Kamamoto Fábio, Paggiaro Andre Oliveira, Rodas Andrea, Herson Marisa Roma, Mathor Monica Beatriz, Ferreira Marcus Castro
Laboratório de Cirurgia Plástica, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Artif Organs. 2003 Aug;27(8):701-5. doi: 10.1046/j.1525-1594.2003.07277.x.
Preventing and treating hypertrophic and keloid scars is difficult because of the lack of knowledge about their genesis. Tissue repair can be studied with biocompatible matrices and ex vivo cultures of different cell types. We used an experimental model where collagen gels populated by human fibroblasts underwent progressive contraction, allowing the study of wound healing remodeling. The fibroblast-populated lattices showed the greater contraction of the gel populated by fibroblasts from keloids versus fibroblasts from normal skin. Moreover, fibroblast growth factor (FGF) and transforming growth factor beta (TGF-beta) involved in scar formation were added to the collagen gels populated by normal skin fibroblasts. TGF-beta caused an increase in gel contraction; FGF did not. The mean percentages of contraction of the gels populated by keloid fibroblasts were very similar to the percentages of gels populated by normal skin fibroblasts with added TGF-beta. These observations confirm the existing hypothesis that TGF-beta may be involved in keloid formation.
由于对肥厚性瘢痕和瘢痕疙瘩的发病机制缺乏了解，其预防和治疗颇具难度。可以通过生物相容性基质和不同细胞类型的体外培养来研究组织修复。我们采用了一种实验模型，即由人成纤维细胞填充的胶原凝胶会逐渐收缩，从而能够研究伤口愈合的重塑过程。与来自正常皮肤的成纤维细胞相比，瘢痕疙瘩来源的成纤维细胞填充的凝胶收缩更为明显。此外，将参与瘢痕形成的成纤维细胞生长因子（FGF）和转化生长因子β（TGF-β）添加到由正常皮肤成纤维细胞填充的胶原凝胶中。TGF-β导致凝胶收缩增加；FGF则没有此作用。瘢痕疙瘩来源的成纤维细胞填充的凝胶的平均收缩百分比与添加了TGF-β的正常皮肤成纤维细胞填充的凝胶的百分比非常相似。这些观察结果证实了现有的假说，即TGF-β可能参与瘢痕疙瘩的形成。
