Publication: The role of water channel aquaporin 3 in the mechanism of TNF-α-mediated proinflammatory events: Implication in periodontal inflammation
Issued Date
2008-11-01
Resource Type
ISSN
00219541
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2-s2.0-51449083993
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Cellular Physiology. Vol.217, No.2 (2008), 338-349
Suggested Citation
S. Tancharoen, T. Matsuyama, K. Abeyama, K. Matsushita, K. Kawahara, V. Sangalungkarn, M. Tokuda, T. Hashiguchi, I. Maruyama, Y. Izumi The role of water channel aquaporin 3 in the mechanism of TNF-α-mediated proinflammatory events: Implication in periodontal inflammation. Journal of Cellular Physiology. Vol.217, No.2 (2008), 338-349. doi:10.1002/jcp.21506 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/18840
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Title
The role of water channel aquaporin 3 in the mechanism of TNF-α-mediated proinflammatory events: Implication in periodontal inflammation
Other Contributor(s)
Mahidol University
Cardiovascular and Respiratory Disorders Kagoshima Graduate School of Medical and Dental Science
Tokyo Medical and Dental University
Kagoshima University Faculty of Medicine
Shin Nippon Biomedical Laboratories, Ltd.
National Center for Geriatrics and Gerontology - National Institute for Longevity Sciences
Kagoshima Graduate School of Medical and Dental Science
Cardiovascular and Respiratory Disorders Kagoshima Graduate School of Medical and Dental Science
Tokyo Medical and Dental University
Kagoshima University Faculty of Medicine
Shin Nippon Biomedical Laboratories, Ltd.
National Center for Geriatrics and Gerontology - National Institute for Longevity Sciences
Kagoshima Graduate School of Medical and Dental Science
Abstract
Aquaporin 3 (AQP3) is the predominant water channel protein in human keratinocytes and acts as an inflammatory mediator in some lesions. A chronic, inflammatory process of periodontitis is related with a dramatic change of surrounding fluid homeostasis to plasma extravasation. The exact pattern of aquaporin (AQP) water channel expression and its mechanism in periodontal disease is still unknown. We describe herein an up-regulated 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 Ca9-22 were strongly increased in response to TNF-α treatment through the 55 kDa TNF-α receptor (TNFR1). In this context, small interfering RNA- (siRNA)-mediated "aqp-3 gene silencing," which could reduce AQP3 expression by more than 65%, significantly attenuated selected proinflammatory events of ICAM-1 expression induced by TNF-α in Ca9-22. A sixfold increase in leukocyte adherence to TNF-α-stimulated epithelial cells was demonstrated by an adherence assay (P < 0.001) and pretreatment with AQP3 siRNA and anti-ICAM-1 antibody reduced leukocyte retention by 85% (P < 0.001). Our study indicates for the first time a novel important mode in the regulation of the inflammatory response through TNF-α/TNFR1 ligation at the site of epithelial lesions by specialized membrane channel AQP3 and ICAM-1 protein, which is closely implicated in the development of periodontitis mechanisms. © 2008 Wiley-Liss, Inc.