{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T10:24:40Z","timestamp":1783592680919,"version":"3.55.0"},"reference-count":43,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,5,6]],"date-time":"2016-05-06T00:00:00Z","timestamp":1462492800000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["SC1CA153325"],"award-info":[{"award-number":["SC1CA153325"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01HL094889"],"award-info":[{"award-number":["R01HL094889"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL28607"],"award-info":[{"award-number":["HL28607"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microcirculation"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>S1P was found to protect the <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> by inhibiting <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> activity\u2010dependent shedding of <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> in cultured endothelial cell studies. We aimed to further test that S1P contributes to the maintenance of normal vascular permeability by protecting the <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> in intact microvessels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We quantified the <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> in post\u2010capillary venules of rat mesentery and measured the vascular permeability to albumin in the presence and absence of 1\u00a0<jats:italic>\u03bc<\/jats:italic>M S1P. We also measured permeability to albumin in the presence of <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> inhibitors and compared the measured permeability with those predicted by a transport model for the inter\u2010endothelial cleft.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that in the absence of S1P, the fluorescence intensity of the <jats:styled-content style=\"fixed-case\">FITC<\/jats:styled-content>\u2010anti\u2013HS\u2010labeled <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> was ~10% of that in the presence of S1P, whereas the measured permeability to albumin was\u00a0~6.5\u2010fold of that in the presence of S1P. Similar results were\u00a0observed with <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content> inhibition. The predictions by the mathematical model further confirmed that S1P maintains microvascular permeability by preserving <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our results show that S1P contributes to the maintenance of normal vascular permeability by protecting the <jats:styled-content style=\"fixed-case\">ESG<\/jats:styled-content> in intact microvessels, consistent with parallel observation in cultured endothelial monolayers.<\/jats:p><\/jats:sec>","DOI":"10.1111\/micc.12278","type":"journal-article","created":{"date-parts":[[2016,3,25]],"date-time":"2016-03-25T13:46:40Z","timestamp":1458913600000},"page":"301-310","source":"Crossref","is-referenced-by-count":70,"title":["Sphingosine\u20101\u2010phosphate Maintains Normal Vascular Permeability by Preserving Endothelial Surface Glycocalyx in Intact Microvessels"],"prefix":"10.1111","volume":"23","author":[{"given":"Lin","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering The City College of the City University of New York New York City New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering The City College of the City University of New York New York City New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering The City College of the City University of New York New York City New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John M.","family":"Tarbell","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering The City College of the City University of New York New York City New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fitz\u2010Roy E.","family":"Curry","sequence":"additional","affiliation":[{"name":"Department of Physiology and Membrane Biology School of Medicine University of California at Davis Davis California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingmei M.","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering The City College of the City University of New York New York City New York 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