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Editorial Hepatic Catabolism of Remnant Lipoproteins: Where the Action Is Richard J. Havel, Robert L. Hamilton rown and Goldstein described the classical pathway of remnant lipoproteins must migrate there together with these recep- low-density lipoprotein (LDL) catabolism in human fibro- tors along the plane of the microvillar membrane. Bblasts, initiated by LDL-binding to the LDL receptor Both HL and apo E are thought to be bound to the surface of liver 11,12 (LDLR) and followed by endocytosis and lysosomal catabolism of cells by HSPGs. Although heparin releases some apo E from its components. The initial steps in the hepatic catabolism of cell surfaces in rat liver, heparin is much less effective in releasing chylomicron remnants and large very-low-density lipoprotein apo E as compared with the negatively charged polyelectrolyte, (VLDL) remnants have turned out to be more complex, involving suramin. Some cell surface apo E may be bound to LRP or initial binding to other cell surface molecules, including heparan LDLR, for which it is a high-affinity ligand. In this regard, suramin, sulfate proteoglycans (HSPGs), apo E, and hepatic lipase (HL), but not heparin, can release -macroglobulin from its high-affinity followed by transfer to endocytic receptors (LDLR and LDLR-
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: Feb 1, 2004
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