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The exact pattern of aquaporin (AQP) water channel expression and its mechanism in periodontal disease is still unknown. We describe herein an up\u2010regulated AQP3 expression in the epithelial lesion with chronic periodontitis and its functional role. The levels of AQP3 expression in inflamed gingival epithelial tissues were significantly higher than those of healthy subjects. Consistent with these results, AQP3 expression (i.e., levels of mRNA and protein) in cultured rat primary gingival epithelial cells and the human gingival epithelial cell line Ca9\u201022 were strongly increased in response to TNF\u2010\u03b1 treatment through the 55 kDa TNF\u2010\u03b1 receptor (TNFR I). In this context, small interfering RNA\u2010 (siRNA)\u2010mediated \u201c<jats:italic>aqp\u20103<\/jats:italic>gene silencing,\u201d which could reduce AQP3 expression by more than 65%, significantly attenuated selected proinflammatory events of ICAM\u20101 expression induced by TNF\u2010\u03b1 in Ca9\u201022. A sixfold increase in leukocyte adherence to TNF\u2010\u03b1\u2010stimulated epithelial cells was demonstrated by an adherence assay (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) and pretreatment with AQP3 siRNA and anti\u2010ICAM\u20101 antibody reduced leukocyte retention by 85% (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001). Our study indicates for the first time a novel important mode in the regulation of the inflammatory response through TNF\u2010\u03b1\/TNFR I ligation at the site of epithelial lesions by specialized membrane channel AQP3 and ICAM\u20101 protein, which is closely implicated in the development of periodontitis mechanisms. J. Cell. Physiol. 217: 338\u2013349, 2008. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21506","type":"journal-article","created":{"date-parts":[[2008,6,9]],"date-time":"2008-06-09T14:52:04Z","timestamp":1213023124000},"page":"338-349","source":"Crossref","is-referenced-by-count":21,"title":["The role of water channel aquaporin 3 in the mechanism of TNF\u2010\u03b1\u2010mediated proinflammatory events: Implication in periodontal inflammation"],"prefix":"10.1002","volume":"217","author":[{"given":"S.","family":"Tancharoen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Matsuyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Abeyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Matsushita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Kawahara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"Sangalungkarn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Tokuda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Hashiguchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Maruyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Izumi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,6,9]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuint.2007.08.006"},{"key":"e_1_2_5_3_1","first-page":"706","article-title":"New 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