A world leader in studying diseases of blood vessels, the Center of Vascular Biology at Weill Cornell Medical College (WCMC) in New York City has received $13 million from the National Heart, Lung and Blood Institute (NHLBI) to continue studying atherosclerosis and thrombosis, which are major risk factors for coronary artery disease, heart attack and stroke.

The grant renews five projects that have already added to our understanding of the biology of artery wall cells, the blood cells that interact with them and the principal cellular and genetic changes in arteries that predispose them to forming plaque and blood clots.

The projects will continue to test the hypothesis that mediators -- such substances as nitrogen oxides, reactive oxygen species and growth factors -- regulate blood-vessel cell activity and plaque formation, and that atherosclerosis acts like a blood clot, forming a "response to injury."

"Perhaps the greatest strength of Weill Cornell's Vascular Biology Program, which began 17 years ago, is its record of high-quality, collaborative scientific interactions and outstanding scientists," said David P. Hajjar, executive vice provost and senior executive vice dean of WCMC, and dean and Frank H.T. Rhodes Distinguished Professor of Cardiovascular Biology and Genetics at Weill Cornell Graduate School of Medical Sciences.

The five NHLBI grant projects were awarded to:

• Aaron J. Marcus (medicine) to study the critical role of a key compound (CD39 NTPDase1) as the prime regulator of blood fluidity and thrombosis;
• Katherine A. Hajjar (cell biology) to study the stress response in vascular cells of Annexin 2, a receptor that mediates the breakdown of a blood clot, as it relates to atherosclerosis;
• Barbara L. Hempstead (medicine) to examine the role of brain-derived neurotrophic factor in promoting blood-vessel formation in heart attack patients;
• Steven S. Gross (pharmacology) to study mitochondria (cells' power plants) in the function and dysfunction of endothelial nitric oxide synthase, an enzyme that relaxes the smooth muscle in blood vessels; and
• David Hajjar (biochemistry and pathology) to study the activation of the enzyme cyclooxygenase in atherosclerosis by nitrogen oxide and the impact this activation has on plaque formation.

By 2011, the Cornell researchers hope to have identified the array of molecular links that define atherogenesis and thrombosis, Hajjar said.