Generic placeholder image

Current Medicinal Chemistry

Editor-in-Chief

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

Review Article

Triglyceride-Rich Lipoproteins as a Source of Proinflammatory Lipids in the Arterial Wall

Author(s): Katariina Öörni*, Satu Lehti, Peter Sjövall and Petri T. Kovanen

Volume 26, Issue 9, 2019

Page: [1701 - 1710] Pages: 10

DOI: 10.2174/0929867325666180530094819

Price: $65

Abstract

Apolipoprotein B –containing lipoproteins include triglyceride-rich lipoproteins (chylomicrons and their remnants, and very low-density lipoproteins and their remnants) and cholesterol-rich low-density lipoprotein particles. Of these, lipoproteins having sizes below 70-80 nm may enter the arterial wall, where they accumulate and induce the formation of atherosclerotic lesions. The processes that lead to accumulation of lipoprotein-derived lipids in the arterial wall have been largely studied with a focus on the low-density lipoprotein particles. However, recent observational and genetic studies have discovered that the triglyceriderich lipoproteins and their remnants are linked with cardiovascular disease risk. In this review, we describe the potential mechanisms by which the triglyceride-rich remnant lipoproteins can contribute to the development of atherosclerotic lesions, and highlight the differences in the atherogenicity between low-density lipoproteins and the remnant lipoproteins.

Keywords: Chylomicron, VLDL, remnant, triglyceride, cholesterol, atherosclerosis, inflammation.

