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  • Title: Smad2 is involved in the apoptosis of murine gingival junctional epithelium associated with inhibition of Bcl-2.
    Author: Fujita T, Alotaibi M, Kitase Y, Kota Y, Ouhara K, Kurihara H, Shuler CF.
    Journal: Arch Oral Biol; 2012 Nov; 57(11):1567-73. PubMed ID: 22964108.
    Abstract:
    OBJECTIVE: Gingival junctional epithelium (JE) actively contributes to the homeostasis of the periodontium. Altered activation of TGF-β signalling is implicated in the epithelium from chronic periodontitis. However, little is known about the effects of TGF-β signalling on the JE. In this study, we investigated the relationship between Smad2, which plays an important role in mediating TGF-β signal, and induction of apoptosis in the JE. METHODS: K14-Smad2 transgenic mice were used to observe the effect of over-expression of Smad2 driven by CK14 promoter in the JE. We performed TUNEL technique to evaluate the epithelial apoptosis. Expression of apoptosis related genes was examined using real-time PCR and immunofluorescence. RESULTS: K14-Smad2 mice showed an increased number of phospho-Smad2 positive JE cells associated with an increase in TGF-β1 expression. K14-Smad2 mice have a significantly higher percentage of TUNEL positive cells in the JE. Immunofluorescence double labelling revealed that TUNEL positive cells showed immunoreactivity to phospho-Smad2. Real-time PCR analysis of apoptosis related gene expression provided evidence of lower expression of Bcl-2 in the gingival tissue from K14-Smad2 mice. There was a strong positive reaction for Bcl-2 protein in the junctional epithelium of wild type mice, while the gingival tissue of K14-Smad2 transgenic mice had only a faint signal for Bcl-2. CONCLUSIONS: The present study provided evidence that Smad2 plays a crucial role in the induction of apoptosis in gingival JE through inhibition of Bcl-2.
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