{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T22:20:19Z","timestamp":1792794019571,"version":"4.5.0"},"reference-count":44,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,9,25]],"date-time":"2019-09-25T00:00:00Z","timestamp":1569369600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:p>\n                    Recent 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\u2010to\u2010mesenchymal 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\n                    <jats:italic>via<\/jats:italic>\n                    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\u2010induced glycocalyx shedding and EndoMT. Antioxidants including\n                    <jats:italic>N<\/jats:italic>\n                    \u2010acetyl 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\n                    <jats:italic>de novo<\/jats:italic>\n                    expression of \u03b1\u2010smooth muscle actin in PTCs. Plasma level of syndecan\u20101 was increased in hyperuricemic rats, which was ameliorated by allopurinol. UA caused a phenotypic transition of endothelial cells\n                    <jats:italic>via<\/jats:italic>\n                    induction of oxidative stress with glycocalyx shedding, which could be one of the mechanisms of UA\u2010induced endothelial dysfunction and kidney disease.\u2014Ko, J., Kang, H.\u2010J., Kim, D.\u2010A., Kim, M.\u2010J., Ryu, E.\u2010S., Lee, S., Ryu, J.\u2010H., Roncal, C., Johnson, R. J., Kang, D.\u2010H. Uric acid induced the phenotype transition of vascular endothelial cells\n                    <jats:italic>via<\/jats:italic>\n                    induction of oxidative stress and glycocalyx shedding. FASEB J. 33, 13334\u201313345 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201901148r","type":"journal-article","created":{"date-parts":[[2019,9,25]],"date-time":"2019-09-25T17:33:00Z","timestamp":1569432780000},"page":"13334-13345","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":85,"title":["Uric acid induced the phenotype transition of vascular endothelial cells\n                    <i>via<\/i>\n                    induction of oxidative stress and glycocalyx shedding"],"prefix":"10.1096","volume":"33","author":[{"given":"Jiyeon","family":"Ko","sequence":"first","affiliation":[{"name":"Division of Nephrology Department of Internal Medicine Ewha Medical Research Center College of Medicine Ewha Womans University Seoul South 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