Login Register Cart 0
Review Article

改良低密度脂蛋白免疫复合物与心血管疾病

卷 26, 期 9, 2019

页: [1680 - 1692] 页: 13

弟呕挨: 10.2174/0929867325666180524114429

价格: $65

摘要

经修饰的低密度脂蛋白，无论是在有机体中自发形成还是在实验室制备，都具有免疫原性。因此，体内形成的抗原-抗体复合物（免疫复合物，IC）可以在外周血中测量，它们的水平是心血管疾病（CVD）的强预测因子。 已经有可能产生识别不同LDL修饰的抗体，从而分析循环IC结构。临床研究表明，IC的抗原构成对CVD的发展具有调节作用。IC与铜氧化低密度脂蛋白（oxldl）抗体反应强烈的患者显示动脉粥样硬化的进展，表现为内膜-中膜厚度增加和冠状动脉钙化评分增加。相比之下，IC与体外制备的严重氧化丙二醛低密度脂蛋白（mda-ldl）抗体发生强烈反应的患者有很高的急性血管事件风险，主要是心肌梗死。体外研究表明，虽然Oxldl-IC同时诱导细胞增殖和轻度到中度巨噬细胞凋亡，但MDA-LDL-IC却诱导更显著的巨噬细胞凋亡，而不是细胞增殖。此外，丙二醛-低密度脂蛋白IC比氧低密度脂蛋白IC诱导更高水平的基质金属蛋白酶和肿瘤坏死因子的释放。高水平的肿瘤坏死因子可能是导致细胞凋亡的主要因素，高水平的金属蛋白酶可能在粥样斑块纤维帽变薄中起作用。细胞凋亡和纤维帽变薄的结合是易损斑块的一个众所周知的特征，易损斑块更容易破裂并导致大多数急性心血管事件。

关键词: 改良的低密度脂蛋白，低密度脂蛋白免疫复合物，丙二醛低密度脂蛋白，凋亡，血管炎症，不稳定斑块，氧低密度脂蛋白

« Previous Next »
[1]
Miller, Y.I.; Choi, S.H.; Fang, L.; Tsimikas, S. Lipoprotein modification and macrophage uptake: role of pathologic cholesterol transport in atherogenesis. Subcell. Biochem., 2010, 51, 229-251.
[2]
Giacco, F.; Brownlee, M. Oxidative stress and diabetic complications. Circ. Res., 2010, 107(9), 1058-1070.
[3]
Holvoet, P. Endothelial dysfunction, oxidation of low-density lipoprotein, and cardiovascular disease. Ther. Apher., 1999, 3(4), 287-293.
[4]
Parthasarathy, S.; Printz, D.J.; Boyd, D.; Joy, L.; Steinberg, D. Macrophage oxidation of low density lipoprotein generates a modified form recognized by the scavenger receptor. Arteriosclerosis, 1986, 6(5), 505-510.
[5]
Silverstein, R.L.; Li, W.; Park, Y.M.; Rahaman, S.O. Mechanisms of cell signaling by the scavenger receptor CD36: implications in atherosclerosis and thrombosis. Trans. Am. Clin. Climatol. Assoc., 2010, 121, 206-220.
[6]
Hoff, H.F.; O’Neil, J.; Chisolm, G.M., III; Cole, T.B.; Quehenberger, O.; Esterbauer, H.; Jürgens, G. Modification of low density lipoprotein with 4-hydroxynonenal induces uptake by macrophages. Arteriosclerosis, 1989, 9(4), 538-549.
[7]
Fogelman, A.M.; Shechter, I.; Seager, J.; Hokom, M.; Child, J.S.; Edwards, P.A. Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages. Proc. Natl. Acad. Sci. USA, 1980, 77(4), 2214-2218.
[8]
Hessler, J.R.; Morel, D.W.; Lewis, L.J.; Chisolm, G.M. Lipoprotein oxidation and lipoprotein-induced cytotoxicity. Arteriosclerosis, 1983, 3(3), 215-222.
[9]
Henriksen, T.; Evensen, S.A.; Carlander, B. Injury to human endothelial cells in culture induced by LDL. Scand. J. Clin. Lab. Invest., 1979, 39, 361-364.