« Previous
[1]
Brown, M.S.; Kovanen, P.T.; Goldstein, J.L. Regulation of plasma cholesterol by lipoprotein receptors. Science, 1981, 212(4495), 628-635.
[2]
Chapman, M.J.; Ginsberg, H.N.; Amarenco, P.; Andreotti, F.; Borén, J.; Catapano, A.L.; Descamps, O.S.; Fisher, E.; Kovanen, P.T.; Kuivenhoven, J.A.; Lesnik, P.; Masana, L.; Nordestgaard, B.G.; Ray, K.K.; Reiner, Z.; Taskinen, M.R.; Tokgözoglu, L.; Tybjærg-Hansen, A.; Watts, G.F. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur. Heart J., 2011, 32(11), 1345-1361.
[3]
Lehti, S.; Sjövall, P.; Käkelä, R.; Mäyränpää, M.I.; Kovanen, P.T.; Öörni, K. Spatial distributions of lipids in atherosclerosis of human coronary arteries studied by time-of-flight secondary ion mass spectrometry. Am. J. Pathol., 2015, 185(5), 1216-1233.
[4]
Nakajima, K.; Nagamine, T.; Fujita, M.Q.; Ai, M.; Tanaka, A.; Schaefer, E. Apolipoprotein B-48: a unique marker of chylomicron metabolism. Adv. Clin. Chem., 2014, 64, 117-177.
[5]
Moreton, J.R. Atherosclerosis and alimentary hyperlipemia. Science, 1947, 106(2748), 190-191.
[6]
Zilversmit, D.B. Role of triglyceride-rich lipoproteins in atherogenesis. Ann. N. Y. Acad. Sci., 1976, 275, 138-144.
[7]
Born, J.; Matikainen, N.; Adiels, M.; Taskinen, M.R. Postprandial hypertriglyceridemia as a coronary risk factor. Clin. Chim. Acta, 2014, 431, 131-142.
[8]
Toth, P.P. Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease. Vasc. Health Risk Manag., 2016, 12, 171-183.
[9]
Varbo, A.; Nordestgaard, B.G. Remnant lipoproteins. Curr. Opin. Lipidol., 2017, 28(4), 300-307.
[10]
Olivecrona, G. Role of lipoprotein lipase in lipid metabolism. Curr. Opin. Lipidol., 2016, 27(3), 233-241.
[11]
Kumpula, L.S.; Kumpula, J.M.; Taskinen, M.R.; Jauhiainen, M.; Kaski, K.; Ala-Korpela, M. Reconsideration of hydrophobic lipid distributions in lipoprotein particles. Chem. Phys. Lipids, 2008, 155(1), 57-62.
[12]
Nordestgaard, B.G.; Stender, S.; Kjeldsen, K. Reduced atherogenesis in cholesterol-fed diabetic rabbits. Giant lipoproteins do not enter the arterial wall. Arteriosclerosis, 1988, 8(4), 421-428.
[13]
Nordestgaard, B.G.; Zilversmit, D.B. Large lipoproteins are excluded from the arterial wall in diabetic cholesterol-fed rabbits. J. Lipid Res., 1988, 29(11), 1491-1500.
[14]
Shaikh, M.; Wootton, R.; Nordestgaard, B.G.; Baskerville, P.; Lumley, J.S.; La Ville, A.E.; Quiney, J.; Lewis, B. Quantitative studies of transfer in vivo of low density, Sf 12-60, and Sf 60-400 lipoproteins between plasma and arterial intima in humans. Arterioscler. Thromb., 1991, 11(3), 569-577.
[15]
Proctor, S.D.; Vine, D.F.; Mamo, J.C. Arterial permeability and efflux of apolipoprotein B-containing lipoproteins assessed by in situ perfusion and three-dimensional quantitative confocal microscopy. Arterioscler. Thromb. Vasc. Biol., 2004, 24(11), 2162-2167.
[16]
Rutledge, J.C.; Mullick, A.E.; Gardner, G.; Goldberg, I.J. Direct visualization of lipid deposition and reverse lipid transport in a perfused artery: roles of VLDL and HDL. Circ. Res., 2000, 86(7), 768-773.
[17]
Björnheden, T.; Babyi, A.; Bondjers, G.; Wiklund, O. Accumulation of lipoprotein fractions and subfractions in the arterial wall, determined in an in vitro perfusion system. Atherosclerosis, 1996, 123(1-2), 43-56.
[18]
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.
[19]
