Piscatelli S J, Michaels B M, Gregory P, Jennings R W, Longaker M T, Harrison M R, Siebert J W
Institute of Reconstructive Plastic Surgery, New York University Medical Center, NY 10010.
Ann Plast Surg. 1994 Jul;33(1):38-45. doi: 10.1097/00000637-199407000-00008.
Wound contraction is an important component of healing but, in the extreme, may lead to excessive scar formation and pathological wound contracture. Fetal rabbit wounds heal without contraction or scarring, whereas excisional fetal sheep wounds have been shown to contract, but no scarring or pathological wound contracture is noted. We used an in vitro model, the fibroblast-populated collagen lattice, to study the ability of fetal fibroblasts to coordinate contraction of a collagen matrix and the modulating effects of epidermal growth factor and transforming growth factor-beta 1 on this contraction. With increasing gestational age, fibroblasts increased the degree of collagen lattice contraction. Epidermal growth factor inhibited contraction by fetal fibroblasts, whereas transforming growth factor-beta 1 stimulated it. These findings suggest that while intrinsic differences between fetal and adult fibroblasts exist, polypeptide growth factors may operate at the site of tissue repair to alter cell phenotype. Further work is underway to delineate the role of soluble protein factors responsible for the absence of scarring and contracture seen in the fetal wound.
伤口收缩是愈合过程中的一个重要组成部分，但在极端情况下，可能会导致过度瘢痕形成和病理性伤口挛缩。胎儿兔的伤口愈合时不会收缩或形成瘢痕，而切除胎儿羊的伤口已被证明会收缩，但未观察到瘢痕形成或病理性伤口挛缩。我们使用一种体外模型，即成纤维细胞填充的胶原晶格，来研究胎儿成纤维细胞协调胶原基质收缩的能力，以及表皮生长因子和转化生长因子-β1对这种收缩的调节作用。随着胎龄增加，成纤维细胞增加了胶原晶格的收缩程度。表皮生长因子抑制胎儿成纤维细胞的收缩，而转化生长因子-β1则刺激其收缩。这些发现表明，虽然胎儿和成体成纤维细胞之间存在内在差异，但多肽生长因子可能在组织修复部位发挥作用，以改变细胞表型。目前正在进行进一步的研究，以阐明负责胎儿伤口无瘢痕和挛缩的可溶性蛋白因子的作用。
