Effect of growth factors on dermal fibroblast contraction in normal skin and hypertrophic scar

We have examined the effects of four 'exogenous' growth factors, i.e. PDGF-BB (5 ng/ml), TGF-beta 1 (5 ng/ml), bFGF (10 ng/ml) and EGF (10 ng/ml) on the contraction of floating collagen type I lattices populated by human normal skin (NS) and hypertrophic scar (HS) fibroblasts (FPCL). Only TGF-beta 1 enhanced the contractility of both NS and HS fibroblasts in the collagen lattice (P < 0.01). Other growth factors (PDGF-BB, bFGF and EGF) did not affect FPCLs contraction at 72 h (P > 0.05). The onset effect of TGF-beta 1 on NS-FPCL contraction was relative early at 24 h after FPCL casting as compared to a 72 h delay on HS-FPCL contraction. Besides, PDGF-BB was found to be able to enhance HS-FPCL contraction (P < 0.05) but not on NS-FPCL contraction on day 4. On the other hand, three enzyme-linked immunosorbent assays (ELISA) were performed to demonstrate quantitatively the 'endogenous' growth factors that fibroblasts secreted into the culture medium 48 h after FPCL casting. No appreciable difference was found between 10 NS and 11 HS samples tested for PDGF-AB immunoassay (11.48 +/- 5.5 pg/ml versus 12.20 +/- 5.34 pg/ml). The same result existed in 7 NS and 13 HS samples for TGF-beta 2 immunoassay (15.15 +/- 6.2 pg/ml versus 11.84 +/- 7.46 pg/ml). In bFGF immunoassay study, relative variable data was noted in both 7 NS (18.18 +/- 13.18 pg/ml) and 12 HS samples (20.41 +/- 22.36 pg/ml). In conclusion, we suppose that TGF-beta role in wound healing may be due to the secondary exogenous influences. The endogenous ability of TGF-beta 2 secretion (quantity) in HS fibroblasts are the same as NS fibroblasts but with delayed timing responses (duality) to exogenous TGF-beta 1 effect in the collagen lattice. Further studies with timing-regulated selective specific monoclonal antibodies against the growth factor receptors may provide the therapeutic applications on HS during wound healing. Copyright (C) 1997 Elsevier Science Ireland Ltd.