Cancel, L.M.; Tarbell, J.M. The role of apoptosis in LDL transport through cultured endothelial cell monolayers. Atherosclerosis, 2010, 208(2), 335-341.
[20]
Puhlmann, M.; Weinreich, D.M.; Farma, J.M.; Carroll, N.M.; Turner, E.M.; Alexander, H.R., Jr Interleukin-1beta induced vascular permeability is dependent on induction of endothelial tissue factor (TF) activity. J. Transl. Med., 2005, 3, 37.
[21]
Rozenberg, I.; Sluka, S.H.; Rohrer, L.; Hofmann, J.; Becher, B.; Akhmedov, A.; Soliz, J.; Mocharla, P.; Borén, J.; Johansen, P.; Steffel, J.; Watanabe, T.; Lüscher, T.F.; Tanner, F.C. Histamine H1 receptor promotes atherosclerotic lesion formation by increasing vascular permeability for low-density lipoproteins. Arterioscler. Thromb. Vasc. Biol., 2010, 30(5), 923-930.
[22]
Bot, I.; Shi, G.P.; Kovanen, P.T. Mast cells as effectors in atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2015, 35(2), 265-271.
[23]
Pal, S.; Semorine, K.; Watts, G.F.; Mamo, J. Identification of lipoproteins of intestinal origin in human atherosclerotic plaque. Clin. Chem. Lab. Med., 2003, 41(6), 792-795.
[24]
Nakano, T.; Nakajima, K.; Niimi, M.; Fujita, M.Q.; Nakajima, Y.; Takeichi, S.; Kinoshita, M.; Matsushima, T.; Teramoto, T.; Tanaka, A. Detection of apolipoproteins B-48 and B-100 carrying particles in lipoprotein fractions extracted from human aortic atherosclerotic plaques in sudden cardiac death cases. Clin. Chim. Acta, 2008, 390(1-2), 38-43.
[25]
Lehti, S.; Nguyen, S.D.; Belevich, I.; Vihinen, H.; Heikkilä, H.M.; Soliymani, R.; Käkelä, R.; Saksi, J.; Jauhiainen, M.; Grabowski, G.A.; Kummu, O.; Hörkkö, S.; Baumann, M.; Lindsberg, P.J.; Jokitalo, E.; Kovanen, P.T.; Öörni, K. Extracellular lipid accumulates in human carotid arteries as distinct three-dimensional structures with proinflammatory properties. Am. J. Pathol., 2018, 188(2), 525-538.
[26]
Proctor, S.D.; Mamo, J.C. Intimal retention of cholesterol derived from apolipoprotein B100- and apolipoprotein B48-containing lipoproteins in carotid arteries of Watanabe heritable hyperlipidemic rabbits. Arterioscler. Thromb. Vasc. Biol., 2003, 23(9), 1595-1600.
[27]
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.
[28]
Botham, K.M.; Wheeler-Jones, C.P. Postprandial lipoproteins and the molecular regulation of vascular homeostasis. Prog. Lipid Res., 2013, 52(4), 446-464.
[29]
Tozer, E.C.; Carew, T.E. Residence time of low-density lipoprotein in the normal and atherosclerotic rabbit aorta. Circ. Res., 1997, 80(2), 208-218.
[30]
Schwenke, D.C.; Carew, T.E. Initiation of atherosclerotic lesions in cholesterol-fed rabbits. II. Selective retention of LDL vs. selective increases in LDL permeability in susceptible sites of arteries. Arteriosclerosis, 1989, 9(6), 908-918.
[31]
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. Arteriosclerosis, 1989, 9(6), 895-907.
[32]
Sluimer, J.C.; Kolodgie, F.D.; Bijnens, A.P.; Maxfield, K.; Pacheco, E.; Kutys, B.; Duimel, H.; Frederik, P.M.; van Hinsbergh, V.W.; Virmani, R.; Daemen, M.J. Thin-walled microvessels in human coronary atherosclerotic plaques show incomplete endothelial junctions relevance of compromised structural integrity for intraplaque microvascular leakage. J. Am. Coll. Cardiol., 2009, 53(17), 1517-1527.
[33]
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.
[34]
