{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,4]],"date-time":"2023-10-04T06:41:58Z","timestamp":1696401718702},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2014,7,4]],"date-time":"2014-07-04T00:00:00Z","timestamp":1404432000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cutan Pathol"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Kaposi sarcoma (<jats:styled-content style=\"fixed-case\">KS<\/jats:styled-content>), caused by the infection of Kaposi sarcoma\u2010associated herpesvirus (<jats:italic><jats:styled-content style=\"fixed-case\">KSHV<\/jats:styled-content><\/jats:italic>), is a disease manifested mainly by dark purple skin and mouth nodules. Cancer care studies showed that co\u2010infection of <jats:styled-content style=\"fixed-case\">KSHV<\/jats:styled-content> and human immunodeficiency virus (<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>) was able to increase the patients' survival, but the underlying mechanisms are still elusive.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>To understand the mechanism underlying the prolonged survival in <jats:styled-content style=\"fixed-case\">KSHV\u2010HIV<\/jats:styled-content> co\u2010infected patients, we performed microarray analysis on <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> extracted from biopsies from <jats:styled-content style=\"fixed-case\">KS<\/jats:styled-content> tumors and adjacent healthy tissues in four <jats:styled-content style=\"fixed-case\">KS<\/jats:styled-content> patients. Subsequently, we performed hierarchical clustering, gene ontology (GO) and ingenuity pathway analysis. We then characterized the roles of tight junction protein claudin\u20102 in the endothelial barrier function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Three hundred and forty\u2010three differentially expressed genes were identified, of which 246 genes exhibited significantly increased expression in the tumor compared to the adjacent healthy tissue and 97 genes showed downregulated expression, including claudin\u20102. Knockdown of claudin\u20102 in cultured endothelial cells enhances barrier function by altering the charge selectivity, but not the size selectivity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Claudin\u20102 expression is decreased in <jats:styled-content style=\"fixed-case\">KS<\/jats:styled-content> tumors from patients co\u2010infected with <jats:styled-content style=\"fixed-case\">KSHV<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>. Decreased claudin\u20102 enhances endothelial barrier function and may play a role in the prolonged survival of patients with <jats:styled-content style=\"fixed-case\">KSHV<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> co\u2010infection.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cup.12332","type":"journal-article","created":{"date-parts":[[2014,7,4]],"date-time":"2014-07-04T07:43:14Z","timestamp":1404459794000},"page":"630-639","source":"Crossref","is-referenced-by-count":6,"title":["Claudin\u20102 downregulation by <scp>KSHV<\/scp> infection is involved in the regulation of endothelial barrier function"],"prefix":"10.1111","volume":"41","author":[{"given":"Xiaohua","family":"Tan","sequence":"first","affiliation":[{"name":"School of Medicine Hangzhou Normal University  Hangzhou Zhejiang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dongmei","family":"Li","sequence":"additional","affiliation":[{"name":"Ministry of 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