[10]
Rajavashisth, T.B.; Andalibi, A.; Territo, M.C. Induction of endothelial cell expression of granulocyte and macrophage colony-stimulating factors by modified LDL. Nature, 1990, 344, 254-257.
[11]
Kugiyama, K.; Sakamoto, T.; Musumi, I.; Sugiyama, S.; Ohgushi, M.; Ogawa, H.; Horiguchi, M.; Yasue, H. Transferrable lipids in oxidized LDL stimulate PAI-1 and inhibt TPA release from endothelial cells. Circ. Res., 1993, 73, 335-343.
[12]
Lundberg, A.M.; Hansson, G.K. Innate immune signals in atherosclerosis. Clin. Immunol., 2010, 134(1), 5-24.
[13]
Andersson, J.; Libby, P.; Hansson, G.K. Adaptive immunity and atherosclerosis. Clin. Immunol., 2010, 134(1), 33-46.
[14]
de Boer, O.J.; van der Wal, A.C.; Verhagen, C.E.; Becker, A.E. Cytokine secretion profiles of cloned T cells from human aortic atherosclerotic plaques. J. Pathol., 1999, 188(2), 174-179.
[15]
Li, W.; Febbraio, M.; Reddy, S.P.; Yu, D.Y.; Yamamoto, M.; Silverstein, R.L. CD36 participates in a signaling pathway that regulates ROS formation in murine VSMCs. J. Clin. Invest., 2010, 120(11), 3996-4006.
[16]
Quinn, M.T.; Parthasarathy, S.; Fong, L.G.; Steinberg, D. Oxidatively modified low density lipoproteins: a potential role in recruitment and retention of monocyte/macrophages during atherogenesis. Proc. Natl. Acad. Sci. USA, 1987, 84(9), 2995-2998.
[17]
Kahn, B.V.; Parthasarathy, S.S.; Alexander, R.W.; Medford, R.M. Modified LDL and its constituents augment cytokine-activated vascular cell adhesion molecule -1 gene expression in human vascular endothelial cells. J. Clin. Invest., 1995, 95, 1262-1270.
[18]
Takei, A.; Huang, Y.; Lopes-Virella, M.F. Expression of adhesion molecules by human endothelial cells exposed to oxidized low density lipoprotein. Influences of degree of oxidation and location of oxidized LDL. Atherosclerosis, 2001, 154(1), 79-86.
[19]
Frostegård, J.; Nilsson, J.; Haegerstrand, A.; Hamsten, A.; Wigzell, H.; Gidlund, M. Oxidized low density lipoprotein induces differentiation and adhesion of human monocytes and the monocytic cell line U937. Proc. Natl. Acad. Sci. USA, 1990, 87(3), 904-908.
[20]
Vlassara, H.; Cai, W.; Crandall, J.; Goldberg, T.; Oberstein, R.; Dardaine, V.; Peppa, M.; Rayfield, E.J. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Proc. Natl. Acad. Sci. USA, 2002, 99(24), 15596-15601.
[21]
Wendt, T.; Bucciarelli, L.; Qu, W.; Lu, Y.; Yan, S.F.; Stern, D.M.; Schmidt, A.M. Receptor for advanced glycation endproducts (RAGE) and vascular inflammation: insights into the pathogenesis of macrovascular complications in diabetes. Curr. Atheroscler. Rep., 2002, 4(3), 228-237.
[22]
Vlassara, H.; Bucala, R.; Striker, L. Pathogenic effects of advanced glycosylation: biochemical, biologic, and clinical implications for diabetes and aging. Lab. Invest., 1994, 70(2), 138-151.
[23]
Schmidt, A.M.; Hori, O.; Chen, J.X.; Li, J.F.; Crandall, J.; Zhang, J.; Cao, R.; Yan, S.D.; Brett, J.; Stern, D. Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes. J. Clin. Invest., 1995, 96(3), 1395-1403.
[24]
Steinbrecher, U.P.; Fisher, M.; Witztum, J.L.; Curtiss, L.K. Immunogenicity of homologous low density lipoprotein after methylation, ethylation, acetylation, or carbamylation: generation of antibodies specific for derivatized lysine. J. Lipid Res., 1984, 25(10), 1109-1116.
[25]
Uchida, K.; Sakai, K.; Itakura, K.; Osawa, T.; Toyokuni, S. Protein modification by lipid peroxidation products: formation of malondialdehyde-derived N(epsilon)-(2-propenol)lysine in proteins. Arch. Biochem. Biophys., 1997, 346(1), 45-52.
