Smad2 overexpression enhances adhesion of gingival epithelial cells
| Autor: | Shinsuke Kochi, Tadashi Yamamoto, Hiroshi Maeda, Masayuki Shimoe, Hidetaka Ideguchi, Keisuke Yamashiro, Kazuya Tomikawa, Shoichi Hongo, Shogo Takashiba, Yuki Ugawa |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Integrins Keratin 14 Integrin Gingiva Mice Transgenic Dioxoles Smad2 Protein Real-Time Polymerase Chain Reaction Transfection Transforming Growth Factor beta1 Mice 03 medical and health sciences Cell Adhesion Animals Humans Cell adhesion General Dentistry biology Cell adhesion molecule Chemistry Soluble cell adhesion molecules Cell Biology General Medicine Adhesion Molar Cell biology 030104 developmental biology Otorhinolaryngology Benzamides biology.protein Neural cell adhesion molecule Signal Transduction |
| Zdroj: | Archives of Oral Biology. 71:46-53 |
| ISSN: | 0003-9969 |
| Popis: | Objective Gingival epithelial cells play an important role in preventing the initiation of periodontitis, by their hemidesmosomal adhesion to the tooth root surface. Adhesion requires integrin-extracellular matrix (ECM) interactions that are intricately regulated by transforming growth factor-β (TGF-β) signaling. However, the mechanisms underlying the interplay between adhesion molecules and TGF-β, especially the respective roles of Smad2 and Smad3, remain elusive. In this study, we examined the effects of Smad overexpression on gingival epithelial cell adhesion and expression profiles of integrin and ECM-related genes. Methods Human gingival epithelial cells immortalized by the SV40 T-antigen were transfected with Smad2- and Smad3-overexpression vectors. A cell adhesion assay involving fluorescence detection of attached cells was performed using the ArrayScan imaging system. Real-time PCR was performed to examine the kinetics of integrin and ECM gene expression. In vitro and in vivo localization of adhesion molecules was examined by immunofluorescence analysis. Results By using SB431542, a specific inhibitor of the TGF-β type I receptor, Smad2/3 signaling was confirmed to be dominant in TGF-β1-induced cell adhesion. The Smad2-transfectant demonstrated higher potency for cell adhesion and integrin expression (α2, α5, β4, and β6) than the Smad3-transfectant, whereas little or no change in ECM expression was observed in either transfectant. Moreover, the gingival epithelium of transgenic mice that overexpressed Smad2 driven by the keratin 14 promoter showed increased integrin α2 expression. Conclusion These findings indicate the crucial role of Smad2 in increased adhesion of gingival epithelial cells via upregulation of integrin α2. |
| Databáze: | OpenAIRE |
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