| Abstract: | Angiogenesis, new vessel growth from existing vessels, is critical to tissue development and healing. Much is known about the molecular and cellular elements of angiogenesis, such as the effects of growth factors and matrix molecules on proliferation and migration. However, it is not clear how these elements are coordinated to produce specific microvascular beds. To address this, the effects of basic fibroblast growth factor (bFGF) on β1 integrin-mediated adhesion relative to migration in human microvessel endothelial cells (HMVEC) was examined. Using two assays of migration that differ in the density of cells being examined, bFGF stimulated single cell migration and reduced cell migration from a confluent monolayer on collagen I. Adhesion to collagen I of HMVEC treated at low density (2−4 × 104 cells/cm2) with bFGF for 22 h was reduced, while bFGF increased cell adhesion of HMVEC treated at high density (6−8 × 104 cells/cm2). Adhesion of both bFGF-treated and untreated HMVEC was mediated by the β1 integrin matrix receptor. Basic FGF treatment did not significantly alter surface expression of the β1 integrin subunit. Reduction in bFGF-mediated adhesion correlated with delayed cell spreading and altered organization of β1 integrin into substrate contacts. Thus, integrin-mediated cell adhesion in microvessel endothelial cells is sensitive to regulation by a growth factor. Furthermore, the nature of the response to this signal depends on another cell regulator, cell density. In addition, modulation of cell adhesion by a growth factor may be a central regulatory feature in controlling endothelial cell migration. © 1996 Wiley-Liss, Inc. |
