2007 Fiscal Year Final Research Report Summary
Analysis of the mechanisms that claudins expressed in periodontal diseased epithelium regulate the permeability of gingival epithelium
| Project/Area Number |
18592264
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NAKAD Hideaki The University of Tokushima, Institute of Health Biosciences, Graduate School, Associated professor (30227730)
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| Co-Investigator(Kenkyū-buntansha) |
SUGE Toshiyuki The University of Tokushima, Medical and Dental Hospital, School, Lecturer (60243713)
YUMOTO Hiromichi The University of Tokushima, Institute of Health Biosciences, Graduate School, Assistant Professor (60284303)
TAKAHASHI Kanako The University of Tokushima, Institute of Health Biosciences, Graduate School, Assistant Professor (80403715)
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| Project Period (FY) |
2006 – 2007
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| Keywords | fight iunction / adherence junction / claudin / cadherin / JAM-A / epithelial cell / periodontal disease / MMP |
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| Research Abstract |
To aim of this study was to determine the roles of claudins, cadherin, and JAM-A, which composed tight junction and adherence junction to regulate the permeability of gingival epithelium in periodontally diseased tissues. RT-PCR analysis showed that claudins, E-cadherin, JAM-A were expressed in human gingival tisseus. Of particular significance, the expression level of claudin-10 was increased in inflamed gingival tissues compared with normal gingival tissues. In situ hybridization and immunohistochemical analysis showed that claudin-10 expression was strongly detected in the basal layer of the epithelium in inflamed gingival tissues. Moreover, claudin-10 was detected not only on cell surfaces but also in cytosol. This result showed that claudin-10 might have other roles. In the monolayer culture of gingival epithelial cells, TNF-a and IL-13 decreased the mRNA expression levels of E-cadherin, occluding, and JAM-A in a dose-dependent manner and increased those of claudin-2. In addition, TNF-α and IL-13 decreased Transepithelial Electrical Resisitance (TER) and increased the transepithelial cell permeability of gingival epithelial cells. These findings suggested that claudin-2 was the key component that regulated the permeability of diseased gingival tissues. Recently, it reported that overexpression of CLDN-10 in hepatocytes was up-regulated matrix metalloproteinase 2 (MMP2) and membrane type 1-MMP (MT1-MMP), claudin-2. Then, we concluded that expression of claudin-10 in diseased periodontal tissues caused increase of expression of claudin-2 which increased the permeability of epithelium and MMP destroyed the gingival tissues.
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