Overexpression of Smad2 inhibits proliferation of gingival epithelial cells

Abstract

The signaling activation triggered by overexpression of Smad2 was dependent on TGF-β type I receptor, and the activated Smad2 increased p15 and p21 expression, responsible for inhibiting cell cycle entry, resulting in antiproliferative effects on gingival epithelial cells. Understanding of Smad2-induced signaling would be useful for possible clinical application to regulate gingival epithelial downgrowth.

Osteogenic differentiation regulated by Rho-kinase in periodontal ligament cells

“…The amplification conditions consisted of an initial 10 min of denaturation at 95 1C, followed by 40 cycles of denaturation at 95 1C for 10 s, annealing at 60 1C for 15 s, and elongation at 72 1C for 20 s. Relative expression is shown after normalization relative to the expression of GAPDH mRNA. The data were quantified using the ΔCt method (Shimoe et al, 2014). The data are presented as means from three different donors, and were analyzed for statistical significance by Student's t test.…”

“…After 14 days in culture, aliquots of 30 μg of total protein from each sample were subjected to Western blotting as described previously (Shimoe et al, 2014) using antibodies specific to F-actin (Abcam, Cambridge, MA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a loading control (Cell Signaling) at a dilution of 1:500 and 1:3000. The signal intensities were quantified by densitometric analysis using ImageJ (http://rsb.info.nih.gov/ij/).…”

Modulation of microenvironment for controlling the fate of periodontal ligament cells: the role of Rho/ROCK signaling and cytoskeletal dynamics

“…TGF-β/Smad2 signaling inhibits the proliferation and migration of gingival epithelium. It also contributes to maintain tissue integrity by increasing epithelial adhesion and mesenchymal collagen content during wound healing (Tomikawa et al 2012;Shimoe et al 2014;Alotaibi et al 2014;Hongo et al 2016). However, long-term effects of Smad2 induce excess apoptosis of gingiva and alveolar bone loss (Fujita et al 2012;Alotaibi et al 2016).…”

Excessive retinoic acid inhibit mouse embryonic palate mesenchymal cell growth through involvement of Smad signaling

“…Smad2 and Smad3 were structurally very closely related and both were involved in signaling from TGF-β, Smad3 could form a complex together with Smad2 in order to regulate the target genes of TGF-βs. Over-expression of Smad2 inhibited the proliferation of junctional epithelium cells by down-regulating c-Myc and up-regulating p15 and p27 which leading to cellcycle arrest (Alotaibi et al 2014), and inhibited oral epithelial cell proliferation by increasing p15 and p21 (Shimoe et al 2014). However, Smad2 was not required for TGF-β-stimulated growth inhibition in hepatocytes (Ju et al 2006).…”