Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques
- Jaime Llodrá*,
- Véronique Angeli*,
- Jianhua Liu†,
- Eugene Trogan‡,
- Edward A. Fisher‡, and
- Gwendalyn J. Randolph*,§
- Departments of *Gene and Cell Medicine and †Surgery, Mount Sinai School of Medicine, New York, NY 10029; and ‡Departments of Medicine (Cardiology) and Cell Biology, The Marc and Ruti Bell Vascular Biology and Disease Program, and New York University Lipid Treatment and Research Center, New York University School of Medicine, New York, NY 10016
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Edited by Ralph M. Steinman, The Rockefeller University, New York, NY, and approved June 23, 2004 (received for review May 10, 2004)
Abstract
Some monocytes normally take up residence in tissues as sessile macrophages, but others differentiate into migratory cells resembling dendritic cells that emigrate to lymph nodes. In an in vitro model of a vessel wall, lipid mediators lysophosphatidic acid and platelet-activating factor, whose signals are implicated in promoting atherosclerosis, blocked conversion of monocytes into migratory cells and favored their retention in the subendothelium. In vivo studies revealed trafficking of monocyte-derived cells from atherosclerotic plaques during lesion regression, but little emigration was detected from progressive plaques. Thus, progression of atherosclerotic plaques may result not only from robust monocyte recruitment into arterial walls but also from reduced emigration of these cells from lesions.
Footnotes
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↵ § To whom correspondence should be addressed. E-mail: gwendalyn.randolph{at}mssm.edu.
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This paper was submitted directly (Track II) to the PNAS office.
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Abbreviations: DC, dendritic cell; PAF, platelet-activating factor; LPA, lysophosphatidic acid; apoE, apolipoprotein E.
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See Commentary on page 11529.
- Copyright © 2004, The National Academy of Sciences
