Abstract
BackgroundPerilipin1, a lipid droplet associated protein has an important role in the regulation of lipolysis and lipid storage in adipocytes. Perilipin1 is also expressed in foam cells of atheroma plaques and could therefore play a role in the accumulation of lipids in arterial wall and in the development of atherosclerosis. The aim of the study was to investigate this possible role of perilipin1 in atherogenesis.MethodsMice deficient in perilipin1 (Plin1-/-) were crossed with Ldlr-/- mice. Ldlr-/- and Plin1-/- Ldlr-/- mice received an atherogenic diet during 10 or 20 weeks. Blood pressure and plasma lipids concentrations were measured. Aortas were collected at the end of the atherogenic diet periods for quantification of atheroma lesions (en face method), histological and immunohistological studiesResultsLdlr-/- and Plin1-/- Ldlr-/- mice had comparable blood pressure and plasma lipids levels. Plin1-/- Ldlr-/- mice had a lower body weight and decreased adiposity. The atherosclerotic lesion area in Plin1-/-Ldlr-/- mice was moderately increased after 10 weeks of atherogenic diet (ns) and significantly higher after 20 weeks (p < 0.01). Histology of atheroma plaques was comparable with no sign of increased inflammation in Plin1-/- Ldlr-/- mice.ConclusionPerilipin1 ablation in mice results in increased atherosclerosis independently of modifications of risk factors such as raised blood pressure or plasma lipids levels. These data strongly support an atheroprotective role for perilipin1.
Highlights
A hallmark of atherosclerosis is the accumulation of free (FC) and esterified (EC) cholesterol in macrophages and smooth muscular cells transforming them in foam cells [1]
Such accumulation depends on the balance between the uptake of cholesterol-rich lipoprotein through scavenger receptors [2] and the efflux of free cholesterol controled by the transporters ABCA1 and ABCG1 [3] and to a lesser extent by SR-B1 [4,5]
Perilipin1 A is expressed in macrophages [18,19,20,21] and vascular smooth muscular cells [18], in arterial wall [18] and is overexpressed in atheroma plaques [18,22], unstable plaques [22]
Summary
A hallmark of atherosclerosis is the accumulation of free (FC) and esterified (EC) cholesterol in macrophages and smooth muscular cells transforming them in foam cells [1] Such accumulation depends on the balance between the uptake of cholesterol-rich lipoprotein through scavenger receptors [2] and the efflux of free cholesterol controled by the transporters ABCA1 and ABCG1 [3] and to a lesser extent by SR-B1 (or CLA-1) [4,5]. Perilipin is expressed in foam cells of atheroma plaques and could play a role in the accumulation of lipids in arterial wall and in the development of atherosclerosis. The aim of the study was to investigate this possible role of perilipin in atherogenesis
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