Abstract
Apoprotein E (apoE) is a multifunctional protein. Its best-characterized function is as a ligand for low-density lipoprotein (LDL) receptor family members to mediate the clearance of apoB-containing atherogenic lipoproteins. Among its other functions, apoE is involved in cholesterol efflux, especially from cholesterol-loaded macrophage foam cells and other atherosclerosis-relevant cells, and in reverse cholesterol transport. Reverse cholesterol transport is a mechanism by which excess cellular cholesterol is transported via lipoproteins in the plasma to the liver where it can be excreted from the body in the feces. This process is thought to have a role in the attenuation of atherosclerosis. This review summarizes studies on the role of apoE in cellular cholesterol efflux and reverse cholesterol transport and discusses the identification of apoE mimetic peptides that may promote these pathways.
Highlights
Apoprotein E is a multifunctional protein [1]
It serves as a ligand for several cell surface receptors, those involved in the clearance of apoB-containing chylomicron and very low density lipoprotein (VLDL) remnants (IDL) from the plasma and reduces plasma lipid levels
Among its other functions is its involvement in cholesterol efflux, especially from the macrophage foam cells that accumulate in the atherosclerotic vessel walls, and reverse cholesterol transport
Summary
Though not in all cell types, e.g., apoE is not expressed in enterocytes It serves as a ligand for several cell surface receptors, those involved in the clearance of apoB-containing chylomicron and very low density lipoprotein (VLDL) remnants (IDL) from the plasma and reduces plasma lipid levels. The loss of apoE-mediated atherogenic lipoprotein clearance and reverse cholesterol transport functions contribute to hyperlipidemia-induced atherosclerosis in this murine model [4]. Synthesis of apoE by macrophages mediates efflux of cholesterol from the cell, as is discussed below, but apoE may serve as a ligand for remnant clearance This is indicated by experiments in which apoE-expressing bone marrow is transplanted into Apoe−/− recipients [5,6]. The remainder of this review is devoted to the efflux of cholesterol from cholesterol-loaded cells mediated by exogenous and cell-autonomous apoE and to apoE’s role in reverse cholesterol transport
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