[26]
Palinski, W.; Ylä-Herttuala, S.; Rosenfeld, M.E.; Butler, S.W.; Socher, S.A.; Parthasarathy, S.; Curtiss, L.K.; Witztum, J.L. Antisera and monoclonal antibodies specific for epitopes generated during oxidative modification of low density lipoprotein. Arteriosclerosis, 1990, 10(3), 325-335.
[27]
Ylä-Herttuala, S.; Palinski, W.; Butler, S.W.; Picard, S.; Steinberg, D.; Witztum, J.L. Rabbit and human atherosclerotic lesions contain IgG that recognizes epitopes of oxidized LDL. Arterioscler. Thromb., 1994, 14(1), 32-40.
[28]
Mironova, M.; Virella, G.; Lopes-Virella, M.F. Isolation and characterization of human antioxidized LDL autoantibodies. Arterioscler. Thromb. Vasc. Biol., 1996, 16(2), 222-229.
[29]
Virella, G.; Koskinen, S.; Krings, G.; Onorato, J.M.; Thorpe, S.R.; Lopes-Virella, M. Immunochemical characterization of purified human oxidized low-density lipoprotein antibodies. Clin. Immunol., 2000, 95(2), 135-144.
[30]
Virella, G.; Thorpe, S.R.; Alderson, N.L.; Derrick, M.B.; Chassereau, C.; Rhett, J.M.; Lopes-Virella, M.F. Definition of the immunogenic forms of modified human LDL recognized by human autoantibodies and by rabbit hyperimmune antibodies. J. Lipid Res., 2004, 45(10), 1859-1867.
[31]
Lopes-Virella, M.F.; Virella, G. Pathogenic role of modified LDL antibodies and immune complexes in atherosclerosis. J. Atheroscler. Thromb., 2013, 20(10), 743-754.
[32]
Orekhov, A.N.; Tertov, V.V. Antibody-like immunoglobulins G against low density lipoprotein that stimulate lipid accumulation in cultured cells. Adv. Exp. Med. Biol., 1991, 285, 399-404.
[33]
Virella, G.; Wilson, K.; Elkes, J.; Hammad, S.M.; Rajab, H.A.; Li, Y.; Chassereau, C.; Huang, Y.; Lopes-Virella, M. Immune complexes containing malondialdehyde (MDA) LDL induce apoptosis in human macrophages. Clin. Immunol., 2018, 187, 1-9.
[34]
Orekhov, A.N.; Tertov, V.V.; Kabakov, A.E.; Adamova, I.; Pokrovsky, S.N.; Smirnov, V.N. Autoantibodies against modified low density lipoprotein. Nonlipid factor of blood plasma that stimulates foam cell formation. Arterioscler. Thromb., 1991, 11(2), 316-326.
[35]
Virella, G.; Thorpe, S.R.; Alderson, N.L.; Stephan, E.M.; Atchley, D.H.; Wagner, F.; Lopes-Virella, M.F.; Group, D.E.R. Autoimmune response to advanced glycosylation end-products of human low density lipoprotein. J. Lipid Res., 2003, 443, 487-493.
[36]
Virella, G.; Lopes-Virella, M.F. Lipoprotein autoantibodies: measurement and significance. Clin. Diagn. Lab. Immunol., 2003, 10(4), 499-505.
[37]
Virella, G.; Carter, R.E.; Saad, A.; Crosswell, E.G.; Game, B.A.; Lopes-Virella, M.F. Distribution of IgM and IgG antibodies to oxidized LDL in immune complexes isolated from patients with type 1 diabetes and its relationship with nephropathy. Clin. Immunol., 2008, 127(3), 394-400.
[38]
Saad, A.F.; Virella, G.; Chassereau, C.; Boackle, R.J.; Lopes-Virella, M.F. OxLDL immune complexes activate complement and induce cytokine production by MonoMac 6 cells and human macrophages. J. Lipid Res., 2006, 47(9), 1975-1983.
[39]
Lopes-Virella, M.F.; Mironova, M.; Virella, G. LDL-containing immune complexes and atherosclerosis in diabetes mellitus. Diabetes Rev. (Alex.), 1997, 58, 410-424.