Nakashima, Y.; Wight, T.N.; Sueishi, K. Early atherosclerosis in humans: role of diffuse intimal thickening and extracellular matrix proteoglycans. Cardiovasc. Res., 2008, 79(1), 14-23.
[35]
Weisgraber, K.H.; Rall, S.C., Jr Human apolipoprotein B-100 heparin-binding sites. J. Biol. Chem., 1987, 262(23), 11097-11103.
[36]
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.
[37]
Flood, C.; Gustafsson, M.; Richardson, P.E.; Harvey, S.C.; Segrest, J.P.; Borén, J. Identification of the proteoglycan binding site in apolipoprotein B48. J. Biol. Chem., 2002, 277(35), 32228-32233.
[38]
Saito, H.; Dhanasekaran, P.; Baldwin, F.; Weisgraber, K.H.; Lund-Katz, S.; Phillips, M.C. Lipid binding-induced conformational change in human apolipoprotein E. Evidence for two lipid-bound states on spherical particles. J. Biol. Chem., 2001, 276(44), 40949-40954.
[39]
Van Craeyveld, E.; Jacobs, F.; Feng, Y.; Thomassen, L.C.; Martens, J.A.; Lievens, J.; Snoeys, J.; De Geest, B. The relative atherogenicity of VLDL and LDL is dependent on the topographic site. J. Lipid Res., 2010, 51(6), 1478-1485.
[40]
Kockx, M.; Jessup, W.; Kritharides, L. Regulation of endogenous apolipoprotein E secretion by macrophages. Arterioscler. Thromb. Vasc. Biol., 2008, 28(6), 1060-1067.
[41]
Olin-Lewis, K.; Krauss, R.M.; La Belle, M.; Blanche, P.J.; Barrett, P.H.; Wight, T.N.; Chait, A. ApoC-III content of apoB-containing lipoproteins is associated with binding to the vascular proteoglycan biglycan. J. Lipid Res., 2002, 43(11), 1969-1977.
[42]
Hiukka, A.; Ståhlman, M.; Pettersson, C.; Levin, M.; Adiels, M.; Teneberg, S.; Leinonen, E.S.; Hultén, L.M.; Wiklund, O.; Oresic, M.; Olofsson, S.O.; Taskinen, M.R.; Ekroos, K.; Borén, J. ApoCIII-enriched LDL in type 2 diabetes displays altered lipid composition, increased susceptibility for sphingomyelinase, and increased binding to biglycan. Diabetes, 2009, 58(9), 2018-2026.
[43]
Naghavi, M.; John, R.; Naguib, S.; Siadaty, M.S.; Grasu, R.; Kurian, K.C.; van Winkle, W.B.; Soller, B.; Litovsky, S.; Madjid, M.; Willerson, J.T.; Casscells, W. pH Heterogeneity of human and rabbit atherosclerotic plaques; a new insight into detection of vulnerable plaque. Atherosclerosis, 2002, 164(1), 27-35.
[44]
Öörni, K.; Rajamäki, K.; Nguyen, S.D.; Lähdesmäki, K.; Plihtari, R.; Lee-Rueckert, M.; Kovanen, P.T. Acidification of the intimal fluid: the perfect storm for atherogenesis. J. Lipid Res., 2015, 56(2), 203-214.
[45]
Sneck, M.; Kovanen, P.T.; Oörni, K. Decrease in pH strongly enhances binding of native, proteolyzed, lipolyzed, and oxidized low density lipoprotein particles to human aortic proteoglycans. J. Biol. Chem., 2005, 280(45), 37449-37454.
[46]
Oörni, K.; Kovanen, P.T. Enhanced extracellular lipid accumulation in acidic environments. Curr. Opin. Lipidol., 2006, 17(5), 534-540.
[47]
Lähdesmäki, K.; Öörni, K.; Alanne-Kinnunen, M.; Jauhiainen, M.; Hurt-Camejo, E.; Kovanen, P.T. Acidity and lipolysis by group V secreted phospholipase A(2) strongly increase the binding of apoB-100-containing lipoproteins to human aortic proteoglycans. Biochim. Biophys. Acta, 2012, 1821(2), 257-267.
[48]
Pentikäinen, M.O.; Oörni, K.; Kovanen, P.T. Lipoprotein lipase (LPL) strongly links native and oxidized low density lipoprotein particles to decorin-coated collagen. Roles for both dimeric and monomeric forms of LPL. J. Biol. Chem., 2000, 275(8), 5694-5701.
[49]
