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U.Va. researchers uncover role of platelets in hardening of the arteries


Scientists at the University of Virginia School of Medicine have discovered a new contributor to atherosclerosis, the most common form of hardening of the arteries. Marked by cholesterol-calcium-lipid deposits, atherosclerosis is the main cause of heart attacks, the number one killer in the U.S. Doctors at U.Va. say research on mice has determined for the first time that activated platelets circulating in the blood, long understood as markers for atherosclerosis, really serve as participants in the process that eventually leads to atherosclerosis. The findings of the two-year study are published in the Dec. 16 online issue of the journal Nature Medicine, found at

"These platelets are time bombs in the blood," said Dr. Klaus Ley, director of the Cardiovascular Research Center and professor of biomedical engineering, molecular physiology and biological physics at U.Va. "The hope now is that we can develop anti-platelet drugs to limit activation, which would be a beneficial, effective preventive measure against heart attack. These important observations could translate into improved therapies for limiting this extremely prevalent disease."

There is a commonly used test for activated platelets, called flow cytometry. Ley believes some patients may want to be tested for the presence of such platelets, in addition to being tested for a compound called C-reactive protein (CRP), which increases when inflammation is present. The American Heart Association is studying whether a CRP test should be part of a routine check-up. "What was surprising is how long these activated platelets stay in the blood," Ley said.

Platelets, round or oval disks, are routinely found in blood and play an important role in clotting. Platelets are activated as part of the blood clotting response to injury or as part of the inflammatory response. They become sticky and are prone to bind with monocytes, a type of white blood cell. It’s believed aspirin plays a role in preventing heart attacks by acting on platelets.

In the study, U.Va. researchers injected activated platelets into mice engineered to have high cholesterol levels (1000 vs. 200 for humans) and studied the interaction with human aortic endothelial cells. They found that activated platelets were able to deposit pro-inflammatory factors, or chemokines, on monocytes and vessel walls, a key element in the formation of atherosclerotic lesions, or altered tissue. The researchers also found that a protein called platelet P-selectin is indispensable for the interaction of the platelets in the formation of atherosclerotic lesions. Researchers at University Hospital in Aachen, Germany and at the Howard Hughes Medical Institute in New York contributed to the study.

*Note: Dr. Ley can be reached for comment at: 434-243-9966 (office) or 434-974-9265 (home) or by email:

Bob Beard | EurekAlert!
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