title: Aggregation of human blood platelets by remnant like lipoprotein particles of plasma chylomicrons and very low density lipoproteins.
abstract: Remnant like lipoprotein particles (RLP) of partially catabolised human plasma chylomicrons (CM) and very low density lipoproteins (VLDL) were separated from CM and VLDL using two monoclonal antibodies, anti apo B-100 (JI-H) and anti apo A-I (H-12) coupled to Sepharose 4B gel to form an immunoaffinity column. Lipoproteins containing apo B-100 or apo E, including VLDL and LDL adsorb to (JI-H)-gel, while CM and HDL with apo A-I adsorb to (H-12)-gel. The unbound fraction (RLP) is rich in apo B-48, apo E and apo E rich apo B-100 which has not been recognized by JI-H. The RLP fraction with a total triglyceride of 12.35 +/- 6.22 mg/ml; total cholesterol, 0.32 +/- 0.08 mg/ml and total protein, 0.72 +/- 0.12 mg/ml (mean +/- S.E.M, n = 9) was added to blood from healthy persons at 2.5-200 microliters/ml and agitated gently at 37 degrees C for 40 s. Platelet aggregation was assessed by measuring the loss of single platelets. At 2.5-10 microliters, RLP induced platelet aggregation increased with the dose of RLP, but decreased at 25-200 microliters. Scanning electron microscopy revealed that within 20 s of agitation in the presence of RLP, activated platelets had appeared on the red cell membrane and within 40 s of agitation, platelet aggregates had formed on the red cells. The platelet responses were unaffected by aspirin (10 or 20 micrograms/ml) but were inhibited by cilostazol, a phosphodiesterase type III inhibitor (0.4 to 1.6 micrograms/ml). It is likely that the platelet effect of RLP is a consequence of RLP dependent red cell-platelet interaction. This is the first report of platelet aggregation induced by RLP without an added platelet agonist.
authors.affiliation: Japan Immunoresearch Laboratories, Takasaki, Japan.
authors.forename: A R
authors.initials: AR
authors.lastname: Saniabadi
authors.forename: K
authors.initials: K
authors.lastname: Umemura
authors.forename: M
authors.initials: M
authors.lastname: Shimoyama
authors.forename: M
authors.initials: M
authors.lastname: Adachi
authors.forename: M
authors.initials: M
authors.lastname: Nakano
authors.forename: M
authors.initials: M
authors.lastname: Nakashima
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D000911:Antibodies, Monoclonal; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D002846:Chromatography, Affinity; D002914:Chylomicrons / Q000097:blood / Q000737:chemistry / Q000494:pharmacology*; D000077407:Cilostazol; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D006400:Hematocrit; D006801:Humans; D066298:In Vitro Techniques; D008074:Lipoproteins / Q000494:pharmacology*; D008079:Lipoproteins, VLDL / Q000097:blood / Q000737:chemistry / Q000494:pharmacology*; D008297:Male; D008855:Microscopy, Electron, Scanning; D008875:Middle Aged; D010446:Peptide Fragments / Q000302:isolation & purification / Q000494:pharmacology*; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects* / Q000502:physiology; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D000911:Antibodies, Monoclonal; D002914:Chylomicrons; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D010446:Peptide Fragments; D010726:Phosphodiesterase Inhibitors; D013777:Tetrazoles; D000244:Adenosine Diphosphate; D000077407:Cilostazol; D001241:Aspirin