Publication | Open Access
Human endothelial cells are chemotactic to endothelial cell growth factor and heparin.
279
Citations
39
References
1985
Year
ImmunologyCellular PhysiologyAngiogenesisFibroblast Growth FactorMatrix BiologyHeparinsModified Boyden ChamberVascular BiologyNeovascularizationVascular Endothelial Growth FactorCell BiologyTumor MicroenvironmentEndothelial BiologyEndothelial DysfunctionCell-matrix InteractionCell MigrationGrowth FactorsWound HealingHuman Endothelial CellsMedicineExtracellular Matrix
Human endothelial cell migration was evaluated in response to various extracellular matrix components and growth factors. Human endothelial cells exhibit enhanced chemotaxis and chemokinesis toward ECGF (10⁻⁹ M), an effect blocked by anti‑ECGF antibody, while heparin (10⁻⁸–10⁻¹⁰ M) is also chemotactic and amplifies ECGF activity, and other ECM proteins elicit weaker responses, indicating that ECGF and heparin may modulate endothelial migration relevant to tumor metastasis, wound healing, and atherogenesis.
The response of human endothelial cell migration to various extracellular matrix components and growth factors has been assessed. Human endothelial cells demonstrate increased chemotaxis and chemokinesis when placed in a modified Boyden chamber with endothelial cell growth factor (ECGF) used at a concentration of 10(-9) M. Anti-ECGF antibody inhibits the chemotactic response. Heparin (10(-8) to 10(-10) M) was also chemotactic and was shown to potentiate the chemotactic activity of ECGF. Although laminin, fibronectin, the polypeptide (epidermal, fibroblast, and nerve) growth factors, and collagen types I, II, III, IV, and V demonstrate a chemotactic response, these activities were one third to one half less than observed with ECGF. These data suggest that ECGF and heparin may play a significant role as response modifiers of human endothelial cell migration which may be relevant to tumor metastasis, wound healing, and atherogenesis.
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