{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T20:38:04Z","timestamp":1773866284143,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,8,20]],"date-time":"2013-08-20T00:00:00Z","timestamp":1376956800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Nasal polyposis is characterized by tissue remodelling and oedematous nasal mucosa. Vascular endothelial growth factor (<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>) plays a significant role in the regulation of remodelling in nasal polyps. <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 activation is associated with <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> expression in murine macrophages and odontoblasts.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>This study aimed to evaluate whether lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>), an inducer of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4, stimulates <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> expression and to determine the mechanism underlying <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> production in nasal polyps.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Nasal polyp\u2010derived fibroblasts (<jats:styled-content style=\"fixed-case\">NPDFs<\/jats:styled-content>) were isolated from 10 patients with nasal polyps and exposed to LPS. LPS from <jats:italic>Rhodobacter sphaeroides<\/jats:italic> (<jats:styled-content style=\"fixed-case\">LRS<\/jats:styled-content>) was used to inhibit the expression levels of <jats:styled-content style=\"fixed-case\">TLR4<\/jats:styled-content>, MyD88 and <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>. Messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>) expression levels of <jats:italic>TLRs, MyD88<\/jats:italic> and <jats:italic>VEGF<\/jats:italic> were determined by gene expression microarray and semiquantitative reverse transcription\u2010PCR. Protein expression levels of <jats:styled-content style=\"fixed-case\">TLR4<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> were analysed using western blot, immunofluorescence staining and enzyme\u2010linked immunosorbent assay (<jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>). Activation of <jats:styled-content style=\"fixed-case\">MAPKs<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>, p38, and <jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content>) and Akt was examined using western blot analysis. The expression level of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> was measured by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content> and western blot analysis in <jats:italic>ex vivo<\/jats:italic> nasal polyp organ culture.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The protein expression level of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> was increased in nasal polyp tissues compared with inferior turbinate tissues. <jats:styled-content style=\"fixed-case\">LRS<\/jats:styled-content> inhibited the <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein expression of <jats:styled-content style=\"fixed-case\">TLR4<\/jats:styled-content>, MyD88 and <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010stimulated <jats:styled-content style=\"fixed-case\">NPDFs<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010activated <jats:styled-content style=\"fixed-case\">MAPKs<\/jats:styled-content> and Akt signals, whereas <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> inhibitors did not inhibit <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> expression, and only Akt inhibitor blocked <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> production. <jats:styled-content style=\"fixed-case\">LRS<\/jats:styled-content> reduced the production of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010stimulated <jats:italic>ex vivo<\/jats:italic> organ culture.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Clinical Relevance<\/jats:title><jats:p>These results suggest that <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> stimulates the production of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> through the <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4\u2010Akt signalling pathway in nasal polyps. <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> may be involved in the pathogenesis of nasal polyp remodelling.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12165","type":"journal-article","created":{"date-parts":[[2013,6,26]],"date-time":"2013-06-26T17:04:51Z","timestamp":1372266291000},"page":"1038-1047","source":"Crossref","is-referenced-by-count":19,"title":["Activation of <scp>TLR<\/scp>4 induces <scp>VEGF<\/scp> expression via Akt pathway in nasal polyps"],"prefix":"10.1111","volume":"43","author":[{"given":"J.\u2010S.","family":"Cho","sequence":"first","affiliation":[{"name":"Biomedical Science Korea University College of Medicine Seoul Korea"},{"name":"Institute for Medical Devices Clinical Trial Center Guro Hospital Korea University Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.\u2010H.","family":"Kang","sequence":"additional","affiliation":[{"name":"Biomedical Science Korea University College of Medicine Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I.\u2010H.","family":"Han","sequence":"additional","affiliation":[{"name":"Biomedical Science Korea University College of Medicine Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.\u2010Y.","family":"Um","sequence":"additional","affiliation":[{"name":"Biomedical Science Korea University College of Medicine Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.\u2010M.","family":"Lee","sequence":"additional","affiliation":[{"name":"Biomedical Science Korea University College of Medicine Seoul Korea"},{"name":"Institute for Medical Devices Clinical Trial Center Guro Hospital Korea University Seoul Korea"},{"name":"Department of Otorhinolaryngology\u2010Head and Neck Surgery Korea University College of Medicine Seoul 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