[40]
Lopes-Virella, M.F.; Virella, G.; Orchard, T.J.; Koskinen, S.; Evans, R.W.; Becker, D.J.; Forrest, K.Y. Antibodies to oxidized LDL and LDL-containing immune complexes as risk factors for coronary artery disease in diabetes mellitus. Clin. Immunol., 1999, 90, 165-172.
[41]
Mironova, M.A.; Klein, R.L.; Virella, G.T.; Lopes-Virella, M.F. Anti-modified LDL antibodies, LDL-containing immune complexes, and susceptibility of LDL to in vitro oxidation in patients with type 2 diabetes. Diabetes, 2000, 49(6), 1033-1041.
[42]
Orekhov, A.N.; Kalenich, O.S.; Tetov, V.V.; Novikov, I.D.; Vorobeva, E.G. Cholesterol level in circulating immune complexes as a marker of coronary atherosclerosis. Adv. Exp. Med. Biol., 1990, 285, 393-397.
[43]
Orekhov, A.N.; Kalenich, O.S.; Tertov, V.V.; Novikov, I.D. Lipoprotein immune complexes as markers of atherosclerosis. Int. J. Tissue React., 1991, 13(5), 233-236.
[44]
Lopes-Virella, M.F.; McHenry, M.B.; Lipsitz, S.; Yim, E.; Wilson, P.F.; Lackland, D.T.; Lyons, T.; Jenkins, A.J.; Virella, G. Immune complexes containing modified lipoproteins are related to the progression of internal carotid intima-media thickness in patients with type 1 diabetes. Atherosclerosis, 2007, 190(2), 359-369.
[45]
Lopes-Virella, M.F.; Baker, N.L.; Hunt, K.J.; Lachin, J.; Nathan, D.; Virella, G. Oxidized LDL immune complexes and coronary artery calcification in type 1 diabetes. Atherosclerosis, 2011, 214(2), 462-467.
[46]
Lopes-Virella, M. F.; Hunt, K. J.; Baker, N. L.; Lachin, J.; Nathan, D. M.; Virella, G. Levels of oxidized LDL and advanced glycation end products-modified LDL in circulating immune complexes are strongly associated with increased levels of carotid intima-media thickness and its progression in type 1 diabetes. 2011, 60, 582-589.
[47]
Lopes-Virella, M.F.; Hunt, K.J.; Baker, N.L.; Virella, G.; Moritz, T. VADT Investigators. The levels of MDA-LDL in circulating immune complexes predict myocardial infarction in the VADT study. Atherosclerosis, 2012, 224(2), 526-531.
[48]
Hernández-Vargas, P.; Ortiz-Muñoz, G.; López-Franco, O.; Suzuki, Y.; Gallego-Delgado, J.; Sanjuán, G.; Lázaro, A.; López-Parra, V.; Ortega, L.; Egido, J.; Gómez-Guerrero, C. Fcgamma receptor deficiency confers protection against atherosclerosis in apolipoprotein E knockout mice. Circ. Res., 2006, 99(11), 1188-1196.
[49]
Li, Y.; Lu, Z.; Huang, Y.; Lopes-Virella, M.F.; Virella, G.F. (ab’)2 fragments of anti-oxidized LDL IgG attenuate vascular inflammation and atherogenesis in diabetic LDL receptor-deficient mice. Clin. Immunol., 2016, 173, 50-56.
[50]
Mallavia, B.; Oguiza, A.; Lopez-Franco, O.; Recio, C.; Ortiz-Muñoz, G.; Lazaro, I.; Lopez-Parra, V.; Egido, J.; Gomez-Guerrero, C. Gene deficiency in activating Fc gamma receptors influences the macrophage phenotypic balance and reduces atherosclerosis in mice. PLoS One, 2013, 8(6), e66754.
[51]
Griffith, R.L.; Virella, G.T.; Stevenson, H.C.; Lopes-Virella, M.F. Low density lipoprotein metabolism by human macrophages activated with low density lipoprotein immune complexes. A possible mechanism of foam cell formation. J. Exp. Med., 1988, 168, 1041-1059.
[52]
Kiener, P.A.; Rankin, B.M.; Davis, P.M.; Yocum, S.A.; Warr, G.A.; Grove, R.I. Immune complexes of LDL induce atherogenic responses in human monocytic cells. Arterioscler. Thromb. Vasc. Biol., 1995, 15(7), 990-999.
