Smad protein mediated transforming growth factor β1 induction of apoptosis in the MDPC-23 odontoblast-like cell line

SummaryObjective: nction of apoptosis and its regulation in odontoblasts remain unclear. In this study, we characterize the possible role of transforming growth factor (TGF)-β 1 in the induction of apoptosis and the molecular mechanisms that mediate TGF-β1-induced apoptosis in odontoblasts. s: n V/propidium iodide staining, cell Death Detection ELISA and DNA ladder were used to examine the effect of TGF-β1 on apoptosis in a mouse odontoblast-like cell line, MDPC-23. Stable cell clones expressing Smad2 or Smad3 dominant negative mutants, or wild-type Smad7 were constructed to investigate the role of Smad proteins in the mediation of apoptosis by TGF-β1 in MDPC-23 cells. The TGF-β1-induced transcriptional activity in stable cell clones expressing Smad proteins was analyzed by a transient transfected TGF-β-responsive reporter gene, p3TP-Lux. s: can induce apoptotic cell death in MDPC-23 cells in a dose-dependent manner. Transfection of dominant negative mutant forms of Smad2 or Smad3 blocked TGF-β1-induced apoptosis; moreover, the Smad3 mutant was more efficient than the Smad2 mutant. Transfection of Smad7, an inhibitory Smad, also significantly inhibited TGF-β1-induced apoptosis of these cells. Over-expression of Smad3 dominant negative mutant or Smad7 significantly inhibited TGF-β1-induced transcriptional activity. sion: results suggest that Smad proteins are involved in TGF-β1-induced apoptosis of odontoblast cells.