JCI table of contents: April 22, 2008

Barry J. Goldstein
Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Phone: (215) 503-1272; Fax: (215) 923-7932; E-mail: .

MEDIA CONTACT:
Debra Kain
University of California at San Diego, San Diego, California, USA.
Phone: (619) 543-6163; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=32691

ACCOMPANYING COMMENTARY
TITLE: Linking adiponectin to proteinuria

AUTHOR CONTACT:
Rexford S. Ahima
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-1872; Fax: (215) 573-5809; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=35655

HEMATOLOGY: A novel role for the protein CD36 in disease-causing blood clot formation

A key step in the formation of a blood clot is the activation and aggregation of cells known as platelets. If a blood clot forms in an intact blood vessel it is known as a thrombus and it can have serious consequences (such as heart disease and stroke) as it restricts, and sometimes even completely blocks, the flow of blood through the vessel. New data, generated by Roy Silverstein and colleagues, at the Cleveland Clinic, has revealed a role for the protein CD36 on platelets in thrombus formation in mice, leading to the suggestion that it might provide a useful new target for the development of anti-thrombotic drugs.

Microparticles are small particles released from cells when they become activated or undergo a form of death known as apoptosis. Physiologically, this means that they are released into the circulation when a blood vessel is injured. In the study, CD36 was shown to mediate binding of human platelets to microparticles derived in vitro from the cells that would be damaged by blood vessel injury and to microparticles isolated from healthy people. Further analysis indicated that CD36 bound a chemical known as phosphatidylserine that is found on the surface of microparticles, and that platelets exposed to microparticles were subsequently easier to activate. Importantly, under certain conditions, the formation of a thrombus in mice was delayed in the absence of CD36 and the thrombi that formed contained fewer microparticles derived from endothelial cells, which are the cells that line blood vessel walls. The rationale for the author’s suggestion that CD36 might provide a useful target for the development of therapeutics to treat individuals with thrombotic disease is supported by the observation that endothelial cell–derived microparticles are found in the blood of patients with several of these diseases.

TITLE: Platelet CD36 mediates interactions with endothelial cell–derived microparticles and contributes to thrombosis in mice

AUTHOR CONTACT:
Roy L. Silverstein
Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Phone: (216) 444-5220; Fax: (216) 444-9404; Email: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=34904