Thromb Haemost 1981; 46(01): 199
DOI: 10.1055/s-0038-1652578
Vessel Wall – IV
Vessel Wall – V
Schattauer GmbH Stuttgart

Microfibrils (MF) Platelet Interaction: Requirement Of Von Willebrand Factor In Platelet Adhesion To A Placenta Microfibrillar Component (PMC)

Authors

  • F Fauvel

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • Y J Legrand

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • N Gutman

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • J P Muh

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • G Tobelem

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • H Souchon

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • A Karniguian

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
  • J P Caen

    Unité de Recherches Thrombose et Hémostase (Unité 150 INSERM) Hôpital Saint-Louis 75475 Paris Cedex 10, France
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Publikationsverlauf

Publikationsdatum:
24. Juli 2018 (online)

Preview

It has been shown that collagenase resistant arterial microfibrils (MF) are able to interact with platelets and therefore represents, besides collagen, a second thrombogenic structure in the vessel wall. In vitro observation using a PMC purified from the villosities of human placenta by a mechanical non denaturing procedure confirm this interaction between platelets and MF. PMC was homogenous under electron microscope (feltwork of MF with a mean diameter of 120 – 130 A) and was glycoproteic in nature. PMC were able to induce an aggregation of human platelets only if the platelets were in plasma. The role of Von Willebrand factor (F VIII/WF) as a cofactor of the aggregation of platelets by MF has been postulated from the fact that twice washed platelets from normal subject resuspended in PPP obtained from a severe Von Willebrand deficient patient were not aggregated by the PMC. Furthermore, aggregation was restored after resuspension of the same platelets in the PPP of the same patient 30 and 120 minutes after perfusion of cryoprecipitate (40 units F VIII/RA per kg).

F VIII/WF mediates platelet adhesion after binding to subendothelium of human artery. Our observation strongly supports the idea that MF are the subendothelial components to which F VIII/WF binds, thus promoting an adhesion of platelets.