title: Triglyceride-rich lipoproteins isolated by selected-affinity anti-apolipoprotein B immunosorption from human atherosclerotic plaque.
abstract: We isolated and characterized immunoreactive apolipoprotein B (apoB)-containing lipoproteins from human atherosclerotic plaque and plasma to determine whether very-low-density lipoprotein (VLDL) can enter and become incorporated into the atherosclerotic lesion and how plaque apoB-containing lipoproteins differ from apoB-containing lipoproteins isolated from plasma. Atherosclerotic plaques were obtained during aortic surgery and processed immediately. Lipoproteins were extracted from minced plaque in a buffered saline solution (extract A). In selected cases a second extraction was done after plaque was incubated with collagenase (extract B). Lipoproteins were then isolated from the extracts by anti-apoB immunosorption and separated into VLDL + intermediate-density lipoprotein (IDL) (d < 1.019 g/mL) and low-density lipoprotein (LDL) (1.019 < d < 1.070 g/mL) fractions by ultracentrifugation. The VLDL + IDL fractions from plaque contained more than one third of the total apoB-associated lipoprotein cholesterol in both extracts A and B. The lipid composition of VLDL + IDL in both extracts was related to that of plasma VLDL + IDL. By electron microscopy mean particle diameters of VLDL + IDL from extracts A and B were 9% and 23%, respectively, greater than VLDL + IDL diameters from plasma. Mean diameters of LDL from extracts A and B were 11% and 31% greater than LDL diameters from plasma. The apoE-apoB ratio of extract A VLDL + IDL was nearly twice that of plasma VLDL + IDL and severalfold higher than that of extract A LDL. Immunoblots of both VLDL + IDL and LDL from extract A demonstrated minimal fragmentation of apoB.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cardiovascular Research Institute, University of California, San Francisco.
authors.forename: J H
authors.initials: JH
authors.lastname: Rapp
authors.forename: A
authors.initials: A
authors.lastname: Lespine
authors.forename: R L
authors.initials: RL
authors.lastname: Hamilton
authors.forename: N
authors.initials: N
authors.lastname: Colyvas
authors.forename: A H
authors.initials: AH
authors.lastname: Chaumeton
authors.forename: J
authors.initials: J
authors.lastname: Tweedie-Hardman
authors.forename: L
authors.initials: L
authors.lastname: Kotite
authors.forename: S T
authors.initials: ST
authors.lastname: Kunitake
authors.forename: R J
authors.initials: RJ
authors.lastname: Havel
authors.forename: J P
authors.initials: JP
authors.lastname: Kane
mesh_terms: D000368:Aged; D000906:Antibodies / Q000276:immunology; D001055:Apolipoproteins B / Q000097:blood / Q000276:immunology / Q000378:metabolism; D001057:Apolipoproteins E / Q000097:blood / Q000378:metabolism; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007122:Immunoelectrophoresis; D007163:Immunosorbent Techniques; D008074:Lipoproteins / Q000097:blood / Q000302:isolation & purification / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010316:Particle Size; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D000906:Antibodies; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D008074:Lipoproteins; D014280:Triglycerides