FIBROBLAST MIGRATION AND PROLIFERATION DURING IN-VITRO WOUND-HEALING - A QUANTITATIVE COMPARISON BETWEEN VARIOUS GROWTH-FACTORS AND A LOW-MOLECULAR-WEIGHT BLOOD DIALYSATE USED IN THE CLINIC TO NORMALIZE IMPAIRED WOUND-HEALING

被引:107
作者
SCHREIER, T
DEGEN, E
BASCHONG, W
机构
[1] UNIV BASEL, BIOCTR, MAURICE E MULLER INST, KLINGELBERGSTR 70, CH-4056 BASEL, SWITZERLAND
[2] SOLCO BASLE, DEPT BIOCHEM, CH-4127 BIRSFELDEN, SWITZERLAND
关键词
FIBROBLASTS; GROWTH FACTORS; DRUGS; WOUND HEALING IN-VITRO; CELL MIGRATION;
D O I
10.1007/BF02576227
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
During the formation of granulation tissue in a dermal wound, platelets, monocytes and other cellular blood constituents release various peptide growth factors to stimulate fibroblasts to migrate into the wound site and proliferate, in order to reconstitute the various connective tissue components. The effect on fibroblast migration and proliferation of these growth factors, and of Solcoseryl (HD), a deproteinized fraction of calf blood used to normalize wound granulation and scar tissue formation, was quantified in vitro. The presence of basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-beta) and hemodialyzate (HD) increased the number of cells in the denuded area, i.e., in the ''wound space'' of an artificially ruptured monolayer of LM-fibroblasts (mouse lung fibroblasts). When cell proliferation was blocked with Mitomycin C, in the first 24 h all factors, i.e., bFGF, PDGF, TGF-beta and HD, promoted cell migration, whereas after 48 h it became obvious that each factor stimulated both migration and proliferation, each in a characteristic way. The effects were significant and more distinct after 48 h, following the order: PDGF (46%) approximately bFGF (87%) > HD (45%) approximately TGF-beta (40%) > control (62%). The relative contributions of migration after inhibiting proliferation are given in brackets. The modulatory activity of HD was localized in its hydrophilic fraction. It was destroyed by acid hydrolysis. Furthermore, this activity could be blocked by protamine sulfate, an inhibitor blocking peptide growth factor receptor binding.
引用
收藏
页码:195 / 205
页数:11
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