Atherosclerosis, characterized by cholesterol-calcium-lipid deposits, is the main cause of heart attacks, which is the leading killer of Americans.
The University of Virginia scientists' research with mice found that activated platelets circulating in the blood act as participants in the process that eventually leads to atherosclerosis. These activated platelets have long been identified as markers for atherosclerosis.
The scientists injected activated platelets into mice that were engineered to have high cholesterol levels. They then studied the interaction with human endothelial cells.
The scientists found that activated platelets deposited pro-inflammatory factors, called chemokines, on monocytes and blood vessel walls, an important factor in the formation of atherosclerosis lesions.
The study also found that a protein called platelet P-selectin is vital for the interaction of the platelets in the formation of atherosclerosis lesions.
Identifying the role of these platelets is the first step. The next step is to develop drugs to limit their activation, which could prove an effective preventive measure against heart attack.
Platelets are round or oval discs routinely found in blood and they play an important role in clotting. They're activated as part of the blood-clotting response to an injury or as part of the body's inflammatory response.
The findings of the two-year study were just published in the online issue of Nature Medicine.
The American Heart Association has more information about atherosclerosis.
SOURCE: University of Virginia, news release, Dec. 16, 2002
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