Autonomous Migration of Human Fetal Skin Fibroblasts into a Denuded Area in a Cell Monolayer Is Mediated by Basic Fibroblast Growth Factor and Collagen

• Published in: In vitro cellular & developmental biology. Animal 1993-12, Vol.29A (12), p.929-935
• Main Authors: Kondo, H, Matsuda, R, Yonezawa, Y
• Format: Article
• Language: English
• Subjects: Antibodies; Antioxidants - pharmacology; Cell growth; Cell Line; Cell motility; Cell Movement - drug effects; Cell Movement - physiology; Collagen - pharmacology; Collagens; Culture Media; Cultured cells; Endothelial cells; Extracellular matrix; Extracellular Matrix - physiology; Fetus; Fibroblast Growth Factor 2 - pharmacology; Fibroblast growth factors; Fibroblasts; Fibroblasts - drug effects; Fibroblasts - physiology; Fibronectins - pharmacology; Growth Substances - pharmacology; Growth, Differentiation, and Senescence; Human growth; Humans; Hydroxybenzoates - pharmacology; Male; Monensin - pharmacology; Skin - cytology; Skin - drug effects; Skin - embryology; Suramin - pharmacology
• ISSN: 1071-2690; 1543-706X
• DOI: 10.1007/BF02634231

Human fetal skin fibroblasts (TIG-3S) were found to migrate into a denuded area in a cell monolayer when cultured in both serum-depleted and serum-supplemented media, unlike adult-donor skin fibroblasts which migrated well only when cultured in serum-supplemented medium. Therefore, a series of experiments was carried out to determine whether autocrine factors are involved in their migration. The migration of TIG-3S cells in serum-depleted medium was suppressed by the addition of suramin, a factor with growth factor antagonist properties, which suggests that growth factors are important for cell migration. The suramin-induced inhibition was reversed completely by adding excess basic fibroblast growth factor (bFGF) to the culture medium and partially by platelet-derived growth factor (PDGF). Treatment with neutralizing anti-PDGF antibody did not suppress TIG-3S cell migration, whereas neutralizing anti-bFGF antibody did, which indicates that bFGF is an autocrine and PDGF a paracrine factor involved in cell migration. Next, an experiment was performed to ascertain whether the extracellular matrix is involved in TIG-3S cell migration. Monensin, an inhibitor of extracellular matrix secretion, inhibited cell migration, which was reversed by adding excess type I collagen, but not excess plasma fibronectin. In addition, further evidence for the involvement of collagen was provided by the observation that ethyl-3,4-dihydroxybenzoate, a specific inhibitor of collagen synthesis, suppressed cell migration. These results suggest that the autonomous migration of TIG-3S human fetal skin fibroblasts is mediated by bFGF and type I collagen, which they produce and secrete.