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• W2150038119 abstract "Objective— To study atherosclerosis regression in mice after plasma lipid reduction to moderately elevated apolipoprotein B (apoB)–lipoprotein levels. Approach and Results— Chow-fed hypomorphic Apoe mice deficient in low-density lipoprotein receptor expression ( Apoe h/h Ldlr –/– Mx1-cre mice) develop hyperlipidemia and atherosclerosis. These mice were studied before and after inducible cre-mediated Apoe gene repair. By 1 week, induced mice displayed a 2-fold reduction in plasma cholesterol and triglyceride levels and a decrease in the non–high-density lipoprotein:high-density lipoprotein-cholesterol ratio from 87%:13% to 60%:40%. This halted atherosclerotic lesion growth and promoted macrophage loss and accumulation of thick collagen fibers for up to 8 weeks. Concomitantly, blood Ly-6C high monocytes were decreased by 2-fold but lesional macrophage apoptosis was unchanged. The expression of several genes involved in extracellular matrix remodeling and cell migration was changed in lesional macrophages 1 week after Apoe gene repair. However, mRNA levels of numerous genes involved in cholesterol efflux and inflammation were not significantly changed at this time point. Conclusions— Restoring apoE expression in Apoe h/h Ldlr –/– Mx1-cre mice resulted in lesion stabilization in the context of a human-like ratio of non–high-density lipoprotein:high-density lipoprotein-cholesterol. Our data suggest that macrophage loss derived in part from reduced blood Ly-6C high monocytes levels and genetic reprogramming of lesional macrophages." @default.
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• W2150038119 date "2013-08-01" @default.
• W2150038119 modified "2023-10-18" @default.
• W2150038119 title "Inducible <i>Apoe</i> Gene Repair in Hypomorphic ApoE Mice Deficient in the Low-Density Lipoprotein Receptor Promotes Atheroma Stabilization with a Human-Like Lipoprotein Profile" @default.
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• W2150038119 doi "https://doi.org/10.1161/atvbaha.112.300605" @default.
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