Pentikäinen, M.O.; Oksjoki, R.; Oörni, K.; Kovanen, P.T. Lipoprotein lipase in the arterial wall: linking LDL to the arterial extracellular matrix and much more. Arterioscler. Thromb. Vasc. Biol., 2002, 22(2), 211-217.
[50]
Jonasson, L.; Bondjers, G.; Hansson, G.K. Lipoprotein lipase in atherosclerosis: its presence in smooth muscle cells and absence from macrophages. J. Lipid Res., 1987, 28(4), 437-445.
[51]
Ylä-Herttuala, S.; Lipton, B.A.; Rosenfeld, M.E.; Goldberg, I.J.; Steinberg, D.; Witztum, J.L. Macrophages and smooth muscle cells express lipoprotein lipase in human and rabbit atherosclerotic lesions. Proc. Natl. Acad. Sci. USA, 1991, 88(22), 10143-10147.
[52]
O’Brien, K.D.; Gordon, D.; Deeb, S.; Ferguson, M.; Chait, A. Lipoprotein lipase is synthesized by macrophage-derived foam cells in human coronary atherosclerotic plaques. J. Clin. Invest., 1992, 89(5), 1544-1550.
[53]
Gustafsson, M.; Levin, M.; Skålén, K.; Perman, J.; Fridén, V.; Jirholt, P.; Olofsson, S.O.; Fazio, S.; Linton, M.F.; Semenkovich, C.F.; Olivecrona, G.; Borén, J. Retention of low-density lipoprotein in atherosclerotic lesions of the mouse: evidence for a role of lipoprotein lipase. Circ. Res., 2007, 101(8), 777-783.
[54]
Oörni, K.; Pentikäinen, M.O.; Ala-Korpela, M.; Kovanen, P.T. Aggregation, fusion, and vesicle formation of modified low density lipoprotein particles: molecular mechanisms and effects on matrix interactions. J. Lipid Res., 2000, 41(11), 1703-1714.
[55]
Oörni, K.; Posio, P.; Ala-Korpela, M.; Jauhiainen, M.; Kovanen, P.T. Sphingomyelinase induces aggregation and fusion of small very low-density lipoprotein and intermediate-density lipoprotein particles and increases their retention to human arterial proteoglycans. Arterioscler. Thromb. Vasc. Biol., 2005, 25(8), 1678-1683.
[56]
Marathe, S.; Choi, Y.; Leventhal, A.R.; Tabas, I. Sphingomyelinase converts lipoproteins from apolipoprotein E knockout mice into potent inducers of macrophage foam cell formation. Arterioscler. Thromb. Vasc. Biol., 2000, 20(12), 2607-2613.
[57]
Parthasarathy, S.; Quinn, M.T.; Schwenke, D.C.; Carew, T.E.; Steinberg, D. Oxidative modification of beta-very low density lipoprotein. Potential role in monocyte recruitment and foam cell formation. Arteriosclerosis, 1989, 9(3), 398-404.
[58]
Horrigan, S.; Campbell, J.H.; Campbell, G.R. Oxidation of beta-very low density lipoprotein by endothelial cells enhances its metabolism by smooth muscle cells in culture. Arterioscler. Thromb., 1991, 11(2), 279-289.
[59]
Botham, K.M. Oxidation of chylomicron remnants and vascular dysfunction. Atheroscler. Suppl., 2008, 9(2), 57-61.
[60]
Mas, S.; Martínez-Pinna, R.; Martín-Ventura, J.L.; Pérez, R.; Gomez-Garre, D.; Ortiz, A.; Fernandez-Cruz, A.; Vivanco, F.; Egido, J. Local non-esterified fatty acids correlate with inflammation in atheroma plaques of patients with type 2 diabetes. Diabetes, 2010, 59(6), 1292-1301.
[61]
Haka, A.S.; Grosheva, I.; Chiang, E.; Buxbaum, A.R.; Baird, B.A.; Pierini, L.M.; Maxfield, F.R. Macrophages create an acidic extracellular hydrolytic compartment to digest aggregated lipoproteins. Mol. Biol. Cell, 2009, 20(23), 4932-4940.
[62]
Hakala, J.K.; Oksjoki, R.; Laine, P.; Du, H.; Grabowski, G.A.; Kovanen, P.T.; Pentikäinen, M.O. Lysosomal enzymes are released from cultured human macrophages, hydrolyze LDL in vitro, and are present extracellularly in human atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol., 2003, 23(8), 1430-1436.
