Articles |
From the Division of Endocrinology and Metabolic Diseases, Thomas Jefferson University, Philadelphia, Pa (K.J.W.), and the Departments of Medicine and Anatomy and Cell Biology, Columbia University, New York, NY (I.T.).
Correspondence to Kevin Jon Williams, MD, Division of Endocrinology and Metabolic Diseases, Thomas Jefferson University, Jefferson Alumni Hall, Suite 349, 1020 Locust St, Philadelphia, PA 19107-6799. E-mail k_williams@lac.jci.tju.edu.
| Introduction |
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| Competing Hypotheses |
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The response-to-injury hypothesis originally presupposed endothelial desquamation as the key event in atherogenesis.7 8 9 It is now clear, however, that developing atheromata are covered by an intact endothelial layer throughout most stages of lesion progression: lipoprotein retention, fatty streak formation, and formation of advanced lesions.5 6 12 13 14 15 In humans, only the most complicated, ulcerated lesions lose their endothelial layer. Furthermore, in some experimental models, an intact endothelium is required for lesion initiation and development, which do not occur in adjacent areas of denudation.16 17 18 Gross endothelial denudation, though presumably important in restenosis after balloon injury19 and in very advanced complicated plaques, does not appear to be central to early atherogenesis.5
A refinement of the response-to-injury hypothesis states that endothelial injuries that are insufficient to cause gross denudation but severe enough to cause functional modifications are key to atherogenesis.10 11 12 20 A major hypothesized change in endothelial function was increased permeability,21 22 particularly to atherogenic lipoproteins.23 24 25 26 27 This idea is related to the lipid infiltration hypothesis,5 which originated with Anichkov and Khalatov28 (reviewed in References 29 and 3029 30 ). Alterations in permeability or even microscopic losses of endothelial cells in excess of those due to normal cell turnover are not mechanistically required for atherogenesis, however, because normal, healthy endothelium transports31 32 or "leaks"26 33 many molecules, including lipoproteins (reviewed in Reference 2727 ). In fact, the rate of LDL entry into the normal, healthy arterial wall vastly exceeds the LDL accumulation rate.34 Most important, seminal studies by Schwenke and Carew35 36 showed in vivo that the early prelesional accumulation of atherogenic lipoproteins within the arterial wall is focally concentrated in sites that are known to be prone to the later development of atheromata, but that the rates of lipoprotein entry into prelesional susceptible versus resistant sites were not different (cf Reference 22 ). These studies indicate that retention, not enhanced endothelial permeability to lipoprotein influx, is the key pathological event in this experimental model. Subsequent studies in several other animal models have demonstrated either increased23 24 25 26 or decreased37 rates of lipoprotein entry into atherosclerosis-susceptible sites, suggesting a nonessential role for alterations in endothelial permeability. All studies agree, however, that prelesional susceptible arterial sites show enhanced retention of apoB-rich, atherogenic lipoproteins.35 36 38 39 40 41 We conclude that alterations in endothelial permeability, though apparently not essential to lesion development, may play a contributory role, eg, in smoking,42 dyslipidemias27 37 (cf Reference 3636 ), and possibly hypertension27 (cf Reference 4343 ), but only if some of the infiltrated material is retained.35
Several other functional modifications have been documented in the endothelial layer in vivo during atherogenesis, but these occur comparatively late. For example, in rabbits, cell adhesion molecules,44 the earliest known being vascular cell adhesion molecule1 (VCAM-1), are expressed by endothelial cells that overlie lesions, but only after more than 4 days of severe hypercholesterolemia and resultant foam cell formation.45 In contrast, lipoprotein retention and aggregation are detectable within minutes to hours after the onset of hypercholesterolemia.31 36 41 46 Furthermore, atherogenic lipoproteins and their components have been shown to regulate endothelial expression of cell-adhesion molecules.12 47 48 49 The most straightforward conclusion is that the earliest known endothelial changes during atherogenesis in vivo, such as VCAM-1 expression, cannot be a cause, and are likely to be a consequence, of the initial retention of lipoproteins within the arterial wall (see "Future Directions").
The effect of turbulent blood flow on the arterial wall deserves special comment, particularly because it can be such an early influence. Arterial segments that are subject to turbulent blood flow, such as those at branch points or during hypertension, show a predisposition to lesion development, though the precise relationship in vivo may be complicated.50 Because of the response-to-injury hypothesis, the connection between blood flow and atherogenesis has led to many studies on the effects of shear stress on the endothelium in cell culture experiments. Many alterations have been reported,12 18 51 such as intracellular calcium mobilization, ion channel activation, cytoskeletal changes, altered cellular alignment, cell surface streamlining,52 increased endothelial cell division,53 stimulation of specific transcription factors,54 and production of potentially atherogenic molecules, such as vasoactive,55 adhesive,56 and growth12 20 57 factors. Somewhat different results are obtained in vitro when shear is low instead of high, constant instead of pulsatile, laminar instead of turbulent, or spatially uniform instead of graded,12 51 53 but the overall findings in vitro strongly support a contributory role for shear stressinduced alterations of the endothelium during atherogenesis.
