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The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis

低密度脂蛋白受体 病变 ABCG1公司 内科学 内分泌学 受体 胆固醇 医学 脂蛋白 生物 病理 ABCA1 生物化学 运输机 基因
作者
Illiana Meurs,Bart Lammers,Ying Zhao,Ruud Out,Reeni B. Hildebrand,Menno Hoekstra,Theo J.C. Van Berkel,Miranda Van Eck
出处
期刊:Atherosclerosis [Elsevier BV]
卷期号:221 (1): 41-47 被引量:63
标识
DOI:10.1016/j.atherosclerosis.2011.11.024
摘要

ObjectiveAs ABCG1 plays a role in cholesterol efflux, macrophage ABCG1 expression has been suggested to protect against atherosclerosis. However, we and others observed varying effects of ABCG1 deficiency on atherosclerotic lesion size. The objective of this study was to define the effect of ABCG1 deficiency during atherosclerotic lesion progression in LDL receptor knockout (LDLr−/−) mice.Methods and resultsABCG1−/−/LDLr−/− and ABCG1+/+/LDLr−/− littermates were fed a Western-type diet for 10 and 12 weeks in order to study the effect of ABCG1 deficiency in the exponential phase of atherosclerotic lesion formation. At 10 weeks of diet feeding, a significant 1.5-fold increase in early atherosclerotic lesion size (130 ± 12 × 103 μm2) was observed in ABCG1−/−/LDLr−/− mice compared to ABCG1+/+/LDLr−/− mice (88 ± 11 × 103 μm2; p < 0.05). Interestingly, in more advanced lesions, induced by 12 weeks of WTD feeding, ABCG1−/−/LDLr−/− mice showed a significant 1.7-fold decrease in atherosclerotic lesion size (160 ± 20 × 103 μm2 vs 273 ± 19 × 103 μm2 in control mice; p < 0.01), indicating that in the ABCG1−/−/LDLr−/− mice progression of lesion formation is retarded as compared to ABCG1+/+/LDLr−/− mice. In addition, correlation analysis performed on 7 independent published studies and the current study confirmed that ABCG1 is atheroprotective in early lesions, while the development of advanced lesions is stimulated.ConclusionsIt appears that the effect of ABCG1 deficiency on lesion development in LDLr−/− mice depends on the stage of atherogenesis, whereby the absence of ABCG1 leads to increased lesions at sizes < 167 × 103 μm2 while in more advanced stages of atherosclerosis enhanced apoptosis and/or compensatory mechanisms lead to retarded lesion progression.

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