Increased level of oxidized LDL-dependent monocytederived microparticles in acute coronary syndrome
Noriko Matsumoto
1
Second Department of Internal Medicine, Kansai Medical University, Osaka Japan
,
Shosaku Nomura
2
First Department of Internal Medicine, Kansai Medical University, Osaka Japan
,
Hiroshi Kamihata
1
Second Department of Internal Medicine, Kansai Medical University, Osaka Japan
,
Yutaka Kimura
1
Second Department of Internal Medicine, Kansai Medical University, Osaka Japan
,
Toshiji Iwasaka
1
Second Department of Internal Medicine, Kansai Medical University, Osaka Japan
› Author AffiliationsFinancial support: This study was supported in part by a grant from the Japan Foundation of Neuropsychiatry and Hematology Research, a Research Grant for Advanced Medical Care from the Ministry of Health and Welfare of Japan, and a Grant (13670760 to S.N.) from the Ministry of Education, Science and Culture of Japan.
We measured and compared the levels of plasma soluble (s) Pselectin, sCD40L, platelet-derived microparticles (PDMP), monocyte-derived microparticles (MDMP), and anti-oxidized LDL antibody, to obtain a better understanding of their potential contribution to vascular complications in acute coronary syndrome (ACS). The concentrations of sP-selectin, sCD40L, PDMP, and MDMP in ACS patients were significantly higher than those in normal controls and patients with stable angina.When levels of these markers were compared with differences in concentration of anti-oxidized LDL antibody, all markers were significantly higher in ACS patients with a high level of antioxidized LDL antibody. Next, a monocytic cell line (THP-1) was incubated with high shear stress-induced platelet aggregates and PDMP. After incubation,THP-1 cells generated tissue factorexpressing MDMPs. This finding was particularly significant in the presence of oxidized LDL. These findings suggest that elevated levels of MDMPs may be a sign of atherosclerotic development in ACS patients, particularly those who exhibit anti-oxidized LDL antibodies.
1
Fuster V,
Badimon L,
Badimon JJ.
et al. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992; 326: 242-50.
3
Mallat Z,
Benamer H,
Hugel B.
et al. Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes. Circulation 2000; 101: 841-3.
4
Philippou H,
Adami A,
Amersey RA.
et al. A novel specific immunoassay for plasma twochain factor VIIa: investigation of FVIIa levels in normal individuals and in patients with acute coronary syndromes. Blood 1997; 89: 767-75.
7
Neumann FJ,
Ott I,
Marx N.
et al. Effect of human recombinant interleukin-6 and interleukin-8 on monocyte procoagulant activity. Arterioscler Thromb Vasc Biol 1997; 17: 3399-405.
9
Furman MI,
Barnard MR,
Krueger LA.
et al. Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction. J Am Coll Cardiol 2001; 38: 1002-6.
10
Satta N,
Toti F,
Feugeas O.
et al. Monocyte vesiculation is a possible mechanism for dissemination of membrane-associated procoagulant activities and adhesion molecules after stimulation by lipopolysaccharide. J Immunol 1994; 153: 3245-55.
13
Diamant M,
Nieuwland R,
Pablo RF.
et al. Elevated numbers of tissue-factor exposing microparticles correlate with components of the metabolic syndrome in uncomplicated type 2 diabetes mellitus. Circulation 2002; 106: 2442-7.
14
Chobanian AV.
Single risk factor intervention may be inadequate to inhibit atherosclerosis progression when hypertension and hypercholesterolemia co-exist. Hypertension 1991; 18: 130-1.
15
Croft KD,
Beilin LJ,
Vandongen R.
et al. Leukocyte and platelet function and eicosanoid production in subjects with hypercholesterolaemia. Atherosclerosis 1990; 83: 101-9.
16
Fogelman AM,
Shechter I,
Seager J.
et al. Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in macrophages. Proc Natl Acad Sci USA 1980; 77: 2214-8.
17
Puurunen M,
Manttari M,
Manninen V.
et al. Antibody against oxidized low-density lipoprotein predicting myocardial infarction. Arch Intern Med 1994; 154: 2605-9.