In vivo, however, it is clear that sheer stressinduced endothelial alterations are neither necessary nor sufficient for atherogenesis. In vivo lesion development at sites of turbulent flow shows an absolute requirement for high plasma concentrations of atherogenic lipoproteins relative to those that occur naturally in nonhuman, nonatherosclerotic mammals: the plasma concentration of LDL cholesterol must exceed 2 mmol/L (80 mg/dL) for atherogenesis, even at sites of high shear stress.58 59 Furthermore, at sufficiently high plasma lipoprotein concentrations, lesions develop even at sites of low shear stress, such as at nonbranch points6 60 or within the pulmonary arteries.60 61 Although stress-induced endothelial changes can play a contributory role in atherogenesis, the most directly relevant functional changes that have been documented at prelesional sites that are susceptible to atherogenesis, including those that are subject to turbulent blood flow, are altered proteoglycan structure62 63 64 65 66 and increased lipoprotein retention36 39 46 67 68 69 (see above).
We therefore propose that the atherogenic effects of sheer stress in vivo are entirely dependent on lipoprotein retention within the arterial wall and are limited to increased local vulnerability to lipoprotein retention and the consequences thereof. Specifically, we hypothesize that the role of shear stress in early atherogenesis is mediated primarily through the stimulation of intramural synthesis of molecules, such as proteoglycans, that promote lipoprotein retention (see References 63, 64, 66, 70, and 7163 64 66 70 71 ). Later, once vessel segments have accumulated retained lipoproteins, the threshold for injury and activation from continued shear stress may be lowered. Many stimuli can activate endothelial cells, and synergy is likely between shear stress and, for example, oxidative breakdown products of retained lipoproteins. The same general lines of reasoning can be used to argue against a central role for other potential activators of the endothelium, such as viruses72 or homocysteine,9 12 20 73 which are likewise neither necessary nor sufficient for lesion development in vivo. Note that these hypotheses about the central role of retained lipoproteins are testable (see "Future Directions").
The second process that has been proposed to be central to atherogenesis is lipoprotein oxidation.74 75 76 Current evidence indicates, however, that pathophysiologically important oxidation can occur only after the retention of lipoproteins within the sequestered microenvironment of the arterial wall. Lipoprotein oxidation by cells or transition metals in vitro is blocked by small concentrations of plasma or plasma proteins,77 such as albumin78 79 80 81 82 83 (cf Reference 8484 ), and any oxidized lipoproteins that might appear in the plasma in vivo would be rapidly removed by the liver,85 86 rather than be deposited into developing lesions within the arterial wall.87 In fact, oxidation may be regarded as a normal, expected consequence of lipoprotein trapping: studies in vitro indicate that once lipoproteins are sequestered from the protective elements of plasma, nearby healthy arterial cells will cause oxidation,75 apparently through their efficient generation of thiols.88 89 In vivo, myeloperoxidases may be involved.90 Note that adherence of LDL to arterial proteoglycans increases LDL's susceptibility to oxidation in vitro71 91 (see below), but that prior oxidation of LDL does not enhance its retention in arteries.87 Consistent with these results, apoB is retained in the human intima before it is detectably oxidized.92 The most straightforward conclusion is that oxidation is a normal, expected consequence of intramural sequestration of sufficient quantities of atherogenic lipoproteins within an otherwise healthy artery.
The importance of lipoprotein oxidation in lesion development is supported by discoveries of many biological consequences in vitro that are consistent with atherogenesis,48 74 75 93 by demonstrations of antiatherogenic effects in experimental animals of compounds with antioxidant actions,94 95 96 and by the findings in humans of oxidized epitopes within lesions92 97 (see Reference 9898 ) and of antioxidized LDL antibodies within lesions99 and in plasma.100 Nevertheless, there are also reports that show the ineffectiveness of antioxidants on atherogenesis. For example, recent reports of humans who consumed antioxidant vitamins101 102 or who were given probucol103 104 and of animals that were given a potent antioxidant analogue of probucol that does not affect plasma lipoprotein concentrations105 106 (see Reference 107107 ) failed to find beneficial effects of these treatments on disease. Note that vitamin E and probucol, which appear to be antiatherogenic in humans102 and animals,94 95 respectively, have many actions besides inhibition of lipoprotein oxidation.102 104 105 108 109 Because even minimal oxidation of LDL, which has been described in human lesions110 (see also Reference 111111 ), produces many potentially harmful biological effects,93 lipoprotein oxidation is unlikely to be a rate-limiting step in atherogenesis. Thus, nearly total inhibition of oxidation of retained lipoproteins may be required before there would be any substantial effect on lesion development in vivo (cf Reference 105105 ).
