Platelet adhesion to vascular cells. The role of exogenous von Willebrand factor in platelet adhesion.

نویسندگان

  • P F Nievelstein
  • P G de Groot
  • P D'Alessio
  • H F Heijnen
  • E Orlando
  • J J Sixma
چکیده

Platelet deposition on cultured fibroblasts and on their extracellular matrix (FBM) was investigated in a flow system with citrated blood and was compared with platelet deposition on cultured endothelial cells, smooth muscle cells, and their extracellular matrices. Platelet deposition was present at all surfaces except on intact endothelial cells. Deposition on FBM consisted of contact platelets, spread platelets, and a few small aggregates. On intact fibroblasts cells, the surface coverage was lower, and platelets formed aggregates. Factors involved in primary hemostasis, particularly the wall shear rate, von Willebrand factor (vWF), and fibronectin, were investigated on FBM. The reactivity of FBM was determined by the passage number of the cultured cells. The vWF was involved in platelet adhesion on FBM at only the high shear rate (greater than 800 s-1). Platelet deposition was independent of plasma fibronectin at all shear rates tested. Matrix-associated fibronectin was involved in adhesion at low and high wall shear rates. We conclude that FBM can be used as a platelet adhesive surface especially to study the contribution of exogenous vWF to platelet adhesion because FBM does not contain vWF.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Different Stages of Platelet Adhesion to the Site of Vascular Injury

Platelet activation and adhesion to the site of vascular injury is a dynamic process comprising reversible and irreversible phases. Platelet adhesion typically occurs in a multi-step process similar to the selectin/integrin-mediated adhesion of neutrophils. This phenomenon is highly regulated and influenced by the cross-talk between platelets and injured endothelium. This cross-talk involves a ...

متن کامل

Role of von Willebrand factor associated to extracellular matrices in platelet adhesion.

The respective role of plasmatic and endothelial extracellular matrix (ECM)-associated von Willebrand factor (vWF) in platelet adhesion was investigated at a high shear rate using a parallel-plate perfusion chamber. Incubation of the endothelial ECM with a monoclonal antibody (MoAb) to vWF, which specifically blocks vWF binding to platelet GP Ib (MoAb 322), inhibited 45% of platelet adhesion. C...

متن کامل

Platelet-independent adhesion of calcium-loaded erythrocytes to von Willebrand factor

Adhesion of erythrocytes to endothelial cells lining the vascular wall can cause vaso-occlusive events that impair blood flow which in turn may result in ischemia and tissue damage. Adhesion of erythrocytes to vascular endothelial cells has been described in multiple hemolytic disorders, especially in sickle cell disease, but the adhesion of normal erythrocytes to endothelial cells has hardly b...

متن کامل

Staphylococcus aureus adhesion via Spa, ClfA, and SdrCDE to immobilized platelets demonstrates shear-dependent behavior.

OBJECTIVE The objective of this study is to delineate the molecular mechanisms responsible for Staphylococcus aureus-platelet adhesion as a function of physiologically relevant wall shear stresses. METHODS AND RESULTS A parallel plate flow chamber was used to quantify adhesion of wild-type, Spa-, ClfA- and SdrCDE- strains to immobilized platelet layers. In the absence of plasma, adhesion incr...

متن کامل

Evidence that the primary binding site of von Willebrand factor that mediates platelet adhesion on subendothelium is not collagen.

We have studied the binding of von Willebrand factor to extracellular matrices of endothelial cells and to the vessel wall of human umbilical arteries in relation to its function in supporting platelet adhesion. CLB-RAg 201, an MAb against von Willebrand factor, completely inhibits the binding of von Willebrand factor to collagen type I and type III. CLB-RAg 201 does not inhibit the binding of ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Arteriosclerosis

دوره 10 3  شماره 

صفحات  -

تاریخ انتشار 1990