2000 年 23 巻 12 号 p. 1517-1520
Wound contraction plays on important role in healing, but in extreme conditions, it may lead to excessive scar formation and pathological wound contracture. To date, the key regulator of excessive contracture is known to be transforming growth factor-beta (TGF-β1). In this study, we have evaluated epidermal growth factor (EGF) antagonism in fibroblast-populated collagen lattice (FPCL)gel contraction, which has been generally used as an in vitro model thought to mimic wound contraction in vivo. As expected, TGF-β1 treatment enhanced normal fibroblast-induced collagen gel concentration in a dose-dependent manner. In contrast, EGF did not affect normal gel formation, but significantly antagonized TGF-β1-induced gel formation (p<0.05 at 100 ng/ml), whereas the other growth factor, platelet-derived growth factor (PDGF), did not altered either normal or TGF-β1-induced gel contractions. Similarly, EGF treatment, but not PDGF, also significantly suppressed TGF-β1 release that was autologously elicited by TGF-β1 treatment (p<0.01 at 100 ng/ml). Therefore, the results suggest that EGF may negatively regulate the role of TGF-β1 through attenuating antologous release of TGF-β1.
