Login Register Cart 0
Generic placeholder image

Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe Translate in Chinese
Review Article

The Role of (Modified) Lipoproteins in Vascular Function: A Duet Between Monocytes and the Endothelium

Author(s): Johan G. Schnitzler, Geesje M. Dallinga-Thie* and Jeffrey Kroon*

Volume 26, Issue 9, 2019

Page: [1594 - 1609] Pages: 16

DOI: 10.2174/0929867325666180316121015

Price: $65

Abstract

Over the last century, many studies have demonstrated that low-density lipoprotein (LDL) is a key risk factor of cardiovascular diseases (CVD) related to atherosclerosis. Thus, for these CVD patients, LDL lowering agents are commonly used in the clinic to reduce the risk for CVD. LDL, upon modification, will develop distinct inflammatory and proatherogenic potential, leading to impaired endothelial integrity, influx of immune cells and subsequent increased foam cell formation. LDL can also directly affect peripheral monocyte composition, rendering them in a more favorable position to migrate and accumulate in the subendothelial space. It has become apparent that other lipoprotein particles, such as triglyceride- rich lipoproteins or remnants (TRL) and lipoprotein(a) [Lp(a)] may also impact on atherogenic pathways. Evidence is accumulating that Lp(a) can promote peripheral monocyte activation, eventually leading to increased transmigration through the endothelium. Similarly, remnant cholesterol has been identified to play a key role in endothelial dysfunction and monocyte behavior. In this review, we will discuss recent developments in understanding the role of different lipoproteins in the context of inflammation at both the level of the monocyte and the endothelium.

Keywords: Lipoproteins, apoB, Lp(a), oxidized phospholipids, remnants, atherogenesis, monocytes, endothelial cells.

« Previous Next »
[1]
Borén, J.; Williams, K.J. The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity. Curr. Opin. Lipidol., 2016, 27(5), 473-483.
[2]
Gisterå, A.; Hansson, G.K. The immunology of atherosclerosis. Nat. Rev. Nephrol., 2017, 13(6), 368-380.
[3]
Dallinga-Thie, G.M.; Franssen, R.; Mooij, H.L.; Visser, M.E.; Hassing, H.C.; Peelman, F.; Kastelein, J.J.; Péterfy, M.; Nieuwdorp, M. The metabolism of triglyceride-rich lipoproteins revisited: new players, new insight. Atheroscler., 2010, 211(1), 1-8.
[4]
Young, S.G.; Zechner, R. Biochemistry and pathophysiology of intravascular and intracellular lipolysis. Genes Dev., 2013, 27(5), 459-484.
[5]
Hussain, M.M. Intestinal lipid absorption and lipoprotein formation. Curr. Opin. Lipidol., 2014, 25(3), 200-206.
[6]
Abumrad, N.A.; Goldberg, I.J. CD36 actions in the heart: Lipids, calcium, inflammation, repair and more? Biochim. Biophys. Acta, 2016, 1861(10), 1442-1449.
[7]
Williams, K.J. Molecular processes that handle -- and mishandle -- dietary lipids. J. Clin. Invest., 2008, 118(10), 3247-3259.
[8]
Goldstein, J.L.; Brown, M.S. Atherosclerosis: the low-density lipoprotein receptor hypothesis. Metabol., 1977, 26(11), 1257-1275.
[9]
Twickler, T.; Dallinga-Thie, G.M.; Chapman, M.J.; Cohn, J.S. Remnant lipoproteins and atherosclerosis. Curr. Atheroscler. Rep., 2005, 7(2), 140-147.
[10]
Chatterjee, C.; Sparks, D.L. Hepatic lipase, high density lipoproteins, and hypertriglyceridemia. Am. J. Pathol., 2011, 178(4), 1429-1433.
[11]
Ketelhuth, D.F.; Hansson, G.K. Cellular immunity, low-density lipoprotein and atherosclerosis: break of tolerance in the artery wall. Thromb. Haemost., 2011, 106(5), 779-786.
[12]
Bernelot Moens, S.J.; Neele, A.E.; Kroon, J.; van der Valk, F.M.; Van den Bossche, J.; Hoeksema, M.A.; Hoogeveen, R.M.; Schnitzler, J.G.; Baccara-Dinet, M.T.; Manvelian, G.; de Winther, M.P.J.; Stroes, E.S.G. PCSK9 monoclonal antibodies reverse the pro-inflammatory profile of monocytes in familial hypercholesterolaemia. Eur. Heart J., 2017, 38(20), 1584-1593.
[13]
Berglund, L.; Brunzell, J.D.; Goldberg, A.C.; Goldberg, I.J.; Sacks, F.; Murad, M.H.; Stalenhoef, A.F. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline. J. Clin. Endocrinol. Metab., 2012, 97(9), 2969-2989.
[14]
Freiberg, J.J.; Tybjaerg-Hansen, A.; Jensen, J.S.; Nordestgaard, B.G. Nonfasting triglycerides and risk of ischemic stroke in the general population. JAMA, 2008, 300(18), 2142-2152.
[15]
Nordestgaard, B.G.; Benn, M.; Schnohr, P.; Tybjaerg-Hansen, A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA, 2007, 298(3), 299-308.
[16]
Varbo, A.; Benn, M.; Tybjærg-Hansen, A.; Jørgensen, A.B.; Frikke-Schmidt, R.; Nordestgaard, B.G. Remnant cholesterol as a causal risk factor for ischemic heart disease. J. Am. Coll. Cardiol., 2013, 61(4), 427-436.
[17]
Utermann, G.; Menzel, H.J.; Kraft, H.G.; Duba, H.C.; Kemmler, H.G.; Seitz, C. Lp(a) glycoprotein phenotypes. Inheritance and relation to Lp(a)-lipoprotein concentrations in plasma. J. Clin. Invest., 1987, 80(2), 458-465.
[18]
White, A.L.; Lanford, R.E. Cell surface assembly of lipoprotein(a) in primary cultures of baboon hepatocytes. J. Biol. Chem., 1994, 269(46), 28716-28723.
[19]
Lobentanz, E.M.; Dieplinger, H. Biogenesis of lipoprotein(a) in human and animal hepatocytes. Electrophoresis, 1997, 18(14), 2677-2681.
[20]
Reyes-Soffer, G.; Ginsberg, H.N.; Ramakrishnan, R. The metabolism of lipoprotein (a): an ever-evolving story. J. Lipid Res., 2017, 58(9), 1756-1764.
[21]
Willeit, P.; Kiechl, S.; Kronenberg, F.; Witztum, J.L.; Santer, P.; Mayr, M.; Xu, Q.; Mayr, A.; Willeit, J.; Tsimikas, S. Discrimination and net reclassification of cardiovascular risk with lipoprotein(a): prospective 15-year outcomes in the Bruneck Study. J. Am. Coll. Cardiol., 2014, 64(9), 851-860.
