RESUMO
Objective: To investigate the effect of endothelial dysfunction in hypertrophic scar regression on the fibroblasts biology. Methods: Scar-derived endothelial cells were isolated and cultured from proliferative scars, regressive scars and mature scars, and the endothelial cells from normal skin as control. After 6 h of culture, the endothelial cell culture medium (ECCM) was harvested. In addition, the fibroblasts from normal skin were cultured and treated with the ECCM. After 48 h, the cell viability, total collagen production, and cell apoptosis were assessed by Alamar blue, sirius red staining, and TUNEL assay, respectively. Furthermore, anti-VEGF (vascular endothelial growth factor), anti-PDGF (platelet derived growth factor), anti-TGF-β1 (transforming growth factor-β1), anti-ET-1 (endothelin 1), and anti-bFGF (basic fibroblast growth factor) neutralizing antibodies were individually added to the ECCM to identify their effects on fibroblasts biology. Results: The results revealed that the ECCM from regressive scars inhibited fibroblasts viability and collagen production, and induced apoptosis (P<0.01). Moreover, after neutralization of TGF-β1, PDGF or bFGF by antibodies, fibroblasts proliferation and collagen production were significantly inhibited (P<0.05), and combined blockade of the three factors could induce apoptosis (P<0.01). Conclusion:Vascular endothelial dysfunction in hypertrophic scars can inhibit fibroblast proliferation and collagen production, and induce cell apoptosis, especially in regressive scars. TGF-β1, PDGF and bFGF may play a major role in this process.