The rockefeller university

Event Details

Type

Friday Lecture Series

Speaker(s)

Edward A. Fisher, M.D., Ph.D., M.P.H., Leon Charney Professor of Cardiovascular Medicine, director, Center for the Prevention of Cardiovascular Disease and director, Marc and Ruti Bell Program in Vascular Biology, New York University School of Medicine

Speaker bio(s)

Blocking the progression of atherosclerotic lesions and inducing their regression are important clinical goals, given that the consequences of atherosclerosis, heart attacks and strokes kill more people in the United States and worldwide than any other disease. Research into the fundamental biology of atherosclerosis was hampered for decades by the lack of powerful and convenient animal models. This changed dramatically in 1992 when Jan Breslow and his colleagues at The Rockefeller University, including then-graduate student Andrew Plump and assistant professor Jonathan Smith, reported in Cell the apoE-deficient (apoE-/-) mouse, an accomplishment considered to be the start of modern atherosclerosis research.

 

Over the past 10 years, Dr. Fisher's laboratory has used the apoE-/- mouse as a platform to study the regression of atherosclerosis and have extended the major results to other models of regression they and their collaborators have introduced. The basic principle has been to reverse the hyperlipidemia of these models after atherosclerotic plaques develop, and then to apply standard and novel modes of analyses. In general, Dr. Fisher and his colleagues have found a remarkably rapid reduction in plaque macrophage content regulated by both “gas pedals” that promote macrophage emigration (in particular, the chemokine receptor CCR7) and “brakes” (such as netrin-1) that retard macrophage movement. Another common feature has a dramatic phenotypic enrichment of plaque macrophages in markers of the anti-inflammatory (M2) state, and most recently have shown a requirement for this shift for the recruitment into the regressing plaques of monocytes from the circulating pool of those that are Ly6C^high. Paradoxically, these monocytes are thought to give rise in most tissues to inflammatory (M1) macrophages, but in the context of atherosclerosis, we now show that the failure to resolve the long-standing inflammation in progressing plaques can be overcome in a regression environment by the recruitment of Ly6C^high cells that when they become macrophages assume the phenotypic characteristics not of M1, but of M2 cells.

Dr. Fisher studies the cell biology of very low density lipoproteins (the precursors of LDL), as well as the regression of atherosclerosis and the development of nanoparticles to target therapies and imaging agents directly to atherosclerotic plaques. Dr. Fisher earned his M.D. at the New York University School of Medicine and did clinical training in pediatrics at Duke University Hospital. He completed clinical fellowships at Boston Children’s Hospital and MIT, and went on to earn his Ph.D. at MIT working in Jan Breslow’s lab at Children’s Hospital on apolipoprotein E metabolism, followed by a fellowship in human and molecular genetics at NIH in Gary Felsenfeld’s lab. Dr. Fisher joined the faculty of the NYU School of Medicine in 2003.

Open to

Public

Reception

Refreshments, 3:15 p.m. - 3:45 p.m., Abby Lounge

Contact

Gloria Phipps

Phone

(212) 327-8967

Sponsor

Gloria Phipps
(212) 327-8967
phippsg@rockefeller.edu