[22]
Merki, E.; Graham, M.; Taleb, A.; Leibundgut, G.; Yang, X.; Miller, E.R.; Fu, W.; Mullick, A.E.; Lee, R.; Willeit, P.; Crooke, R.M.; Witztum, J.L.; Tsimikas, S. Antisense oligonucleotide lowers plasma levels of apolipoprotein (a) and lipoprotein (a) in transgenic mice. J. Am. Coll. Cardiol., 2011, 57(15), 1611-1621.
[23]
Nordestgaard, B.G.; Langsted, A. Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology. J. Lipid Res., 2016, 57(11), 1953-1975.
[24]
Tsimikas, S.A. Test in context: lipoprotein(a): diagnosis, prognosis, controversies, and emerging therapies. J. Am. Coll. Cardiol., 2017, 69(6), 692-711.
[25]
van der Valk, F.M.; Bekkering, S.; Kroon, J.; Yeang, C.; Van den Bossche, J.; van Buul, J.D.; Ravandi, A.; Nederveen, A.J.; Verberne, H.J.; Scipione, C.; Nieuwdorp, M.; Joosten, L.A.; Netea, M.G.; Koschinsky, M.L.; Witztum, J.L.; Tsimikas, S.; Riksen, N.P.; Stroes, E.S. Oxidized Phospholipids on Lipoprotein(a) Elicit Arterial Wall Inflammation and an Inflammatory Monocyte Response in Humans. Circulation, 2016, 134(8), 611-624.
[26]
Capoulade, R.; Chan, K.L.; Yeang, C.; Mathieu, P.; Bossé, Y.; Dumesnil, J.G.; Tam, J.W.; Teo, K.K.; Mahmut, A.; Yang, X.; Witztum, J.L.; Arsenault, B.J.; Després, J.P.; Pibarot, P.; Tsimikas, S. Oxidized phospholipids, lipoprotein(a), and progression of calcific aortic valve stenosis. J. Am. Coll. Cardiol., 2015, 66(11), 1236-1246.
[27]
Tsimikas, S.; Mallat, Z.; Talmud, P.J.; Kastelein, J.J.; Wareham, N.J.; Sandhu, M.S.; Miller, E.R.; Benessiano, J.; Tedgui, A.; Witztum, J.L.; Khaw, K.T.; Boekholdt, S.M. Oxidation-specific biomarkers, lipoprotein(a), and risk of fatal and nonfatal coronary events. J. Am. Coll. Cardiol., 2010, 56(12), 946-955.
[28]
Erqou, S.; Kaptoge, S.; Perry, P.L.; Di Angelantonio, E.; Thompson, A.; White, I.R.; Marcovina, S.M.; Collins, R.; Thompson, S.G.; Danesh, J.; Danesh, J. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009, 302(4), 412-423.
[29]
Erqou, S.; Thompson, A.; Di Angelantonio, E.; Saleheen, D.; Kaptoge, S.; Marcovina, S.; Danesh, J. Apolipoprotein(a) isoforms and the risk of vascular disease: systematic review of 40 studies involving 58,000 participants. J. Am. Coll. Cardiol., 2010, 55(19), 2160-2167.
[30]
Kamstrup, P.R.; Benn, M.; Tybjaerg-Hansen, A.; Nordestgaard, B.G. Extreme lipoprotein(a) levels and risk of myocardial infarction in the general population: the Copenhagen City Heart Study. Circulation, 2008, 117(2), 176-184.
[31]
Langsted, A.; Kamstrup, P.R.; Nordestgaard, B.G. Lipoprotein(a): fasting and nonfasting levels, inflammation, and cardiovascular risk. Atheroscler., 2014, 234(1), 95-101.
[32]
Boerwinkle, E.; Leffert, C.C.; Lin, J.; Lackner, C.; Chiesa, G.; Hobbs, H.H. Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J. Clin. Invest., 1992, 90(1), 52-60.
[33]
Utermann, G. The mysteries of lipoprotein(a). Sci., 1989, 246(4932), 904-910.
[34]
Tardif, J.C.; Grégoire, J.; L’Allier, P.L.; Ibrahim, R.; Lespérance, J.; Heinonen, T.M.; Kouz, S.; Berry, C.; Basser, R.; Lavoie, M.A.; Guertin, M.C.; Rodés-Cabau, J. Effects of reconstituted high-density lipoprotein infusions on coronary atherosclerosis: a randomized controlled trial. JAMA, 2007, 297(15), 1675-1682.
[35]
Libby, P. Managing the risk of atherosclerosis: the role of high-density lipoprotein. Am. J. Cardiol., 2001, 88(12A), 3N-8N.
[36]
Kontush, A.; Chapman, M.J. Functionally defective high-density lipoprotein: a new therapeutic target at the crossroads of dyslipidemia, inflammation, and atherosclerosis. Pharmacol. Rev., 2006, 58(3), 342-374.
[37]
Ross, R. Atherosclerosis--an inflammatory disease. N. Engl. J. Med., 1999, 340(2), 115-126.
[38]
Hahn, C.; Schwartz, M.A. The role of cellular adaptation to mechanical forces in atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2008, 28(12), 2101-2107.
[39]
Baratchi, S.; Khoshmanesh, K.; Woodman, O.L.; Potocnik, S.; Peter, K.; McIntyre, P. Molecular sensors of blood flow in endothelial cells. Trends Mol. Med., 2017, 23(9), 850-868.
[40]
Cunningham, K.S.; Gotlieb, A.I. The role of shear stress in the pathogenesis of atherosclerosis. Lab. Invest., 2005, 85(1), 9-23.
[41]
Traub, O.; Berk, B.C. Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force. Arterioscler. Thromb. Vasc. Biol., 1998, 18(5), 677-685.
[42]
Pan, S. Molecular mechanisms responsible for the atheroprotective effects of laminar shear stress. Antioxid. Redox Signal., 2009, 11(7), 1669-1682.
[43]
VanderLaan, P.A.; Reardon, C.A.; Getz, G.S. Site specificity of atherosclerosis: site-selective responses to atherosclerotic modulators. Arterioscler. Thromb. Vasc. Biol., 2004, 24(1), 12-22.
[44]
Zhou, J.; Li, Y.S.; Chien, S. Shear stress-initiated signaling and its regulation of endothelial function. Arterioscler. Thromb. Vasc. Biol., 2014, 34(10), 2191-2198.
[45]
Won, D.; Zhu, S.N.; Chen, M.; Teichert, A.M.; Fish, J.E.; Matouk, C.C.; Bonert, M.; Ojha, M.; Marsden, P.A.; Cybulsky, M.I. Relative reduction of endothelial nitric-oxide synthase expression and transcription in atherosclerosis-prone regions of the mouse aorta and in an in vitro model of disturbed flow. Am. J. Pathol., 2007, 171(5), 1691-1704.
[46]
Heinecke, J.W.; Baker, L.; Rosen, H.; Chait, A. Superoxide-mediated modification of low density lipoprotein by arterial smooth muscle cells. J. Clin. Invest., 1986, 77(3), 757-761.
