Tissue engineering of dentin-pulp complex-like structures by human dental mesenchymal cells / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To establish three-dimensional culture model of human dental mesenchymal cells and bioengineer in vivo with ceramic bovine bone (CBB) and Collagraft as scaffolds.</p><p><b>METHODS</b>Human dental mesenchymal cells induced upon stimulation of bFGF and IGF-1 or TGF-beta(1) were implanted onto CBB and Collagraft containing the same kinds of growth factors respectively. Then cell/scaffold constructs were transplanted into nude mice to establish in vivo culture model of dental mesenchymal cells. Control groups were set up at the same time. After 4 weeks or 10 weeks, the implants were taken out for histological and immunohistochemical analysis.</p><p><b>RESULTS</b>Within 10-week implant tissues, typical dentin-pulp complex-like structures were generated in scaffolds containing growth factors. Human dentin sialoprotein (DSP) was expressed in the newly formed dentin. This phenomenon wasn't observed in control groups and 4-week implants.</p><p><b>CONCLUSIONS</b>Dentin-pulp complex-like structures could be bioengineered successfully with human dental mesenchymal cells and CBB or Collagrafts containing growth factors in nude mice.</p>

The roles of Smad 2/3 in transforming growth factor-beta 1 signaling in human dental pulp cells / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To explore the roles of Smad 2/3 in transforming growth factor-beta(1) (TGF-beta(1)) signaling by human dental pulp cells.</p><p><b>METHODS</b>Laser scanning confocal microscope was used to observe translocation of Smad 2/3 from plasma into nucleus in cultured dental pulp cells at early stage of TGF-beta(1) treatment, and changes of Smad 2/3 protein expression at later stage were evaluated by Western blot analyses.</p><p><b>RESULTS</b>The expression of Smad 2/3 (fluorescence intensity) kept decreasing in cytoplasm but increasing in nucleus within 2 h after TGF-beta(1) treatment, forming a trend that Smad 2/3 translocated into nucleus from cytoplasma. The total amount of Smad 2 protein remained unchanged before and after TGF-beta(1) treatment, but the expression level of Smad 3 decreased markedly after 24 h treatment and kept dropping by 48 h.</p><p><b>CONCLUSIONS</b>The results suggest that the Smad 2/3 may be the downstream signal transducers of TGF-beta(1) in human dental pulp cells and Smad 2/3 may mediate TGF-beta(1) signaling by translocation early in TGF-beta(1) treatment, while down-regulation of Smad 3 expression by TGF-beta(1) at later stage is involved in negative modulation of TGF-beta(1) signaling.</p>