[53]
Klimov, A.N.; Denisenko, A.D.; Popov, A.V.; Nagornev, V.A.; Pleskov, V.M.; Vinogradov, A.G.; Denisenko, T.V.; Magracheva, E.Y.; Kheifes, G.M.; Kuznetzov, A.S. Lipoprotein-antibody immune complexes. Their catabolism and role in foam cell formation. Atherosclerosis, 1985, 58(1-3), 1-15.
[54]
Klimov, A.N.; Denisenko, A.D.; Vinogradov, A.G.; Nagornev, V.A.; Pivovarova, Y.I.; Sitnikova, O.D.; Pleskov, V.M. Accumulation of cholesteryl esters in macrophages incubated with human lipoprotein-antibody autoimmune complex. Atherosclerosis, 1988, 74(1-2), 41-46.
[55]
Lopes-Virella, M.F.; Griffith, R.L.; Shunk, K.A.; Virella, G.T. Enhanced uptake and impaired intracellular metabolism of low density lipoprotein complexed with anti-low density lipoprotein antibodies. Arterioscler. Thromb., 1991, 11(5), 1356-1367.
[56]
Virella, G.; Muñoz, J.F.; Galbraith, G.M.; Gissinger, C.; Chassereau, C.; Lopes-Virella, M.F. Activation of human monocyte-derived macrophages by immune complexes containing low-density lipoprotein. Clin. Immunol. Immunopathol., 1995, 75(2), 179-189.
[57]
Virella, G.; Atchley, D.; Koskinen, S.; Zheng, D.; Lopes-Virella, M.F. Proatherogenic and proinflammatory properties of immune complexes prepared with purified human oxLDL antibodies and human oxLDL. Clin. Immunol., 2002, 105(1), 81-92.
[58]
Ylä-Herttuala, S. Macrophages and oxidized low density lipoproteins in the pathogenesis of atherosclerosis. Ann. Med., 1991, 23(5), 561-567.
[59]
Hörl, G.; Froehlich, H.; Ferstl, U.; Ledinski, G.; Binder, J.; Cvirn, G.; Stojakovic, T.; Trauner, M.; Koidl, C.; Tafeit, E.; Amrein, K.; Scharnagl, H.; Jürgens, G.; Hallström, S. Simvastatin efficiently lowers small LDL-IgG immune complex levels: A therapeutic quality beyond the lipid-lowering effect. PLoS One, 2016, 11(2), e0148210.
[60]
Hunt, K.J.; Baker, N.; Cleary, P.; Backlund, J.Y.; Lyons, T.; Jenkins, A.; Virella, G.; Lopes-Virella, M.F. Oxidized LDL and AGE-LDL in circulating immune complexes strongly predict progression of carotid artery IMT in type 1 diabetes. Atherosclerosis, 2013, 231(2), 315-322.
[61]
Orekhov, A.N.; Bobryshev, Y.V.; Sobenin, I.A.; Melnichenko, A.A.; Chistiakov, D.A. Modified low density lipoprotein and lipoprotein-containing circulating immune complexes as diagnostic and prognostic biomarkers of atherosclerosis and type 1 diabetes macrovascular disease. Int. J. Mol. Sci., 2014, 15(7), 12807-12841.
[62]
Prasad, A.; Clopton, P.; Ayers, C.; Khera, A.; de Lemos, J.A.; Witztum, J.L.; Tsimikas, S. Relationship of autoantibodies to MDA-LDL and ApoB-immune complexes to sex, ethnicity, subclinical atherosclerosis, and cardiovascular events. Arterioscler. Thromb. Vasc. Biol., 2017, 37(6), 1213-1221.
[63]
Sobenin, I.A.; Karagodin, V.P.; Melnichenko, A.C.; Bobryshev, Y.V.; Orekhov, A.N. Diagnostic and prognostic value of low density lipoprotein-containing circulating immune complexes in atherosclerosis. J. Clin. Immunol., 2013, 33(2), 489-495.
[64]
Sobenin, I.A.; Salonen, J.T.; Zhelankin, A.V.; Melnichenko, A.A.; Kaikkonen, J.; Bobryshev, Y.V.; Orekhov, A.N. Low density lipoprotein-containing circulating immune complexes: role in atherosclerosis and diagnostic value. BioMed Res. Int., 2014, 2014, 205697.