[47]
Botti, H.; Trostchansky, A.; Batthyány, C.; Rubbo, H. Reactivity of peroxynitrite and nitric oxide with LDL. IUBMB Life, 2005, 57(6), 407-412.
[48]
von Eckardstein, A.; Rohrer, L. Transendothelial lipoprotein transport and regulation of endothelial permeability and integrity by lipoproteins. Curr. Opin. Lipidol., 2009, 20(3), 197-205.
[49]
Schwenke, D.C.; Carew, T.E. Initiation of atherosclerotic lesions in cholesterol-fed rabbits. I. Focal increases in arterial LDL concentration precede development of fatty streak lesions. Arterioscler., 1989, 9(6), 895-907.
[50]
Tabas, I.; Williams, K.J.; Borén, J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications. Circulation, 2007, 116(16), 1832-1844.
[51]
Sun, S.W.; Zu, X.Y.; Tuo, Q.H.; Chen, L.X.; Lei, X.Y.; Li, K.; Tang, C.K.; Liao, D.F. Caveolae and caveolin-1 mediate endocytosis and transcytosis of oxidized low density lipoprotein in endothelial cells. Acta Pharmacol. Sin., 2010, 31(10), 1336-1342.
[52]
Frank, P.G.; Pavlides, S.; Cheung, M.W.; Daumer, K.; Lisanti, M.P. Role of caveolin-1 in the regulation of lipoprotein metabolism. Am. J. Physiol. Cell Physiol., 2008, 295(1), C242-C248.
[53]
Fogelstrand, P.; Borén, J. Retention of atherogenic lipoproteins in the artery wall and its role in atherogenesis. Nutr. Metab. Cardiovasc. Dis., 2012, 22(1), 1-7.
[54]
Cancel, L.M.; Fitting, A.; Tarbell, J.M. In vitro study of LDL transport under pressurized (convective) conditions. Am. J. Physiol. Heart Circ. Physiol., 2007, 293(1), H126-H132.
[55]
Dabagh, M.; Jalali, P.; Tarbell, J.M. The transport of LDL across the deformable arterial wall: the effect of endothelial cell turnover and intimal deformation under hypertension. Am. J. Physiol. Heart Circ. Physiol., 2009, 297(3), H983-H996.
[56]
Kang, H.; Cancel, L.M.; Tarbell, J.M. Effect of shear stress on water and LDL transport through cultured endothelial cell monolayers. Atheroscler., 2014, 233(2), 682-690.
[57]
Armstrong, S.M.; Sugiyama, M.G.; Fung, K.Y.; Gao, Y.; Wang, C.; Levy, A. `S.; Azizi, P.; Roufaiel, M.; Zhu, S. N.; Neculai, D.; Yin, C.; Bolz, S.S.; Seidah, N.G.; Cybulsky, M. I.; Heit, B.; Lee, W. L. A novel assay uncovers an unexpected role for SR-BI in LDL transcytosis. Cardiovasc. Res., 2015, 108(2), 268-277.
[58]
Velagapudi, S.; Yalcinkaya, M.; Piemontese, A.; Meier, R.; Nørrelykke, S.F.; Perisa, D.; Rzepiela, A.; Stebler, M.; Stoma, S.; Zanoni, P.; Rohrer, L.; von Eckardstein, A. VEGF-A regulates cellular localization of sr-bi as well as transendothelial transport of HDL but not LDL. Arterioscler. Thromb. Vasc. Biol., 2017, 37(5), 794-803.
[59]
Kraehling, J.R.; Chidlow, J.H.; Rajagopal, C.; Sugiyama, M.G.; Fowler, J.W.; Lee, M.Y.; Zhang, X.; Ramírez, C.M.; Park, E.J.; Tao, B.; Chen, K.; Kuruvilla, L.; Larriveé, B.; Folta-Stogniew, E.; Ola, R.; Rotllan, N.; Zhou, W.; Nagle, M.W.; Herz, J.; Williams, K.J.; Eichmann, A.; Lee, W.L.; Fernández-Hernando, C.; Sessa, W.C. Genome-wide RNAi screen reveals ALK1 mediates LDL uptake and transcytosis in endothelial cells. Nat. Commun., 2016, 7, 13516.
[60]
Skålén, K.; Gustafsson, M.; Rydberg, E.K.; Hultén, L.M.; Wiklund, O.; Innerarity, T.L.; Borén, J. Subendothelial retention of atherogenic lipoproteins in early atherosclerosis. Nature, 2002, 417(6890), 750-754.
[61]
Borén, J.; Olin, K.; Lee, I.; Chait, A.; Wight, T.N.; Innerarity, T.L. Identification of the principal proteoglycan-binding site in LDL. A single-point mutation in apo-B100 severely affects proteoglycan interaction without affecting LDL receptor binding. J. Clin. Invest., 1998, 101(12), 2658-2664.
[62]
Boren, J.; Lee, I.; Zhu, W.; Arnold, K.; Taylor, S.; Innerarity, T.L. Identification of the low density lipoprotein receptor-binding site in apolipoprotein B100 and the modulation of its binding activity by the carboxyl terminus in familial defective apo-B100. J. Clin. Invest., 1998, 101(5), 1084-1093.
[63]
Gerhardt, T.; Ley, K. Monocyte trafficking across the vessel wall. Cardiovasc. Res., 2015, 107(3), 321-330.
[64]
Timmerman, I.; Daniel, A.E.; Kroon, J.; van Buul, J.D. Leukocytes crossing the endothelium: a matter of communication. Int. Rev. Cell Mol. Biol., 2016, 322, 281-329.
[65]
Woollard, K.J.; Geissmann, F. Monocytes in atherosclerosis: subsets and functions. Nat. Rev. Cardiol., 2010, 7(2), 77-86.
[66]
Moore, K.J.; Sheedy, F.J.; Fisher, E.A. Macrophages in atherosclerosis: a dynamic balance. Nat. Rev. Immunol., 2013, 13(10), 709-721.
[67]
Nourshargh, S.; Hordijk, P.L.; Sixt, M. Breaching multiple barriers: leukocyte motility through venular walls and the interstitium. Nat. Rev. Mol. Cell Biol., 2010, 11(5), 366-378.
[68]
Boring, L.; Gosling, J.; Cleary, M.; Charo, I.F. Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis. Nature, 1998, 394(6696), 894-897.
[69]
Carman, C.V.; Springer, T.A. A transmigratory cup in leukocyte diapedesis both through individual vascular endothelial cells and between them. J. Cell Biol., 2004, 167(2), 377-388.
[70]
Carman, C.V.; Sage, P.T.; Sciuto, T.E.; de la Fuente, M.A.; Geha, R.S.; Ochs, H.D.; Dvorak, H.F.; Dvorak, A.M.; Springer, T.A. Transcellular diapedesis is initiated by invasive podosomes. Immunity, 2007, 26(6), 784-797.
