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JCI online early table of contents: Dec. 1, 2010
Date:12/1/2010

, Columbia University, New York, New York, USA.
Phone: 212.305.5565; Fax: 212.851.4540; E-mail: drb25@columbia.edu.

Hamid Reza Rezvani
INSERM U876, Bordeaux, F-33000 France.
Phone: 33.557.571.373; Fax: 33.556.983.348; E-mail: hamidreza.rezvani@u-bordeaux2.fr.

View this article at: http://www.jci.org/articles/view/40087?key=28190d52dba2e3e01752


HEMATOLOGY: A tale of unwanted blood clots

Antiphospholipid syndrome is a medical condition that causes blood clots to form within the arteries and veins, causing blockages that can damage tissues and organs. The blood clots are triggered by immune molecules known as antibodies. Specifically, antibodies that recognize proteins in the blood rather than invading microbes. Exactly how these antibodies trigger blood clot formation, is, however, not clear. But now, a team of researchers, led by Chieko Mineo, at the University of Texas Southwestern Medical Center, Dallas, has identified in mice a molecular pathway by which a subset of antibodies that cause antiphospholipid syndrome trigger blood clot formation. The team suggests that targeting this pathway might provide insight into new approaches for developing treatments for individuals with antiphospholipid syndrome.

TITLE: Antiphospholipid antibodies promote leukocyteendothelial cell adhesion and thrombosis in mice by antagonizing eNOS via beta-2GPI and apoER2

AUTHOR CONTACT:
Chieko Mineo
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214.648.2015; Fax: 214.648.2098; E-mail: Chieko.mineo@utsouthwestern.edu.

View this article at: http://www.jci.org/
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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