Effect of metabolic inhibitors on platelet attachment, spreading and aggregation on collagen-coated surfaces.
The interaction of human gel-filtered platelets (GFP) with surfaces coated with fibrillar calf skin collagen (CSC) or monomeric human type I, III, IV, and V collagen (CI, CIII, CIV, CV) includes both energy dependent and independent stages. Incubation of platelets with a collagen-coated surface at 4 degrees C versus 37 degrees C reduces only shape change and the spreading response of adhering platelets, but does not affect the initial attachment. Additionally, the energy dependence was evident from the reduction of platelet spreading and platelet aggregate formation in the presence of 2-Deoxy-D-glucose (2DG). Antimycin A (AMA), Oligomycin (OM), or 2,4-Dinitrophenol (DNP) did not abolish the adhesion-induced platelet activation, indicating that the energy is supplied by glycolysis rather than by oxydative phosphorylation. In contrast, neither inhibition of glycolysis, nor inhibition of the respiratory chain did affect the initial attachment of nonactivated platelets to the collagen-coated surface. The present data suggest (i) that during the interaction of platelets with collagenous substrates there exists an initial energy independent attachment stage, and (ii) that the following stages of adhesion-induced platelet activation require metabolic energy supported mainly by anaerobic glycolysis.[1]References
- Effect of metabolic inhibitors on platelet attachment, spreading and aggregation on collagen-coated surfaces. Misselwitz, F., Leytin, V.L., Repin, V.S. Thromb. Res. (1987) [Pubmed]
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