[71]
van Gils, J.M.; Ramkhelawon, B.; Fernandes, L.; Stewart, M.C.; Guo, L.; Seibert, T.; Menezes, G.B.; Cara, D.C.; Chow, C.; Kinane, T.B.; Fisher, E.A.; Balcells, M.; Alvarez-Leite, J.; Lacy-Hulbert, A.; Moore, K.J. Endothelial expression of guidance cues in vessel wall homeostasis dysregulation under proatherosclerotic conditions. Arterioscler. Thromb. Vasc. Biol., 2013, 33(5), 911-919.
[72]
Ly, N.P.; Komatsuzaki, K.; Fraser, I.P.; Tseng, A.A.; Prodhan, P.; Moore, K.J.; Kinane, T.B. Netrin-1 inhibits leukocyte migration in vitro and in vivo. Proc. Natl. Acad. Sci. USA, 2005, 102(41), 14729-14734.
[73]
Zwaginga, J.J.; Torres, H.I.; Lammers, J.; Sixma, J.J.; Koenderman, L.; Kuijper, P.H. Minimal platelet deposition and activation in models of injured vessel wall ensure optimal neutrophil adhesion under flow conditions. Arterioscler. Thromb. Vasc. Biol., 1999, 19(6), 1549-1554.
[74]
Huo, Y.; Schober, A.; Forlow, S.B.; Smith, D.F.; Hyman, M.C.; Jung, S.; Littman, D.R.; Weber, C.; Ley, K. Circulating activated platelets exacerbate atherosclerosis in mice deficient in apolipoprotein E. Nat. Med., 2003, 9(1), 61-67.
[75]
Langer, H.F.; Gawaz, M. Platelet-vessel wall interactions in atherosclerotic disease. Thromb. Haemost., 2008, 99(3), 480-486.
[76]
da Costa Martins, P.; van den Berk, N.; Ulfman, L.H.; Koenderman, L.; Hordijk, P.L.; Zwaginga, J.J. Platelet-monocyte complexes support monocyte adhesion to endothelium by enhancing secondary tethering and cluster formation. Arterioscler. Thromb. Vasc. Biol., 2004, 24(1), 193-199.
[77]
van Gils, J.M.; da Costa Martins, P.A.; Mol, A.; Hordijk, P.L.; Zwaginga, J.J. Transendothelial migration drives dissociation of plateletmonocyte complexes. Thromb. Haemost., 2008, 100(2), 271-279.
[78]
Badrnya, S.; Schrottmaier, W.C.; Kral, J.B.; Yaiw, K.C.; Volf, I.; Schabbauer, G.; Söderberg-Nauclér, C.; Assinger, A. Platelets mediate oxidized low-density lipoprotein-induced monocyte extravasation and foam cell formation. Arterioscler. Thromb. Vasc. Biol., 2014, 34(3), 571-580.
[79]
Libby, P.; Ridker, P.M.; Hansson, G.K. Progress and challenges in translating the biology of atherosclerosis. Nature, 2011, 473(7347), 317-325.
[80]
Frohman, E.M.; Racke, M.K.; Raine, C.S. Multiple sclerosis--the plaque and its pathogenesis. N. Engl. J. Med., 2006, 354(9), 942-955.
[81]
Dutta, P.; Nahrendorf, M. Monocytes in myocardial infarction. Arterioscler. Thromb. Vasc. Biol., 2015, 35(5), 1066-1070.
[82]
Goldstein, J.L.; Brown, M.S. The low-density lipoprotein pathway and its relation to atherosclerosis. Annu. Rev. Biochem., 1977, 46, 897-930.
[83]
Steinberg, D. Oxidative Modification of LDL in the pathogenesis of atherosclerosis. Am. J. Geriatr. Cardiol., 1993, 2(5), 38-41.
[84]
Gleissner, C.A.; Leitinger, N.; Ley, K. Effects of native and modified low-density lipoproteins on monocyte recruitment in atherosclerosis. Hypertension, 2007, 50(2), 276-283.
[85]
Smalley, D.M.; Lin, J.H.; Curtis, M.L.; Kobari, Y.; Stemerman, M.B.; Pritchard, K.A., Jr Native LDL increases endothelial cell adhesiveness by inducing intercellular adhesion molecule-1. Arterioscler. Thromb. Vasc. Biol., 1996, 16(4), 585-590.
[86]
Zhu, Y.; Lin, J.H.; Liao, H.L.; Friedli, O., Jr; Verna, L.; Marten, N.W.; Straus, D.S.; Stemerman, M.B. LDL induces transcription factor activator protein-1 in human endothelial cells. Arterioscler. Thromb. Vasc. Biol., 1998, 18(3), 473-480.
[87]
Verna, L.; Ganda, C.; Stemerman, M.B. In vivo low-density lipoprotein exposure induces intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 correlated with activator protein-1 expression. Arterioscler. Thromb. Vasc. Biol., 2006, 26(6), 1344-1349.
[88]
Lin, J.H.; Zhu, Y.; Liao, H.L.; Kobari, Y.; Groszek, L.; Stemerman, M.B. Induction of vascular cell adhesion molecule-1 by low-density lipoprotein. Atheroscler., 1996, 127(2), 185-194.
[89]
Allen, S.; Khan, S.; Al-Mohanna, F.; Batten, P.; Yacoub, M. Native low density lipoprotein-induced calcium transients trigger VCAM-1 and E-selectin expression in cultured human vascular endothelial cells. J. Clin. Invest., 1998, 101(5), 1064-1075.
[90]
Blacklow, S.C. Versatility in ligand recognition by LDL receptor family proteins: advances and frontiers. Curr. Opin. Struct. Biol., 2007, 17(4), 419-426.
[91]
Steinberg, D. The LDL modification hypothesis of atherogenesis: an update. J. Lipid Res., 2009, 50(Suppl.), S376-S381.
[92]
Saremi, A.; Arora, R. Vitamin E and cardiovascular disease. Am. J. Ther., 2010, 17(3), e56-e65.
[93]
Gregson, J.M.; Freitag, D.F.; Surendran, P.; Stitziel, N.O.; Chowdhury, R.; Burgess, S.; Kaptoge, S.; Gao, P.; Staley, J.R.; Willeit, P.; Nielsen, S.F.; Caslake, M.; Trompet, S.; Polfus, L.M.; Kuulasmaa, K.; Kontto, J.; Perola, M.; Blankenberg, S.; Veronesi, G.; Gianfagna, F.; Männistö, S.; Kimura, A.; Lin, H.; Reilly, D.F.; Gorski, M.; Mijatovic, V.; Munroe, P.B.; Ehret, G.B.; Thompson, A.; Uria-Nickelsen, M.; Malarstig, A.; Dehghan, A.; Vogt, T.F.; Sasaoka, T.; Takeuchi, F.; Kato, N.; Yamada, Y.; Kee, F.; Müller-Nurasyid, M.; Ferrières, J.; Arveiler, D.; Amouyel, P.; Salomaa, V.; Boerwinkle, E.; Thompson, S.G.; Ford, I.; Wouter Jukema, J.; Sattar, N.; Packard, C.J.; Shafi Majumder, A.A.; Alam, D.S.; Deloukas, P.; Schunkert, H.; Samani, N.J.; Kathiresan, S.; Nordestgaard, B.G.; Saleheen, D.; Howson, J.M.; Di Angelantonio, E.; Butterworth, A.S.; Danesh, J. Genetic invalidation of Lp-PLA2 as a therapeutic target: Large-scale study of five functional Lp-PLA2-lowering alleles. Eur. J. Prev. Cardiol., 2017, 24(5), 492-504.
