A new study by NYU Langone Medical Center researchers identified anew culprit that leads to atherosclerosis, the accumulation of fatand cholesterol that hardens into plaque and narrows arteries. The research,published online by Nature Immunology on January 8, 2012, explains why cholesterol-laden, coronaryartery disease-causing cells called macrophages, accumulate inartery plaques. "We have discovered that macrophages that accumulate in plaquessecrete a molecule called netrin-1," said Kathryn J. Moore, PhD,senior author of the study and associate professor in theDepartments of Medicine and Cell Biology at NYU Langone MedicalCenter. "Our study shows that netrin-1 blocks the normal migrationof macrophages out of arteries, causing these immune cells toaccumulate and promote the progression of atherosclerosis." Artery plaques that break off causing vessel blockages, orpotentially fatal heart attacks and strokes are known to have high macrophage cell content. Atherosclerosis isfueled by the presence of these cholesterol-laden macrophages inthe artery wall. Typically, the immune system sends macrophages toclean up cholesterol deposits in arteries, but once they fill upwith the unhealthy form of cholesterol they get stuck in thearteries, triggering the body's inflammatory response. The bloatedmacrophages then become major components of plaque lining arterywalls. Until now, the mechanism by which macrophages become trappedhas remained unknown. In this new study, researchers show why macrophages remain inartery plaques leading to atherosclerosis. Netrin-1 promotesatherosclerosis by retaining macrophages in the artery wall. Infact, netrin-1 signals macrophages to stop migrating and as aresult these cells accumulate within the plaque. In addition, studyexperiments show, genetically deleting netrin-1 can minimizeatherosclerosis, reduce the level of macrophages in plaque andpromote the migration of macrophages from plaques. In the study researchers used a florescent tracking technique tolabel and monitor the movement of macrophage cells in and out ofplaques. This experiment showed how macrophages were immobilizedand retained in plaque by netrin-1 expression and also demonstratedmacrophage emigration from plaque after the deletion of netrin-1. "Our study identifies netrin-1 as a novel target for futuretherapeutic intervention for the treatment of atherosclerosis andcardiovascular disease," said Janine M. van Gils, PhD, lead authorof the study and a post-doctoral researcher in the Marc and RutiBell Vascular Biology and Disease Program, Leon H. Charney Divisionof Cardiology, Department of Medicine at NYU Langone MedicalCenter. "This discovery provides new clues to help reduce theamount of plaque in arteries and the threat of atherosclerosis, amajor cause of mortality in Western countries. The development of anew strategy to diminish macrophage accumulation in plaque offersgreat promise to reducing the occurrence of fatal cardiac events." Additional References Citations. The e-commerce company in China offers quality products such as Automobile GPS Tracking Device Manufacturer , GPS Monitoring Solutions, and more. For more , please visit Motorcycle GPS Tracker today!
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