SALT LAKE CITY -- It's a case of miscommunication with catastrophic consequences.
Two human blood cells that help fight blood loss, infection, and inflammation are responsible as well for starting a series of molecular events that results in overproduction of Cox-2, an enzyme involved in heart attack, stroke, atherosclerosis, and other inflammatory diseases.
The finding by researchers at the University of Utah and University of South Carolina means scientists may be able to develop drugs to prevent or lessen the severity of inflammatory diseases, such as atherosclerosis and heart attack. Discovery of the signaling mechanism will be invaluable in sorting out the roles Cox-2 plays in those diseases, according to Guy A. Zimmerman, M.D., University of Utah School of Medicine professor of internal medicine, senior author of the study detailing the research.
"This discovery has immediate clinical relevance," said Zimmerman, director of the medical school's Program in Human Molecular Biology and Genetics. "This opens the potential of developing medications for both the prevention of long-term atherosclerosis (clogged arteries) and the acute events of heart attack."
The study, reported in the Journal of Clinical Investigation online, also was led by Dan A. Dixon, a former member of Zimmerman's lab now at South Carolina.
The researchers identified a biochemical signaling pathway between human blood platelets, cells essential for blood clotting, and monocytes, white blood cells the body makes to fight inflammation and infection. But, according to Zimmerman, the biological systems involved in blood clotting and inflammation also are related to a host of human diseases.
The Utah and South Carolina researchers discovered that the blood platelet signals the monocyte two times, triggering production of Cox-2, an enzyme that helps regulate inflammation. But when blood platelets and monocytes get their signals crossed,
Contact: Phil Sahm
University of Utah Health Sciences Center