ROLE OF GROWTH-FACTORS IN SCAR CONTRACTION - AN IN-VITRO ANALYSIS

Excessive scar contracture by wound fibroblasts can have devastating c onsequences, ranging from body disfigurement to joint immobility. The ability of fibroblasts isolated from lesions of hypertrophic scars, ke loids, normal skin, or normal scars in contracting the provisional wou nd matrix (i.e., fibrin clot) was compared and analyzed. Hypertrophic scar fibroblasts showed a consistently higher basal level of fibrin ma trix gel (FMG) contraction than other fibroblasts. This heightened bas al level of contractility may be attributed partially to the autocrine effect of transforming growth factor-beta(1) (TGF-beta(1)). Normal an d keloid fibroblasts exhibited similar basal rates of FMG contraction, and both responded to platelet-derived growth factor (PDGF) and TGF-b eta by increasing FMG contraction two- to threefold, However, 45% of t he TGF-beta-induced increase in FMG contraction by keloid fibroblasts, but not normal fibroblasts, was mediated by the autocrine production of PDGF. Therefore, fibroblasts isolated from different scars exhibit varied degrees of FMG contraction. In addition, the mechanism underlyi ng growth factor-mediated contraction differed vastly among fibroblast s of different scar origin. The significance of these differences in g rowth factor-mediated FMG contraction is discussed.