A new study by NYU Langone Medical Center researchers identified a new culprit that leads to atherosclerosis, the accumulation of fat and cholesterol that hardens into plaque and narrows arteries. The research, published online by Nature Immunology on January 8, 2012, explains why cholesterol-laden, coronary artery disease-causing cells called macrophages, accumulate in artery plaques.
"We have discovered that macrophages that accumulate in plaques secrete a molecule called netrin-1," said Kathryn J. Moore, PhD, senior author of the study and associate professor in the Departments of Medicine and Cell Biology at NYU Langone Medical Center. "Our study shows that netrin-1 blocks the normal migration of macrophages out of arteries, causing these immune cells to accumulate and promote the progression of atherosclerosis."
Artery plaques that break off causing vessel blockages, or potentially fatal heart attacks and strokes are known to have high macrophage cell content. Atherosclerosis is fueled by the presence of these cholesterol-laden macrophages in the artery wall. Typically, the immune system sends macrophages to clean up cholesterol deposits in arteries, but once they fill up with the unhealthy form of cholesterol they get stuck in the arteries, triggering the body's inflammatory response. The bloated macrophages then become major components of plaque lining artery walls. Until now, the mechanism by which macrophages become trapped has remained unknown.
In this new study, researchers show why macrophages remain in artery plaques leading to atherosclerosis. Netrin-1 promotes atherosclerosis by retaining macrophages in the artery wall. In fact, netrin-1 signals macrophages to stop migrating and as a result these cells accumulate within the plaque. In addition, study experiments show, genetically deleting netrin-1 can minimize atherosclerosis, reduce the level of macrophages in plaque and promote the migration of macrophages
|Contact: Lauren Woods|
NYU Langone Medical Center / New York University School of Medicine