[63]
Lähdesmäki, K.; Plihtari, R.; Soininen, P.; Hurt-Camejo, E.; Ala-Korpela, M.; Oörni, K.; Kovanen, P.T. Phospholipase A(2)-modified LDL particles retain the generated hydrolytic products and are more atherogenic at acidic pH. Atherosclerosis, 2009, 207(2), 352-359.
[64]
Chung, B.H.; Tallis, G.A.; Cho, B.H.; Segrest, J.P.; Henkin, Y. Lipolysis-induced partitioning of free fatty acids to lipoproteins: effect on the biological properties of free fatty acids. J. Lipid Res., 1995, 36(9), 1956-1970.
[65]
Yu, X.H.; Fu, Y.C.; Zhang, D.W.; Yin, K.; Tang, C.K. Foam cells in atherosclerosis. Clin. Chim. Acta, 2013, 424, 245-252.
[66]
Allahverdian, S.; Chehroudi, A.C.; McManus, B.M.; Abraham, T.; Francis, G.A. Contribution of intimal smooth muscle cells to cholesterol accumulation and macrophage-like cells in human atherosclerosis. Circulation, 2014, 129(15), 1551-1559.
[67]
Witztum, J.L. You are right too! J. Clin. Invest., 2005, 115(8), 2072-2075.
[68]
Kruth, H.S. Receptor-independent fluid-phase pinocytosis mechanisms for induction of foam cell formation with native low-density lipoprotein particles. Curr. Opin. Lipidol., 2011, 22(5), 386-393.
[69]
Takahashi, S.; Sakai, J.; Fujino, T.; Hattori, H.; Zenimaru, Y.; Suzuki, J.; Miyamori, I.; Yamamoto, T.T. The very low-density lipoprotein (VLDL) receptor: characterization and functions as a peripheral lipoprotein receptor. J. Atheroscler. Thromb., 2004, 11(4), 200-208.
[70]
Nakajima, K.; Nakano, T.; Tanaka, A. The oxidative modification hypothesis of atherosclerosis: the comparison of atherogenic effects on oxidized LDL and remnant lipoproteins in plasma. Clin. Chim. Acta, 2006, 367(1-2), 36-47.
[71]
Mietus-Snyder, M.; Gowri, M.S.; Pitas, R.E. Class A scavenger receptor up-regulation in smooth muscle cells by oxidized low density lipoprotein. Enhancement by calcium flux and concurrent cyclooxygenase-2 up-regulation. J. Biol. Chem., 2000, 275(23), 17661-17670.
[72]
Chellan, B.; Reardon, C.A.; Getz, G.S.; Hofmann Bowman, M.A. Enzymatically Modified Low-Density Lipoprotein Promotes Foam Cell Formation in Smooth Muscle Cells via Macropinocytosis and Enhances Receptor-Mediated Uptake of Oxidized Low-Density Lipoprotein. Arterioscler. Thromb. Vasc. Biol., 2016, 36(6), 1101-1113.
[73]
Argmann, C.A.; Sawyez, C.G.; Li, S.; Nong, Z.; Hegele, R.A.; Pickering, J.G.; Huff, M.W. Human smooth muscle cell subpopulations differentially accumulate cholesteryl ester when exposed to native and oxidized lipoproteins. Arterioscler. Thromb. Vasc. Biol., 2004, 24(7), 1290-1296.
[74]
Boström, P.; Magnusson, B.; Svensson, P.A.; Wiklund, O.; Borén, J.; Carlsson, L.M.; Ståhlman, M.; Olofsson, S.O.; Hultén, L.M. Hypoxia converts human macrophages into triglyceride-loaded foam cells. Arterioscler. Thromb. Vasc. Biol., 2006, 26(8), 1871-1876.
[75]
Lu, M.; Kho, T.; Munford, R.S. Prolonged triglyceride storage in macrophages: pHo trumps pO2 and TLR4. J. Immunol., 2014, 193(3), 1392-1397.
[76]
Huang, Y.L.; Morales-Rosado, J.; Ray, J.; Myers, T.G.; Kho, T.; Lu, M.; Munford, R.S. Toll-like receptor agonists promote prolonged triglyceride storage in macrophages. J. Biol. Chem., 2014, 289(5), 3001-3012.
[77]
Mattsson, L.; Johansson, H.; Ottosson, M.; Bondjers, G.; Wiklund, O. Expression of lipoprotein lipase mRNA and secretion in macrophages isolated from human atherosclerotic aorta. J. Clin. Invest., 1993, 92(4), 1759-1765.
