Dietary fish oil reduces intercellular adhesion molecule 1 and scavenger receptor expression on murine macrophages

Citation
Ea. Miles et al., Dietary fish oil reduces intercellular adhesion molecule 1 and scavenger receptor expression on murine macrophages, ATHEROSCLER, 152(1), 2000, pp. 43-50
Citations number
39
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
ATHEROSCLEROSIS
ISSN journal
00219150 → ACNP
Volume
152
Issue
1
Year of publication
2000
Pages
43 - 50
Database
ISI
SICI code
0021-9150(200009)152:1<43:DFORIA>2.0.ZU;2-0
Abstract
During atherogenesis, a pathological accumulation of lipids occurs within a ortic intimal macrophages through uptake of oxidised low-density lipoprotei n (LDL) via scavenger receptors. Here we investigate whether some of the an ti-atherosclerotic effects ascribed to dietary fish oil are mediated throug h effects on macrophage intercellular adhesion molecule 1 (ICAM-1) and scav enger receptor expression. Mice were fed on a low fat diet (containing 25 g /kg corn oil) or on high fat diets containing 200 g/kg coconut oil, safflow er oil or fish oil. Thioglycollate-elicited peritoneal macrophages were ana lysed for fatty acid composition by gas chromatography. Macrophage scavenge r receptor A (MSR-A) type I + type II and ICAM-1 expression were measured b y how cytometry and the levels of mRNA coding for MSR-A type I, MSR-A type II and ICAM-I were measured by reverse-transcription polymerase chain react ion. Feeding mice diets enriched with different fats resulted in significan t changes in the fatty acid profile of macrophages, which reflected the fat ty acid compositions of the diets. Macrophages from the fish oil fed mice h ad the lowest expression of ICAM-I and MSR-A at the level of both mRNA and cell surface expression. The reduced expression of ICAM-I and MSR-A on macr ophages from mice fed on a fish oil-rich diet supports our hypothesis that part of the protective effect of fish oil against atherosclerosis might be due to an altered macrophage phenotype and function ameliorating macrophage -induced plaque formation. (C) 2000 Elsevier Science Ireland Ltd. All right s reserved.