Effects of TGF-βs on the growth, collagen synthesis and collagen lattice contraction of human dental pulp fibroblasts in vitro

Transforming growth factor-β (TGF-β) is important in regulating the repair and regeneration of damaged dental pulp. For further elucidating the roles of different isoforms of TGF-β in the healing and inflammatory processes of human dental pulp, we found that TGF-β1, TGF-β2 and TGF-β3 inhibited the g...

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Veröffentlicht in:Archives of oral biology 2005-05, Vol.50 (5), p.469-479
Hauptverfasser: Chan, C.P., Lan, W.H., Chang, M.C., Chen, Y.J., Lan, W.C., Chang, H.H., Jeng, J.H.
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Sprache:eng
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Zusammenfassung:Transforming growth factor-β (TGF-β) is important in regulating the repair and regeneration of damaged dental pulp. For further elucidating the roles of different isoforms of TGF-β in the healing and inflammatory processes of human dental pulp, we found that TGF-β1, TGF-β2 and TGF-β3 inhibited the growth of two human dental pulp cell strains in vitro by 19–29, 18–25 and 23–26%, respectively, at a concentration of 0.5 ng/ml. TGF-β also differentially stimulated the collagen synthesis of pulp cells. Collagen synthesis increased by 1 ng/ml of TGF-β1 and TGF-β2 by 42 and 51%, respectively. TGF-β3 (0.1–1 ng/ml) lacked of stimulatory effect on collagen synthesis of pulp cells. Pulp cells have the intrinsic capacity to contract collagen lattice, leading to decreasing of lattice diameter. An 8 h exposure to TGF-β1 and TGF-β2 enhanced the pulp cell-populated collagen lattice contraction at concentrations ranging from 0.2 to 3 ng/ml. At similar concentrations, TGF-β3 lacked of this stimulatory effect. When collagen lattice were detached after 24 h of exposure, TGF-β1 and TGF-β2 (0.6–3 ng/ml) induced the pulp cells-populated collagen lattice contraction within 4–8 h of gel detachment. These results indicate that TGF-β-induced collagen lattice contraction is a late cellular event. These in vitro results indicate that effects of TGF-β isoforms on the growth, collagen synthesis and collagen lattice contraction of pulp cells may play crucial roles in the pathobiological processes of dental pulp.
ISSN:0003-9969
1879-1506
DOI:10.1016/j.archoralbio.2004.10.005