© 2000 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE-/-/ICAM-1-/-) Fed a Fat or a Chow Diet
From INSERM U331/Faculté de Médecine RTH Laënnec, Lyon, France (M.-C.B., C.C., E.C., G.B., J.L.M.); and the Department of Experimental Pathology, UMDS, Guy’s Hospital, London, UK (R.N.P.).
Correspondence to Marie-Claude Bourdillon, MD, INSERM, Unit 331/Site Cardiologique, 22 Avenue Doyen Lépine, Case Postale 18, F-69675 BRON Cedex France. E-mail bourdillon{at}lyon151.inserm.fr
Abstract—Intercellular adhesion molecule (ICAM)-1, a major adhesion molecule, plays a critical role in the homing of leukocytes to sites of atherosclerotic lesions. However, very little is known on the role of ICAM-1 in initiating and perpetuating vascular lesions in ApoE-/- mice fed a chow or a fat diet. This study has investigated the mean aortic lesions in mice (C57BL6 background) with a single-knockout (ApoE-/-) or double-knockout (DKO; ApoE-/-, ICAM-1-/-) fed a chow or a fat diet over a period of 3, 6, 15, and 20 weeks. A 3-fold reduction in lesion size was observed at all time points in DKO mice fed a chow diet. However, in DKO mice fed a fat diet, a marked reduction in the aortic lesion was observed at 3 and 15 weeks, which did not reach a significant level at 6 and 20 weeks. This study shows in essence that DKO mice are protected from developing significant lesions for up to 6 weeks when fed a chow diet and from 3 to 6 weeks when fed a fat diet. After 6 weeks, the lesion size of the DKO mice follows that of the single-knockout mice when fed a chow diet and gets to the same level in mice fed a fat diet. Plasma cholesterol levels were not altered as a result of ICAM-1 deficiency. These studies show that ICAM-1 is implicated in the formation and progression of atherosclerotic lesions.
Key Words: atherosclerosis • ICAM-1 • apolipoprotein E–deficient mice • aortic lesions
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