[94]
Tellis, C.C.; Tselepis, A.D. Pathophysiological role and clinical significance of lipoprotein-associated phospholipase A2 (Lp-PLA2) bound to LDL and HDL. Curr. Pharm. Des., 2014, 20(40), 6256-6269.
[95]
Steinbrecher, U.P.; Parthasarathy, S.; Leake, D.S.; Witztum, J.L.; Steinberg, D. Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids. Proc. Natl. Acad. Sci. USA, 1984, 81(12), 3883-3887.
[96]
Steinbrecher, U.P. Oxidation of human low density lipoprotein results in derivatization of lysine residues of apolipoprotein B by lipid peroxide decomposition products. J. Biol. Chem., 1987, 262(8), 3603-3608.
[97]
Steinbrecher, U.P.; Witztum, J.L.; Parthasarathy, S.; Steinberg, D. Decrease in reactive amino groups during oxidation or endothelial cell modification of LDL. Correlation with changes in receptor-mediated catabolism. Arterioscler., 1987, 7(2), 135-143.
[98]
Lubos, E.; Handy, D.E.; Loscalzo, J. Role of oxidative stress and nitric oxide in atherothrombosis. Front. Biosci., 2008, 13, 5323-5344.
[99]
Berliner, J.A.; Heinecke, J.W. The role of oxidized lipoproteins in atherogenesis. Free Radic. Biol. Med., 1996, 20(5), 707-727.
[100]
Chen, C.; Khismatullin, D.B. Oxidized low-density lipoprotein contributes to atherogenesis via co-activation of macrophages and mast cells. PLoS One, 2015, 10(3), e0123088.
[101]
Esterbauer, H.; Jürgens, G.; Quehenberger, O.; Koller, E. Autoxidation of human low density lipoprotein: loss of polyunsaturated fatty acids and vitamin E and generation of aldehydes. J. Lipid Res., 1987, 28(5), 495-509.
[102]
Jürgens, G.; Hoff, H.F.; Chisolm, G.M., III; Esterbauer, H. Modification of human serum low density lipoprotein by oxidation--characterization and pathophysiological implications. Chem. Phys. Lipids, 1987, 45(2-4), 315-336.
[103]
Orr, A.W.; Hahn, C.; Blackman, B.R.; Schwartz, M.A. p21-activated kinase signaling regulates oxidant-dependent NF-kappa B activation by flow. Circ. Res., 2008, 103(6), 671-679.
[104]
Yurdagul, A., Jr; Chen, J.; Funk, S.D.; Albert, P.; Kevil, C.G.; Orr, A.W. Altered nitric oxide production mediates matrix-specific PAK2 and NF-κB activation by flow. Mol. Biol. Cell, 2013, 24(3), 398-408.
[105]
Flood, C.; Gustafsson, M.; Pitas, R.E.; Arnaboldi, L.; Walzem, R.L.; Borén, J. Molecular mechanism for changes in proteoglycan binding on compositional changes of the core and the surface of low-density lipoprotein-containing human apolipoprotein B100. Arterioscler. Thromb. Vasc. Biol., 2004, 24(3), 564-570.
[106]
Fu, Z.; Zhou, E.; Wang, X.; Tian, M.; Kong, J.; Li, J.; Ji, L.; Niu, C.; Shen, H.; Dong, S.; Liu, C.; Vermorken, A.; Willard, B.; Zu, L.; Zheng, L. Oxidized low-density lipoprotein-induced microparticles promote endothelial monocyte adhesion via intercellular adhesion molecule 1. Am. J. Physiol. Cell Physiol., 2017, 313(5), C567-C574.
[107]
Yan, F.X.; Li, H.M.; Li, S.X.; He, S.H.; Dai, W.P.; Li, Y.; Wang, T.T.; Shi, M.M.; Yuan, H.X.; Xu, Z.; Zhou, J.G.; Ning, D.S.; Mo, Z.W.; Ou, Z.J.; Ou, J.S. The oxidized phospholipid POVPC impairs endothelial function and vasodilation via uncoupling endothelial nitric oxide synthase. J. Mol. Cell. Cardiol., 2017, 112, 40-48.
[108]
Zhang, C.; Adamos, C.; Oh, M.J.; Baruah, J.; Ayee, M.A.A.; Mehta, D.; Wary, K.K.; Levitan, I. oxLDL induces endothelial cell proliferation via Rho/ROCK/Akt/p27kip1 signaling: opposite effects of oxLDL and cholesterol loading. Am. J. Physiol. Cell Physiol., 2017, 313(3), C340-C351.
[109]
Ahmadian, M.; Abbott, M.J.; Tang, T.; Hudak, C.S.; Kim, Y.; Bruss, M.; Hellerstein, M.K.; Lee, H.Y.; Samuel, V.T.; Shulman, G.I.; Wang, Y.; Duncan, R.E.; Kang, C.; Sul, H.S. Desnutrin/ATGL is regulated by AMPK and is required for a brown adipose phenotype. Cell Metab., 2011, 13(6), 739-748.
[110]
Le Master, E.; Huang, R.T.; Zhang, C.; Bogachkov, Y.; Coles, C.; Shentu, T.P.; Sheng, Y.; Fancher, I.S.; Ng, C.; Christoforidis, T.; Subbaiah, P.V.; Berdyshev, E.; Qain, Z.; Eddington, D.T.; Lee, J.; Cho, M.; Fang, Y.; Minshall, R.D.; Levitan, I. Proatherogenic flow increases endothelial stiffness via enhanced CD36 (Cluster of Differentiation 36)-Mediated OxLDL (Oxidized Low-Density Lipoprotein) uptake. Arterioscler. Thromb. Vasc. Biol., 2018, 38(1), 64-75.
[111]
Sawamura, T.; Kume, N.; Aoyama, T.; Moriwaki, H.; Hoshikawa, H.; Aiba, Y.; Tanaka, T.; Miwa, S.; Katsura, Y.; Kita, T.; Masaki, T. An endothelial receptor for oxidized low-density lipoprotein. Nature, 1997, 386(6620), 73-77.
[112]
Afonso, M.S.; Castilho, G.; Lavrador, M.S.; Passarelli, M.; Nakandakare, E.R.; Lottenberg, S.A.; Lottenberg, A.M. The impact of dietary fatty acids on macrophage cholesterol homeostasis. J. Nutr. Biochem., 2014, 25(2), 95-103.
[113]
Mollace, V.; Gliozzi, M.; Musolino, V.; Carresi, C.; Muscoli, S.; Mollace, R.; Tavernese, A.; Gratteri, S.; Palma, E.; Morabito, C.; Vitale, C.; Muscoli, C.; Fini, M.; Romeo, F. Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression. Int. J. Cardiol., 2015, 184, 152-158.