[65]
Virella, G.; Derrick, M.B.; Pate, V.; Chassereau, C.; Thorpe, S.R.; Lopes-Virella, M.F. Development of capture assays for different modifications of human low-density lipoprotein. Clin. Diagn. Lab. Immunol., 2005, 12(1), 68-75.
[66]
Virella, G.; Colglazier, J.; Chassereau, C.; Hunt, K.J.; Baker, N.L.; Lopes-Virella, M.F. Immunoassay of modified forms of human low density lipoprotein in isolated circulating immune complexes. J. Immunoassay Immunochem., 2013, 34(1), 61-74.
[67]
Libby, P.; Theroux, P. Pathophysiology of coronary artery disease. Circulation, 2005, 111(25), 3481-3488.
[68]
Shah, P.K. Pathophysiology of coronary thrombosis: role of plaque rupture and plaque erosion. Prog. Cardiovasc. Dis., 2002, 44(5), 357-368.
[69]
Galis, Z.S.; Sukhova, G.K.; Lark, M.W.; Libby, P. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J. Clin. Invest., 1994, 94(6), 2493-2503.
[70]
Seimon, T.; Tabas, I. Mechanisms and consequences of macrophage apoptosis in atherosclerosis. J. Lipid Res., 2009, 50(Suppl.), S382-S387.
[71]
Virella, G.; Lopes-Virella, M.F. Humoral immunity and atherosclerosis. Nat. Med., 2003, 9(3), 243-244.
[72]
Lopes-Virella, M.F.; Binzafar, N.; Rackley, S.; Takei, A.; La Via, M.; Virella, G. The uptake of LDL-IC by human macrophages: predominant involvement of the Fc gamma RI receptor. Atherosclerosis, 1997, 135(2), 161-170.
[73]
Shaw, P.X.; Hörkkö, S.; Tsimikas, S.; Chang, M.K.; Palinski, W.; Silverman, G.J.; Chen, P.P.; Witztum, J.L. Human-derived anti-oxidized LDL autoantibody blocks uptake of oxidized LDL by macrophages and localizes to atherosclerotic lesions in vivo. Arterioscler. Thromb. Vasc. Biol., 2001, 21(8), 1333-1339.
[74]
Fu, Y.; Huang, Y.; Bandyopadhyay, S.; Virella, G.; Lopes-Virella, M.F. LDL immune complexes stimulate LDL receptor expression in U937 histiocytes via extracellular signal-regulated kinase and AP-1. J. Lipid Res., 2003, 44(7), 1315-1321.
[75]
Hammad, S.M.; Twal, W.O.; Barth, J.L.; Smith, K.J.; Saad, A.F.; Virella, G.; Argraves, W.S.; Lopes-Virella, M.F. Oxidized LDL immune complexes and oxidized LDL differentially affect the expression of genes involved with inflammation and survival in human U937 monocytic cells. Atherosclerosis, 2009, 202(2), 394-404.
[76]
Tohyama, Y.; Yamamura, H. Protein tyrosine kinase, syk: a key player in phagocytic cells. J. Biochem., 2009, 145(3), 267-273.
[77]
Crowley, M.T.; Costello, P.S.; Fitzer-Attas, C.J.; Turner, M.; Meng, F.; Lowell, C.; Tybulewicz, V.L.; DeFranco, A.L. A critical role for Syk in signal transduction and phagocytosis mediated by Fcgamma receptors on macrophages. J. Exp. Med., 1997, 186(7), 1027-1039.
[78]
Luo, Y.; Pollard, J.W.; Casadevall, A. Fcgamma receptor cross-linking stimulates cell proliferation of macrophages via the ERK pathway. J. Biol. Chem., 2010, 285(6), 4232-4242.
[79]
Huang, Y.; Jaffa, A.; Koskinen, S.; Takei, A.; Lopes-Virella, M.F. Oxidized LDL-containing immune complexes induce Fcgamma receptor I-mediated mitogen-activated protein kinase activation in THP-1 macrophages. Arterioscler. Thromb. Vasc. Biol., 1999, 19(7), 1600-1607.
