ABSTRACT
Heparin affects both dermal fibroblast proliferation and collagen and may mediate these effects by altering the levels of basic fibroblast growth factor (bFGF) and transforming growth factor-beta1 (TGF-beta1) production as a wound healing modulator. The purpose of this study is to probe the effect of heparin on bFGF and TGF-beta1 production by human normal skin and hyperplastic scar fibroblasts. This research investigates the effect of heparin on bFGF and TGF-beta1 production by human normal skin and hyperplastic scar fibroblasts with exposure to 0, 100, 300, or 600 microg/ml heparin for 24, 48, 72, or 96 hours in a serum-free in vitro model. Levels of bFGF and TGF-beta1 in the supernatants were determined by enzyme-linked immunosorbant assay. All doses of heparin significantly stimulated production of bFGF by normal skin (393% to 1019% increase) and hyperplastic scar fibroblasts (405% to 899% increase) at all time points (P < .05). Heparin (300 and 600 microg/ml) also stimulated TGF-beta1 production by normal skin (26% to 83%) and hyperplastic scar fibroblasts (63% to 85%) with statistical significance (P < .05) at various time points. These effects of heparin on normal skin and hyperplastic scar fibroblasts may have implications for hyperplastic scar formation and wound healing in vivo.
Subject(s)
Cicatrix/drug therapy , Fibroblast Growth Factors/drug effects , Fibroblasts/drug effects , Heparin/pharmacology , Hyperplasia/prevention & control , Skin/drug effects , Transforming Growth Factor beta1/drug effects , Wound Healing/physiology , Adult , Cicatrix/prevention & control , Collagen/drug effects , Heparin/therapeutic use , Humans , In Vitro TechniquesABSTRACT
OBJECTIVE: To investigate the pathogenesy deference between multiple and single site keloid by detecting gene mutation of Poly A site of transforming growth factor-beta1 receptor type II (TbetaR II). METHODS: Collecting 20 keloid samples (6 multiple sites keloid samples and 14 single site keloid samples) and extracting DNA from them; designing and synthesizing the primers of Poly A site, then amplifying T1beta II DNA by PCR, analyzing the single strand conformation polymorphism about the products of PCR. After purifying the product of PCR, the site and type of the mutation rate of Poly A site was sequenced directly on the automatic sequencing equipment. RESULTS: It had been found that the Poly A site of TbetaR II in keloid has deletion mutation, its mutation rate in multiple sites keloid was 50% (3/6), in single site keloid 7.1% (1/14). The mutation rate of Poly A site in multiple sites keloid was significant higher than that in single site keloid (P < 0.05) CONCLUSION: It has been supposed that there are some deference in pathogenesy between the multiple and the single site keloid.
