Contribution of distinct adhesive interactions to platelet aggregation in flowing blood

Blood. 1999 Jul 1;94(1):172-8.

Abstract

Aggregation of blood platelets contributes to the arrest of bleeding at sites of vascular injury, but it can occlude atherosclerotic arteries and precipitate diseases such as myocardial infarction. The bonds that link platelets under flow conditions were identified using confocal videomicroscopy in real time. Glycoprotein (GP) Ibalpha and von Willebrand factor (vWF) acted in synergy with alphaIIbbeta3 and fibrinogen to sustain platelet accrual at the apex of thrombi where three-dimensional growth resulted in increasing shear rates. The specific function of distinct adhesion pathways in response to changing hemodynamic conditions helps to explain hemostatic and thrombotic processes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blood Platelets / cytology*
  • Blood Platelets / physiology*
  • Fibrinogen / physiology
  • Fibrinogen / ultrastructure
  • Humans
  • Microscopy, Confocal
  • Platelet Adhesiveness / physiology*
  • Platelet Glycoprotein GPIIb-IIIa Complex / physiology
  • Platelet Glycoprotein GPIIb-IIIa Complex / ultrastructure
  • Platelet Glycoprotein GPIb-IX Complex / physiology
  • Platelet Glycoprotein GPIb-IX Complex / ultrastructure
  • von Willebrand Factor / physiology
  • von Willebrand Factor / ultrastructure

Substances

  • Platelet Glycoprotein GPIIb-IIIa Complex
  • Platelet Glycoprotein GPIb-IX Complex
  • von Willebrand Factor
  • Fibrinogen