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TGF-? Signaling Regulates Cementum Formation through Osterix Expression #MMPMID27180803
Choi H; Ahn YH; Kim TH; Bae CH; Lee JC; You HK; Cho ES
Sci Rep 2016[]; 6 (ä): ä PMID27180803show ga
TGF-?/BMPs have widely recognized roles in mammalian development, including in bone and tooth formation. To define the functional relevance of the autonomous requirement for TGF-? signaling in mouse tooth development, we analyzed osteocalcin-Cre mediated Tgfbr2 (OCCreTgfbr2fl/fl) conditional knockout mice, which lacks functional TGF-? receptor II (T?RII) in differentiating cementoblasts and cementocytes. Strikingly, OCCreTgfbr2fl/fl mutant mice exhibited a sharp reduction in cellular cementum mass with reduced matrix secretion and mineral apposition rates. To explore the molecular mechanisms underlying the roles of TGF-? signaling through T?RII in cementogenesis, we established a mouse cementoblast model with decreased T?RII expression using OCCM-30 cells. Interestingly, the expression of osterix (Osx), one of the major regulators of cellular cementum formation, was largely decreased in OCCM-30 cells lacking T?RII. Consequently, in those cells, functional ALP activity and the expression of genes associated with cementogenesis were reduced and the cells were partially rescued by Osx transduction. We also found that TGF-? signaling directly regulates Osx expression through a Smad-dependent pathway. These findings strongly suggest that TGF-? signaling plays a major role as one of the upstream regulators of Osx in cementoblast differentiation and cementum formation.