. UA induced EndoMT in HUVECs with a generation of reactive oxygen species via the activation of membranous NADPH oxidase (from 15 min) and mitochondria (from 6 h) along with glycocalyx shedding (from 6 h), which were blocked by probenecid. GM6001, an inhibitor of matrix metalloproteinase, alleviated UA-induced glycocalyx shedding and EndoMT. Antioxidants including N-acetyl cysteine, apocynin, and mitotempo ameliorated EndoMT; however, they did not change glycocalyx shedding in HUVECs. In the kidney of hyperuricemic rats, endothelial staining in peritubular capillaries (PTCs) was substantially decreased with a de novo expression of alpha-smooth muscle actin in PTCs. Plasma level of syndecan-1 was increased in hyperuricemic rats, which was ameliorated by allopurinol. UA caused a phenotypic transition of endothelial cells via induction of oxidative stress with glycocalyx shedding, which could be one of the mechanisms of UA-induced endothelial dysfunction and kidney disease.-
dc.languageEnglish-
dc.publisherFEDERATION AMER SOC EXP BIOL-
dc.subjectEndoMT-
dc.subjectreactive oxygen species-
dc.subjecthyperuricemia-
dc.subjectsyndecan-1-
dc.titleUric acid induced the phenotype transition of vascular endothelial cells via induction of oxidative stress and glycocalyx shedding-
dc.typeArticle-
dc.relation.issue12-
dc.relation.volume33-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage13334-
dc.relation.lastpage13345-
dc.relation.journaltitleFASEB JOURNAL-
dc.identifier.doi10.1096/fj.201901148R-
dc.identifier.wosidWOS:000507466100024-
dc.identifier.scopusid2-s2.0-85075962441-
dc.author.googleKo, Jiyeon-
dc.author.googleKang, Hyun-Jung-
dc.author.googleKim, Dal-Ah-
dc.author.googleKim, Mi-Jin-
dc.author.googleRyu, Eun-Sun-
dc.author.googleLee, Shina-
dc.author.googleRyu, Jung-Hwa-
dc.author.googleRoncal, Carlos-
dc.author.googleJohnson, Richard J.-
dc.author.googleKang, Duk-Hee-
dc.contributor.scopusid강덕희(17233695600)-
dc.contributor.scopusid김달아(57193326495)-
dc.date.modifydate20200517081002-
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의과대학 > 의학과 > Journal papers
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