18
Erkkila AT,
Narvanen O,
Lehto S.
et al. Autoantibodies against oxidized low-density lipoprotein and cardiolipin in patients with coronary heart disease. Arterioscler Thromb Vasc Biol 2000; 20: 204-9.
19
Nomura S,
Suzuki M,
Katsura K.
et al. Platelet-derived microparticles may influence the development of atherosclerosis in diabetes mellitus. Atherosclerosis 1995; 116: 235-40.
20
Miyazaki Y,
Nomura S,
Miyake T.
et al. High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles. Blood 1996; 88: 3456-64.
21
Nomura S,
Nakamura T,
Cone J.
et al. Cytometric analysis of high shear-induced platelet microparticles and effect of cytokines on microparticle generation. Cytometry 2000; 40: 173-81.
22
Miyake T,
Nomura S,
Komiyama Y.
et al. Effect of a new monoclonal anti-glycoprotein IX antibody, KMP-9, on high shear-induced platelet aggregation. Thromb Haemost 1997; 78: 902-9.
23
Omoto S,
Nomura S,
Shouzu A.
et al. Detection of monocyte-derived microparticles in patients with type 2 diabetes mellitus. Diabetologia 2002; 45: 550-5.
24
Dachary-Prigent J,
Freyssinet JM,
Pasquet JM.
et al. Annexin V as a probe of aminophospholipid exposure and platelet membrane vesiculation: a flow cytometry study showing a role for free sulfhydryl groups. Blood 1993; 81: 2554-65.
26
Lane P,
Brocker T,
Hubele S.
et al. Soluble CD40 ligand can replace the normal T cell derived CD40 ligand signal to B cells in T cell-dependent activation. J Exp Med 1993; 177: 1209-13.
27
Ikeda Y,
Handa M,
Kawano K.
et al. The role of von Willebrand factor and fibrinogen in platelet aggregation under varying shear stress. J Clin Invest 1991; 87: 1234-40.
28
Bradford MM.
A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein dye binding. Anal Biochem 1976; 72: 248-54.
29
Heller JI,
Crowley JR,
Hazen SL.
et al. Phydroxyphenylacetaldehyde, an aldehyde generated by myeloperoxidase, modifies phospholipid amino groups of low density lipoprotein in human atherosclerotic intima. J Biol Chem 2000; 275: 9957-62.
31
Sims PJ,
Faioni EM,
Wiedmer T.
et al. Complement proteins C5b-9 cause release of membrane vesicles from the platelet surface that are enriched in the membrane receptor for coagulation factor Va and expres prothrombinase activity. J Biol Chem 1988; 263: 1820512.
33
Nomura S,
Shouzu A,
Omoto S.
et al. Effect of cilostazol on soluble adhesion molecules and platelet-derived microparticles in patients with diabetes. Thromb Haemost 1998; 80: 388-92.
34
Nomura S,
Tandon NN,
Nakamura T.
et al. High-shear-stress-induced activation of platelets and microparticles enhances expression of cell adhesion molecules in THP-1 and endothelial cells. Atherosclerosis 2001; 158: 277-87.
36
Neumann FJ,
Marx N,
Gawaz M.
et al. Induction of cytokine expression in leukocytes by binding of thrombin stimulated platelets. Circulation 1997; 95: 2387-94.
38
Laszik Z,
Jansen PJ,
Cummings RD.
et al. Pselectin glycoprotein ligand-1 is broadly expressed in cells of myeloid, lymphoid, and dendritic lineage and in some nonhematopoietic cells. Blood 1996; 88: 3010-21.
42
Wada H,
Kaneko T,
Wakita Y.
et al. Effect of lipoproteins on tissue factor activity and PAI-II antigen in human monocytes and macrophages. Int J Cardiol 1994; 47: S21-5.
43
Combes V,
Simon AC,
Grau GE.
et al. In vitro generation of endothelial microparticles and possible prothrombotic activity in patients with lupus anticoagulant. J Clin Invest 1999; 104: 93-102.