[78]
Smith, E.B.; Keen, G.A.; Grant, A. Factors influencing the accumulation in fibrous plaques of lipid derived from low density lipoprotein. I. Relation between fibrin and immobilization of apo B-containing lipoprotein. Atherosclerosis, 1990, 84(2-3), 165-171.
[79]
Kutkut, I.; Meens, M.J.; McKee, T.A.; Bochaton-Piallat, M.L.; Kwak, B.R. Lymphatic vessels: an emerging actor in atherosclerotic plaque development. Eur. J. Clin. Invest., 2015, 45(1), 100-108.
[80]
Wang, L.; Gill, R.; Pedersen, T.L.; Higgins, L.J.; Newman, J.W.; Rutledge, J.C. Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J. Lipid Res., 2009, 50(2), 204-213.
[81]
Libby, P.; Hansson, G.K. Inflammation and immunity in diseases of the arterial tree: players and layers. Circ. Res., 2015, 116(2), 307-311.
[82]
Varbo, A.; Benn, M.; Tybjærg-Hansen, A.; Nordestgaard, B.G. Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation, 2013, 128(12), 1298-1309.
[83]
Schwartz, E.A.; Reaven, P.D. Lipolysis of triglyceride-rich lipoproteins, vascular inflammation, and atherosclerosis. Biochim. Biophys. Acta, 2012, 1821(5), 858-866.
[84]
Lee, J.Y.; Ye, J.; Gao, Z.; Youn, H.S.; Lee, W.H.; Zhao, L.; Sizemore, N.; Hwang, D.H. Reciprocal modulation of Toll-like receptor-4 signaling pathways involving MyD88 and phosphatidylinositol 3-kinase/AKT by saturated and polyunsaturated fatty acids. J. Biol. Chem., 2003, 278(39), 37041-37051.
[85]
Lee, J.Y.; Zhao, L.; Youn, H.S.; Weatherill, A.R.; Tapping, R.; Feng, L.; Lee, W.H.; Fitzgerald, K.A.; Hwang, D.H. Saturated fatty acid activates but polyunsaturated fatty acid inhibits Toll-like receptor 2 dimerized with Toll-like receptor 6 or 1. J. Biol. Chem., 2004, 279(17), 16971-16979.
[86]
Wong, S.W.; Kwon, M.J.; Choi, A.M.; Kim, H.P.; Nakahira, K.; Hwang, D.H. Fatty acids modulate Toll-like receptor 4 activation through regulation of receptor dimerization and recruitment into lipid rafts in a reactive oxygen species-dependent manner. J. Biol. Chem., 2009, 284(40), 27384-27392.
[87]
Rajamäki, K.; Lappalainen, J.; Oörni, K.; Välimäki, E.; Matikainen, S.; Kovanen, P.T.; Eklund, K.K. Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation. PLoS One, 2010, 5(7), e11765.
[88]
Duewell, P.; Latz, E. Assessment and quantification of crystal-induced lysosomal damage. Methods Mol. Biol., 2013, 1040, 19-27.
[89]
Sheedy, F.J.; Grebe, A.; Rayner, K.J.; Kalantari, P.; Ramkhelawon, B.; Carpenter, S.B.; Becker, C.E.; Ediriweera, H.N.; Mullick, A.E.; Golenbock, D.T.; Stuart, L.M.; Latz, E.; Fitzgerald, K.A.; Moore, K.J. CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation. Nat. Immunol., 2013, 14(8), 812-820.
[90]
Schwartz, E.A.; Zhang, W.Y.; Karnik, S.K.; Borwege, S.; Anand, V.R.; Laine, P.S.; Su, Y.; Reaven, P.D. Nutrient modification of the innate immune response: a novel mechanism by which saturated fatty acids greatly amplify monocyte inflammation. Arterioscler. Thromb. Vasc. Biol., 2010, 30(4), 802-808.
[91]
Deevska, G.M.; Sunkara, M.; Morris, A.J.; Nikolova-Karakashian, M.N. Characterization of secretory sphingomyelinase activity, lipoprotein sphingolipid content and LDL aggregation in ldlr-/- mice fed on a high-fat diet. Biosci. Rep., 2012, 32(5), 479-490.

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy