{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T10:15:51Z","timestamp":1769076951960,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,2,18]],"date-time":"2013-02-18T00:00:00Z","timestamp":1361145600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 DE14079"],"award-info":[{"award-number":["R01 DE14079"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2013,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Vascular endothelial growth factor (<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>) is a critical angiogenic factor affecting endothelial cells, inflammatory cells and neuronal cells. In addition to its well\u2010defined positive role in wound healing, pathological roles for <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> have been described in cancer and inflammatory diseases (<jats:italic>i.e<\/jats:italic>. atherosclerosis, rheumatoid arthritis, inflammatory bowel disease and osteoarthritis). Recently, we showed that transcription factors <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content> affected the inflammatory response. This study builds upon our previous results in testing the role of mouse <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content> in the regulation of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\u2010mediated processes. Cells cotransfected with a series of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> promoter deletions along with truncated forms of <jats:styled-content style=\"fixed-case\">mLITAF<\/jats:styled-content> and\/or <jats:styled-content style=\"fixed-case\">mSTAT<\/jats:styled-content>6B identified a <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> binding site (between \u2212338 and \u2212305 upstream of the transcription site) important in <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content> and\/or <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content>\u2010mediated transcriptional regulation of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content> corresponding protein sites were identified. In addition, si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010mediated knockdown of <jats:styled-content style=\"fixed-case\">mLITAF<\/jats:styled-content> and\/or <jats:styled-content style=\"fixed-case\">mSTAT<\/jats:styled-content>6B leads to significant reduction in <jats:styled-content style=\"fixed-case\">VEGF mRNA<\/jats:styled-content> levels and inhibits <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> secretion in mouse <jats:styled-content style=\"fixed-case\">RAW<\/jats:styled-content> 264.7 cells. Furthermore, <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> treatment of mouse macrophage or endothelial cells induces <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content> nuclear translocation and cell migration. To translate these observations <jats:italic>in vivo<\/jats:italic>,<jats:styled-content style=\"fixed-case\"> VEGF<\/jats:styled-content>164\u2010soaked matrigel were implanted in whole\u2010body <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\u2010deficient animals (Tam<jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content><jats:sup>\u2212\/\u2212<\/jats:sup>), wild\u2010type mice silenced for <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content>, and in respective control animals. Vessel formation was found significantly reduced in Tam<jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content><jats:sup>\u2212\/\u2212<\/jats:sup> as well as in <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content>\u2010silenced wild\u2010type animals compared with control animals. The present data demonstrate that <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> regulation by <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content> and\/or <jats:styled-content style=\"fixed-case\">STAT6B<\/jats:styled-content> is important in angiogenesis signalling pathways and may be a useful target in the treatment of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> diseases.<\/jats:p>","DOI":"10.1111\/jcmm.12020","type":"journal-article","created":{"date-parts":[[2013,2,19]],"date-time":"2013-02-19T00:43:42Z","timestamp":1361234622000},"page":"386-397","source":"Crossref","is-referenced-by-count":27,"title":["Novel transcriptional regulation of <scp>VEGF<\/scp> in inflammatory processes"],"prefix":"10.1111","volume":"17","author":[{"given":"Xiaoren","family":"Tang","sequence":"first","affiliation":[{"name":"Center for Anti\u2010Inflammatory Therapeutics Boston University Goldman School of Dental Medicine Boston MA 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