[80]
Oksjoki, R.; Kovanen, P.T.; Lindstedt, K.A.; Jansson, B.; Pentikäinen, M.O. OxLDL-IgG immune complexes induce survival of human monocytes. Arterioscler. Thromb. Vasc. Biol., 2006, 26(3), 576-583.
[81]
Datta, S.R.; Brunet, A.; Greenberg, M.E. Cellular survival: a play in three Akts. Genes Dev., 1999, 13(22), 2905-2927.
[82]
Al Gadban, M.M.; Smith, K.J.; Soodavar, F.; Piansay, C.; Chassereau, C.; Twal, W.O.; Klein, R.L.; Virella, G.; Lopes-Virella, M.F.; Hammad, S.M. Differential trafficking of oxidized LDL and oxidized LDL immune complexes in macrophages: Impact on oxidative stress. PLoS One, 2010, 5(9), e12534.
[83]
Smith, K.J.; Twal, W.O.; Soodavar, F.; Virella, G.; Lopes-Virella, M.F.; Hammad, S.M. Heat shock protein 70B′ (HSP70B′) expression and release in response to human oxidized low density lipoprotein immune complexes in macrophages. J. Biol. Chem., 2010, 285(21), 15985-15993.
[84]
de Boer, O.J.; van der Wal, A.C.; Houtkamp, M.A.; Ossewaarde, J.M.; Teeling, P.; Becker, A.E. Unstable atherosclerotic plaques contain T-cells that respond to Chlamydia pneumoniae. Cardiovasc. Res., 2000, 48(3), 402-408.
[85]
Lim, W.S.; Timmins, J.M.; Seimon, T.A.; Sadler, A.; Kolodgie, F.D.; Virmani, R.; Tabas, I. Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo. Circulation, 2008, 117(7), 940-951.
[86]
Kinscherf, R.; Claus, R.; Wagner, M.; Gehrke, C.; Kamencic, H.; Hou, D.; Nauen, O.; Schmiedt, W.; Kovacs, G.; Pill, J.; Metz, J.; Deigner, H.P. Apoptosis caused by oxidized LDL is manganese superoxide dismutase and p53 dependent. FASEB J., 1998, 12(6), 461-467.
[87]
Hamilton, J.A.; Whitty, G.; Jessup, W. Oxidized LDL can promote human monocyte survival. Arterioscler. Thromb. Vasc. Biol., 2000, 20(10), 2329-2331.
[88]
Hundal, R.S.; Gómez-Muñoz, A.; Kong, J.Y.; Salh, B.S.; Marotta, A.; Duronio, V.; Steinbrecher, U.P. Oxidized low density lipoprotein inhibits macrophage apoptosis by blocking ceramide generation, thereby maintaining protein kinase B activation and Bcl-XL levels. J. Biol. Chem., 2003, 278(27), 24399-24408.
[89]
Oksjoki, R.; Kovanen, P.T.; Pentikäinen, M.O. Role of complement activation in atherosclerosis. Curr. Opin. Lipidol., 2003, 14(5), 477-482.
[90]
Hammad, S.M.; Taha, T.A.; Nareika, A.; Johnson, K.R.; Lopes-Virella, M.F.; Obeid, L.M. Oxidized LDL immune complexes induce release of sphingosine kinase in human U937 monocytic cells. Prostaglandins Other Lipid Mediat., 2006, 79(1-2), 126-140.
[91]
Schulze-Osthoff, K.; Ferrari, D.; Los, M.; Wesselborg, S.; Peter, M.E. Apoptosis signaling by death receptors. Eur. J. Biochem., 1998, 254(3), 439-459.
[92]
Tsujimoto, Y. Role of Bcl-2 family proteins in apoptosis: apoptosomes or mitochondria? Genes Cells, 1998, 3(11), 697-707.
[93]
Czabotar, P.E.; Lessene, G.; Strasser, A.; Adams, J.M. Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy. Nat. Rev. Mol. Cell Biol., 2014, 15(1), 49-63.
[94]
Hoff, H.F.; Zyromski, N.; Armstrong, D.; O’Neil, J. Aggregation as well as chemical modification of LDL during oxidation is responsible for poor processing in macrophages. J. Lipid Res., 1993, 34(11), 1919-1929.

Rights & Permissions Print Cite
Article Metrics
45
7
© 2024 Bentham Science Publishers | Privacy Policy