Rittenberg T, Burd D A, Ehrlich H P
Shriner Burns Institute, Massachusetts General Hospital, Harvard Medical School, Boston.
Exp Mol Pathol. 1990 Feb;52(1):132-40. doi: 10.1016/0014-4800(90)90065-l.
Closure of full-thickness open wounds in loose-skinned animals is accomplished by wound contraction. Fibroblast-populated collagen lattice (FPCL) contraction is an in vitro model for studying wound contraction. Fibroblasts suspended in a collagen matrix reorient the surrounding collagen fibers, resulting in a reduction in the size of the FPCL. The organization of collagen fibers by fibroblast-generated forces produces lattice contraction. An open wound in a rat begins to show contraction by 3 days, and its size will be reduced by 50% at 7 days. Fluid from 3- and 7-day-old rat wounds was examined for its ability to affect in vitro lattice contraction. Wound fluid was found to inhibit lattice contraction. The fractions which inhibit lattice contraction had molecular weights ranging between 10,000 and 20,000, as revealed by molecular sieve chromatography, and a high positive charge, as demonstrated by ion exchange chromatography. The factor(s) was only slightly affected by added indomethacin in the FPCL contraction model. This suggests a mechanism independent of the generation of prostaglandins. The factor(s) was tested in an ATP-induced model of fibroblast contraction where it was shown to be ineffective at altering cell contraction. The factor(s) did, however, prevent cell spreading and elongation on glass surfaces. Wound fluid has a factor(s) which hinders fibroblast spreading and elongation and which inhibits FPCL contraction.
在皮肤松弛的动物中，全层开放性伤口通过伤口收缩实现愈合。成纤维细胞填充的胶原晶格（FPCL）收缩是研究伤口收缩的体外模型。悬浮在胶原基质中的成纤维细胞使周围的胶原纤维重新定向，导致FPCL尺寸减小。成纤维细胞产生的力对胶原纤维的组织作用导致晶格收缩。大鼠的开放性伤口在3天时开始出现收缩，7天时其大小会减小50%。检测了3日龄和7日龄大鼠伤口的液体影响体外晶格收缩的能力。发现伤口液体可抑制晶格收缩。通过分子筛色谱显示，抑制晶格收缩的组分分子量在10,000至20,000之间，通过离子交换色谱证明其带高正电荷。在FPCL收缩模型中，添加吲哚美辛对该因子的影响很小。这表明存在一种独立于前列腺素生成的机制。在ATP诱导的成纤维细胞收缩模型中对该因子进行了测试，结果表明它在改变细胞收缩方面无效。然而，该因子确实可防止细胞在玻璃表面铺展和伸长。伤口液体含有一种因子，它会阻碍成纤维细胞铺展和伸长，并抑制FPCL收缩。