[114]
Marcovecchio, P.M.; Thomas, G.D.; Mikulski, Z.; Ehinger, E.; Mueller, K.A.L.; Blatchley, A.; Wu, R.; Miller, Y.I.; Nguyen, A.T.; Taylor, A.M.; McNamara, C.A.; Ley, K.; Hedrick, C.C. Scavenger receptor CD36 directs nonclassical monocyte patrolling along the endothelium during early atherogenesis. Arterioscler. Thromb. Vasc. Biol., 2017, 37(11), 2043-2052.
[115]
Syväranta, S.; Alanne-Kinnunen, M.; Oörni, K.; Oksjoki, R.; Kupari, M.; Kovanen, P.T.; Helske-Suihko, S. Potential pathological roles for oxidized low-density lipoprotein and scavenger receptors SR-AI, CD36, and LOX-1 in aortic valve stenosis. Atheroscler., 2014, 235(2), 398-407.
[116]
Chen, M.; Masaki, T.; Sawamura, T. LOX-1, the receptor for oxidized low-density lipoprotein identified from endothelial cells: implications in endothelial dysfunction and atherosclerosis. Pharmacol. Ther., 2002, 95(1), 89-100.
[117]
Xu, S.; Ogura, S.; Chen, J.; Little, P.J.; Moss, J.; Liu, P. LOX-1 in atherosclerosis: biological functions and pharmacological modifiers. Cell. Mol. Life Sci., 2013, 70(16), 2859-2872.
[118]
Lawrence, T. The nuclear factor NF-kappa B pathway in inflammation. Cold Spring Harb. Perspect. Biol., 2009, 1(6), a001651.
[119]
Cominacini, L.; Pasini, A.F.; Garbin, U.; Davoli, A.; Tosetti, M.L.; Campagnola, M.; Rigoni, A.; Pastorino, A.M.; Lo Cascio, V.; Sawamura, T. Oxidized low density lipoprotein (ox-LDL) binding to ox-LDL receptor-1 in endothelial cells induces the activation of NF-kappa B through an increased production of intracellular reactive oxygen species. J. Biol. Chem., 2000, 275(17), 12633-12638.
[120]
Tang, Y.; Zhao, J.; Shen, L.; Jin, Y.; Zhang, Z.; Xu, G.; Huang, X. ox-LDL induces endothelial dysfunction by promoting Arp2/3 complex expression. Biochem. Biophys. Res. Commun., 2016, 475(2), 182-188.
[121]
Hong, D.; Bai, Y.P.; Gao, H.C.; Wang, X.; Li, L.F.; Zhang, G.G.; Hu, C.P. Ox-LDL induces endothelial cell apoptosis via the LOX-1-dependent endoplasmic reticulum stress pathway. Atheroscler., 2014, 235(2), 310-317.
[122]
Tang, F.; Yang, T.L.; Zhang, Z.; Li, X.G.; Zhong, Q.Q.; Zhao, T.T.; Gong, L. MicroRNA-21 suppresses ox-LDL-induced human aortic endothelial cells injuries in atherosclerosis through enhancement of autophagic flux: Involvement in promotion of lysosomal function. Exp. Cell Res., 2017, 359(2), 374-383.
[123]
Lv, J.; Yang, L.; Guo, R.; Shi, Y.; Zhang, Z.; Ye, J. Ox-LDL-induced microRNA-155 promotes autophagy in human endothelial cells via repressing the Rheb/ mTOR pathway. Cell. Physiol. Biochem., 2017, 43(4), 1436-1448.
[124]
Qin, B.; Cao, Y.; Yang, H.; Xiao, B.; Lu, Z. MicroRNA-221/222 regulate ox-LDL-induced endothelial apoptosis via Ets-1/p21 inhibition. Mol. Cell. Biochem., 2015, 405(1-2), 115-124.
[125]
Gencer, B.; Kronenberg, F.; Stroes, E.S.; Mach, F. Lipoprotein(a): the revenant. Eur. Heart J., 2017, 38(20), 1553-1560.
[126]
Leibundgut, G.; Scipione, C.; Yin, H.; Schneider, M.; Boffa, M.B.; Green, S.; Yang, X.; Dennis, E.; Witztum, J.L.; Koschinsky, M.L.; Tsimikas, S. Determinants of binding of oxidized phospholipids on apolipoprotein (a) and lipoprotein (a). J. Lipid Res., 2013, 54(10), 2815-2830.
[127]
Bergmark, C.; Dewan, A.; Orsoni, A.; Merki, E.; Miller, E.R.; Shin, M.J.; Binder, C.J.; Hörkkö, S.; Krauss, R.M.; Chapman, M.J.; Witztum, J.L.; Tsimikas, S.A. Novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma. J. Lipid Res., 2008, 49(10), 2230-2239.
[128]
Haque, N.S.; Zhang, X.; French, D.L.; Li, J.; Poon, M.; Fallon, J.T.; Gabel, B.R.; Taubman, M.B.; Koschinsky, M.; Harpel, P.C. CC chemokine I-309 is the principal monocyte chemoattractant induced by apolipoprotein(a) in human vascular endothelial cells. Circulation, 2000, 102(7), 786-792.
[129]
Nakagami, F.; Nakagami, H.; Osako, M.K.; Iwabayashi, M.; Taniyama, Y.; Doi, T.; Shimizu, H.; Shimamura, M.; Rakugi, H.; Morishita, R. Estrogen attenuates vascular remodeling in Lp(a) transgenic mice. Atheroscler., 2010, 211(1), 41-47.
[130]
Zhao, S.P.; Xu, D.Y. Oxidized lipoprotein(a) enhanced the expression of P-selectin in cultured human umbilical vein endothelial cells. Thromb. Res., 2000, 100(6), 501-510.
[131]
Takami, S.; Yamashita, S.; Kihara, S.; Ishigami, M.; Takemura, K.; Kume, N.; Kita, T.; Matsuzawa, Y. Lipoprotein(a) enhances the expression of intercellular adhesion molecule-1 in cultured human umbilical vein endothelial cells. Circulation, 1998, 97(8), 721-728.
[132]
Pellegrino, M.; Furmaniak-Kazmierczak, E.; LeBlanc, J.C.; Cho, T.; Cao, K.; Marcovina, S.M.; Boffa, M.B.; Côté, G.P.; Koschinsky, M.L. The apolipoprotein(a) component of lipoprotein(a) stimulates actin stress fiber formation and loss of cell-cell contact in cultured endothelial cells. J. Biol. Chem., 2004, 279(8), 6526-6533.
[133]
Park, S.Y.; Lee, J.H.; Kim, Y.K.; Kim, C.D.; Rhim, B.Y.; Lee, W.S.; Hong, K.W. Cilostazol prevents remnant lipoprotein particle-induced monocyte adhesion to endothelial cells by suppression of adhesion molecules and monocyte chemoattractant protein-1 expression via lectin-like receptor for oxidized low-density lipoprotein receptor activation. J. Pharmacol. Exp. Ther., 2005, 312(3), 1241-1248.
