Q--What did one blood platelet say to the other?
A--Want to stick around awhile?
In fact, a "matchmaker" protein may help pair sticky fibrinogen with hook-like receptors on blood platelets, thereby setting the stage for clots, which can trigger heart attacks, strokes and arterial inflammation, a University of Delaware scientist explains.
Studies of the matchmaker protein--dubbed CIB for its calcium and integrin binding function--may someday suggest new strategies for preventing sudden deaths caused by heart attacks, says Ulhas P. Naik, an assistant professor of biological sciences at UD. The research remains fundamental for now, he cautions, but it should prove useful to drug companies in the future.
"If we can learn exactly what lures these cells together, it might be possible to develop better remedies for blocking platelet aggregation, or clustering," Naik says. "The dating rituals of these cells also may shed light on how cells migrate from place to place, and how white blood cells--the body's police officers--reach the site of an infection."
In 1996, Naik's identification of the CIB protein earned him the American Heart Association's Young Investigator Prize in Thrombosis, awarded every two years to a single researcher whose work is judged best in the world.
Since then, his investigations have focused on yet another player in the courtship of clot-related cells. His latest discovery, nicknamed PAM-1 (for platelet adhesive molecule), seems to prowl the corridors of the bloodstream, arranging dates for various cell pairs.
CIB, on the other hand, is an inside operator, similar to known "regulatory" proteins, which works within platelets to attract the protein fibers that form a framework for blood clots.
When a blood vessel is injured, biochemical catalysts (agonists) such as
thrombin send signals into platelets, changing the shape of a receptor or
"integrin" protruding from the cell's surface. A sticky, fibrous protein in the
Contact: Ginger Pinholster
University of Delaware