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Thromb Haemost 2002; 88(05): 843-850
DOI: 10.1055/s-0037-1613312
Review Article
Schattauer GmbH

F11-Receptor (F11R/JAM) Mediates Platelet Adhesion to Endothelial Cells: Role in Inflammatory Thrombosis[*]

Anna Babinska
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Mamdouh H. Kedees   **
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Humra Athar   **
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Tahir Ahmed
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Olcay Batuman
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Yigal H. Ehrlich
1   Program in Neuroscience, Department of Biology, CSI/City University of New York, Staten Island, NY, USA
,
M. Mahmood Hussain
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
,
Elizabeth Kornecki
2   Department of Anatomy/Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA
› Institutsangaben
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Publikationsverlauf

Received 08. April 2002

Accepted after revision 15. Juli 2002

Publikationsdatum:
08. Dezember 2017 (online)

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Summary

The F11 receptor (F11R) is a cell adhesion molecule (CAM), member of the immunoglobulin superfamily found on the surface of human platelets, and determined to play a role in platelet aggregation, secretion, adhesion and spreading. The same molecule is present also at tight junctions of endothelial cells (EC) where it is known as JAM and acts as a CAM through homophilic interactions. The role of F11R/JAM in the interaction of platelets with endothelial cells was investigated in the current studies. We report here that washed human platelets adhere specifically to a matrix made of immobilized, recombinant sF11R. Furthermore, platelets adhere to cytokine(TNF-α, INF-γ) stimulated human umbilical vein endothelial cells (HUVEC), and approximately 40-60% of the adhesive force is exerted by homophilic interactions between the F11R of platelets and EC. This is evidenced by the inhibition of platelet adhesion to endothelial cells by recombinant soluble form of the F11R, and by two F11R peptides with amino acid sequences of the N-terminal region, and in the 1st Ig fold of the F11R, respectively. This study suggests a role for F11R in the adhesion of platelets to cytokine-inflamed endothelial cells and thus in thrombosis and atherosclerosis induced in non-denuded blood vessels by inflammatory processes. Agents that block the F11R-mediated adhesion of platelets to EC may be of therapeutic value in controlling thrombosis and preventing heart attacks and stroke.

Keywords

Human platelet F11 receptor (F11R) - junctional adhesion molecule (JAM) - platelet aggregation - adhesion - F11R peptides - HUVEC

* Part of this work was presented as symposium at the XVIIIth ISTH, July, Paris, France, 2001), and in abstract form (Abstract number: PSY942) in the Supplement to the journal Thrombosis and Haemostasis (see ref. 32)


** M. H. Kedees and H. Athar contributed equally to this work.


 

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