[134]
Adams, D.H.; Shaw, S. Leucocyte-endothelial interactions and regulation of leucocyte migration. Lancet, 1994, 343(8901), 831-836.
[135]
Norata, G.D.; Grigore, L.; Raselli, S.; Seccomandi, P.M.; Hamsten, A.; Maggi, F.M.; Eriksson, P.; Catapano, A.L. Triglyceride-rich lipoproteins from hypertriglyceridemic subjects induce a pro-inflammatory response in the endothelium: Molecular mechanisms and gene expression studies. J. Mol. Cell. Cardiol., 2006, 40(4), 484-494.
[136]
Williams, C.M.; Maitin, V.; Jackson, K.G. Triacylglycerol-rich lipoprotein-gene interactions in endothelial cells. Biochem. Soc. Trans., 2004, 32(Pt 6), 994-998.
[137]
Maggi, F.M.; Raselli, S.; Grigore, L.; Redaelli, L.; Fantappiè, S.; Catapano, A.L. Lipoprotein remnants and endothelial dysfunction in the postprandial phase. J. Clin. Endocrinol. Metab., 2004, 89(6), 2946-2950.
[138]
Wilmink, H.W.; Twickler, M.B.; Banga, J.D.; Dallinga-Thie, G.M.; Eeltink, H.; Erkelens, D.W.; Rabelink, T.J.; Stroes, E.S. Effect of statin versus fibrate on postprandial endothelial dysfunction: role of remnant-like particles. Cardiovasc. Res., 2001, 50(3), 577-582.
[139]
Ceriello, A.; Assaloni, R.; Da Ros, R.; Maier, A.; Piconi, L.; Quagliaro, L.; Esposito, K.; Giugliano, D. Effect of atorvastatin and irbesartan, alone and in combination, on postprandial endothelial dysfunction, oxidative stress, and inflammation in type 2 diabetic patients. Circulation, 2005, 111(19), 2518-2524.
[140]
Shin, H.K.; Kim, Y.K.; Kim, K.Y.; Lee, J.H.; Hong, K.W. Remnant lipoprotein particles induce apoptosis in endothelial cells by NAD(P)H oxidase-mediated production of superoxide and cytokines via lectin-like oxidized low-density lipoprotein receptor-1 activation: prevention by cilostazol. Circulation, 2004, 109(8), 1022-1028.
[141]
Wang, L.; Sapuri-Butti, A.R.; Aung, H.H.; Parikh, A.N.; Rutledge, J.C. Triglyceride-rich lipoprotein lipolysis increases aggregation of endothelial cell membrane microdomains and produces reactive oxygen species. Am. J. Physiol. Heart Circ. Physiol., 2008, 295(1), H237-H244.
[142]
Dichtl, W.; Nilsson, L.; Goncalves, I.; Ares, M.P.; Banfi, C.; Calara, F.; Hamsten, A.; Eriksson, P.; Nilsson, J. Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells. Circ. Res., 1999, 84(9), 1085-1094.
[143]
Bernelot Moens, S.J.; Verweij, S.L.; Schnitzler, J.G.; Stiekema, L.C.A.; Bos, M.; Langsted, A.; Kuijk, C.; Bekkering, S.; Voermans, C.; Verberne, H.J.; Nordestgaard, B.G.; Stroes, E.S.G.; Kroon, J. Remnant cholesterol elicits arterial wall inflammation and a multilevel cellular immune response in humans. Arterioscler. Thromb. Vasc. Biol., 2017, 37(5), 969-975.
[144]
Tarkin, J.M.; Joshi, F.R.; Rudd, J.H. PET imaging of inflammation in atherosclerosis. Nat. Rev. Cardiol., 2014, 11(8), 443-457.
[145]
Rosenson, R.S.; Brewer, H.B., Jr; Ansell, B.J.; Barter, P.; Chapman, M.J.; Heinecke, J.W.; Kontush, A.; Tall, A.R.; Webb, N.R. Dysfunctional HDL and atherosclerotic cardiovascular disease. Nat. Rev. Cardiol., 2016, 13(1), 48-60.
[146]
Haase, C.L.; Tybjærg-Hansen, A.; Qayyum, A.A.; Schou, J.; Nordestgaard, B.G.; Frikke-Schmidt, R. LCAT, HDL cholesterol and ischemic cardiovascular disease: a Mendelian randomization study of HDL cholesterol in 54,500 individuals. J. Clin. Endocrinol. Metab., 2012, 97(2), E248-E256.
[147]
Di Angelantonio, E.; Gao, P.; Pennells, L.; Kaptoge, S.; Caslake, M.; Thompson, A.; Butterworth, A.S.; Sarwar, N.; Wormser, D.; Saleheen, D.; Ballantyne, C.M.; Psaty, B.M.; Sundström, J.; Ridker, P.M.; Nagel, D.; Gillum, R.F.; Ford, I.; Ducimetiere, P.; Kiechl, S.; Koenig, W.; Dullaart, R.P.; Assmann, G.; D’Agostino, R.B., Sr; Dagenais, G.R.; Cooper, J.A.; Kromhout, D.; Onat, A.; Tipping, R.W.; Gómez-de-la-Cámara, A.; Rosengren, A.; Sutherland, S.E.; Gallacher, J.; Fowkes, F.G.; Casiglia, E.; Hofman, A.; Salomaa, V.; Barrett-Connor, E.; Clarke, R.; Brunner, E.; Jukema, J.W.; Simons, L.A.; Sandhu, M.; Wareham, N.J.; Khaw, K.T.; Kauhanen, J.; Salonen, J.T.; Howard, W.J.; Nordestgaard, B.G.; Wood, A.M.; Thompson, S.G.; Boekholdt, S.M.; Sattar, N.; Packard, C.; Gudnason, V.; Danesh, J.; Danesh, J. Lipid-related markers and cardiovascular disease prediction. JAMA, 2012, 307(23), 2499-2506.
[148]
Campbell, S.; Genest, J. HDL-C: clinical equipoise and vascular endothelial function. Expert Rev. Cardiovasc. Ther., 2013, 11(3), 343-353.
[149]
Annema, W.; von Eckardstein, A. Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy. Transl. Res., 2016, 173, 30-57.
[150]
Aviram, M. Atherosclerosis: cell biology and lipoproteins--inflammation and oxidative stress in atherogenesis: protective role for paraoxonases. Curr. Opin. Lipidol., 2011, 22(3), 243-244.
[151]
Nofer, J.R.; Geigenmüller, S.; Göpfert, C.; Assmann, G.; Buddecke, E.; Schmidt, A. High density lipoprotein-associated lysosphingolipids reduce E-selectin expression in human endothelial cells. Biochem. Biophys. Res. Commun., 2003, 310(1), 98-103.
[152]
Mosig, S.; Rennert, K.; Büttner, P.; Krause, S.; Lütjohann, D.; Soufi, M.; Heller, R.; Funke, H. Monocytes of patients with familial hypercholesterolemia show alterations in cholesterol metabolism. BMC Med. Genomics, 2008, 1, 60.
[153]
Tacke, F.; Alvarez, D.; Kaplan, T.J.; Jakubzick, C.; Spanbroek, R.; Llodra, J.; Garin, A.; Liu, J.; Mack, M.; van Rooijen, N.; Lira, S.A.; Habenicht, A.J.; Randolph, G.J. Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques. J. Clin. Invest., 2007, 117(1), 185-194.
[154]
den Hartigh, L.J.; Connolly-Rohrbach, J.E.; Fore, S.; Huser, T.R.; Rutledge, J.C. Fatty acids from very low-density lipoprotein lipolysis products induce lipid droplet accumulation in human monocytes. J. Immunol., 2010, 184(7), 3927-3936.
[155]
Gower, R.M.; Wu, H.; Foster, G.A.; Devaraj, S.; Jialal, I.; Ballantyne, C.M.; Knowlton, A.A.; Simon, S.I. CD11c/CD18 expression is upregulated on blood monocytes during hypertriglyceridemia and enhances adhesion to vascular cell adhesion molecule-1. Arterioscler. Thromb. Vasc. Biol., 2011, 31(1), 160-166.
[156]
Xu, L.; Dai Perrard, X.; Perrard, J.L.; Yang, D.; Xiao, X.; Teng, B.B.; Simon, S.I.; Ballantyne, C.M.; Wu, H. Foamy monocytes form early and contribute to nascent atherosclerosis in mice with hypercholesterolemia. Arterioscler. Thromb. Vasc. Biol., 2015, 35(8), 1787-1797.
[157]
Wu, H.; Gower, R.M.; Wang, H.; Perrard, X.Y.; Ma, R.; Bullard, D.C.; Burns, A.R.; Paul, A.; Smith, C.W.; Simon, S.I.; Ballantyne, C.M. Functional role of CD11c+ monocytes in atherogenesis associated with hypercholesterolemia. Circulation, 2009, 119(20), 2708-2717.
[158]
Sotiriou, S.N.; Orlova, V.V.; Al-Fakhri, N.; Ihanus, E.; Economopoulou, M.; Isermann, B.; Bdeir, K.; Nawroth, P.P.; Preissner, K.T.; Gahmberg, C.G.; Koschinsky, M.L.; Chavakis, T. Lipoprotein(a) in atherosclerotic plaques recruits inflammatory cells through interaction with Mac-1 integrin. FASEB J., 2006, 20(3), 559-561.
[159]
Patel, S.; Drew, B.G.; Nakhla, S.; Duffy, S.J.; Murphy, A.J.; Barter, P.J.; Rye, K.A.; Chin-Dusting, J.; Hoang, A.; Sviridov, D.; Celermajer, D.S.; Kingwell, B.A. Reconstituted high-density lipoprotein increases plasma high-density lipoprotein anti-inflammatory properties and cholesterol efflux capacity in patients with type 2 diabetes. J. Am. Coll. Cardiol., 2009, 53(11), 962-971.
[160]
Patel, V.K.; Williams, H.; Li, S.C.H.; Fletcher, J.P.; Medbury, H.J. Monocyte inflammatory profile is specific for individuals and associated with altered blood lipid levels. Atheroscler., 2017, 263, 15-23.
[161]
Murphy, A.J.; Woollard, K.J.; Hoang, A.; Mukhamedova, N.; Stirzaker, R.A.; McCormick, S.P.; Remaley, A.T.; Sviridov, D.; Chin-Dusting, J. High-density lipoprotein reduces the human monocyte inflammatory response. Arterioscler. Thromb. Vasc. Biol., 2008, 28(11), 2071-2077.
[162]
Iqbal, A.J.; Barrett, T.J.; Taylor, L.; McNeill, E.; Manmadhan, A.; Recio, C.; Carmineri, A.; Brodermann, M.H.; White, G.E.; Cooper, D.; DiDonato, J.A.; Zamanian-Daryoush, M.; Hazen, S.L.; Channon, K.M.; Greaves, D.R.; Fisher, E.A. Acute exposure to apolipoprotein A1 inhibits macrophage chemotaxis in vitro and monocyte recruitment in vivo. eLife, 2016, 5, 5.
[163]
Ginhoux, F.; Jung, S. Monocytes and macrophages: developmental pathways and tissue homeostasis. Nat. Rev. Immunol., 2014, 14(6), 392-404.
[164]
Dutta, P.; Sager, H.B.; Stengel, K.R.; Naxerova, K.; Courties, G.; Saez, B.; Silberstein, L.; Heidt, T.; Sebas, M.; Sun, Y.; Wojtkiewicz, G.; Feruglio, P.F.; King, K.; Baker, J.N.; van der Laan, A.M.; Borodovsky, A.; Fitzgerald, K.; Hulsmans, M.; Hoyer, F.; Iwamoto, Y.; Vinegoni, C.; Brown, D.; Di Carli, M.; Libby, P.; Hiebert, S.W.; Scadden, D.T.; Swirski, F.K.; Weissleder, R.; Nahrendorf, M. Myocardial infarction activates CCR2(+) hematopoietic stem and progenitor cells. Cell Stem Cell, 2015, 16(5), 477-487.
[165]
Libby, P.; Nahrendorf, M.; Swirski, F.K. Leukocytes link local and systemic inflammation in ischemic cardiovascular disease: an expanded “cardiovascular continuum”. J. Am. Coll. Cardiol., 2016, 67(9), 1091-1103.
[166]
Morrison, S.J.; Scadden, D.T. The bone marrow niche for haematopoietic stem cells. Nature, 2014, 505(7483), 327-334.
[167]
Suda, T.; Arai, F.; Hirao, A. Hematopoietic stem cells and their niche. Trends Immunol., 2005, 26(8), 426-433.
[168]
Rahman, M.S.; Murphy, A.J.; Woollard, K.J. Effects of dyslipidaemia on monocyte production and function in cardiovascular disease. Nat. Rev. Cardiol., 2017, 14(7), 387-400.
[169]
Blue, E.K.; Ballman, K.; Boyle, F.; Oh, E.; Kono, T.; Quinney, S.K.; Thurmond, D.C.; Evans-Molina, C.; Haneline, L.S. Fetal hyperglycemia and a high-fat diet contribute to aberrant glucose tolerance and hematopoiesis in adult rats. Pediatr. Res., 2015, 77(2), 316-325.
[170]
Yvan-Charvet, L.; Pagler, T.; Gautier, E.L.; Avagyan, S.; Siry, R.L.; Han, S.; Welch, C.L.; Wang, N.; Randolph, G.J.; Snoeck, H.W.; Tall, A.R. ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation. Sci., 2010, 328(5986), 1689-1693.

Rights & Permissions Print Cite
Article Metrics
63
6
World Chagas Disease
© 2024 Bentham Science Publishers | Privacy Policy