| Evidence to Support Retention as the Key Event |
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Several lines of evidence indicate that intramural retention of atherogenic lipoproteins involves extracellular matrix, chiefly proteoglycans1 71 and perhaps other structural elements,114 115 116 117 118 119 and lipolytic enzymes, chiefly lipoprotein lipase (LpL)120 121 122 123 124 125 126 127 and sphingomyelinase (SMase).127 128 129 130 First, all of these molecules are present to varying degrees within the normal arterial wall.70 71 120 128 131 132 133 Thus, they are available to participate in the earliest stages of atherogenesis. Second, retained apoB in extremely early46 69 as well as advanced64 71 lesions is closely associated with arterial proteoglycans. Purified arterial proteoglycans, particularly those from lesion-prone sites,66 134 bind LDL in vitro, particularly LDL from patients with coronary artery disease.135 136 This interaction involves several well-defined, positively charged segments of apoB.71 137 Third, LpL enhances adherence of LDL in vitro to the matrix that is derived from normal endothelial125 138 and smooth muscle127 cells and to normal cell-surface proteoglycans.122 123 124 125 126 127 139 This adherence is independent of LpL enzymatic activity122 123 125 127 (cf References 120 and 121120 121 ) and appears to occur in vessels enriched in situ with LpL.140 Fourth, a linkage between peritoneal macrophage production of LpL and susceptibility to atherosclerosis has been documented in recombinant inbred mice.141 Results in humans indicate a linkage between LpL polymorphisms and coronary artery disease, though without a linkage between LpL polymorphisms and specific plasma lipoprotein patterns, thus suggesting that the effects on lesion development are independent of plasma changes.142 A genetic absence of LpL in humans has long been known to cause hyperlipidemia without increased atherosclerosis,121 presumably because of poor generation of small, cholesteryl esterrich particles143 that are able to enter the arterial wall27 and loss of LpL-facilitated binding to arterial proteoglycans.122 123 124 125 126 127 More recent work in humans indicates that the single most important determinant of lesion development in homozygous familial hypercholesterolemia is the postheparin plasma concentration of LpL mass, not enzymatic activity; this is consistent with a structural effect.144 Fifth, SMase causes the formation of LDL microaggregates129 that morphologically resemble the intramural particles seen 2 hours after rapid induction of hypercholesterolemia,46 and LpL and SMase synergistically interact to cause massive retention and aggregation of LDL and Lp(a) in vitro to arterial cell proteoglycans and matrix.127 The arterial wall SMase128 was recently shown to act on the LDL retained in aortic strips ex vivo.130 At later stages, once atherogenesis has begun, the content of specific proteoglycans,64 65 66 71 145 LpL,120 131 132 133 146 147 148 and SMase128 increases in lesional areas, thereby apparently accelerating the disease.
The factors responsible for focal retention of lipoproteins and subsequent lesion development, however, are not clear. Because prelesional differences in lipoprotein retention between susceptible versus resistant arterial sites are so rapidly apparent after induction of hypercholesterolemia,35 there are likely to be preexisting local differences in apoB-retentive molecules. Proteoglycan variations alone may not explain the focal development of early lesions, because potentially atherogenic proteoglycans are abundant and ubiquitous throughout the arterial tree,70 though focal alterations in proteoglycans have been documented in prelesional63 64 65 66 and lesional145 149 sites. The enzymes LpL and SMase show enhanced expression in established human133 146 148 and animal133 lesions, and arterial contents of LpL were shown two decades ago to correlate strongly with the arterial accumulation of cholesteryl ester during atherogenesis in rabbits (r=0.9).121 Nevertheless, the status of proteoglycans, LpL, SMase, and possibly other apoB-retentive molecules in prelesional susceptible versus prelesional resistant sites remains an important area for study (see "Future Directions").
| Consequences of Retention |
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B and stimulation of apoptosis or
mitogenesis.156 157 LDL that has been aggregated or otherwise modified by arterial proteoglycans under a variety of conditions in vitro is avidly taken up by normal cultured macrophages and smooth muscle cells,134 leading to foam cell formation.136 151 158 This avid uptake may involve several different receptors,122 123 124 125 126 134 139 158 159 of which only the LDL receptors are known to be nonessential, in that their genetic absence does not impede arterial lipoprotein accumulation160 or atherogenesis60 161 in vivo, in contrast to the situation with LpL deficiency (see above). The conversion of macrophages to foam cells stimulates the release of more LpL133 146 147 148 162 163 and other potentially atherogenic factors164 165 166 and has been shown to alter proteoglycan metabolism.167 Retained, altered lipoproteins155 168 169 and nearby macrophages170 171 can stimulate chemotaxis and transformation of smooth muscle cells from the contractile to the proliferative state, which in smooth muscle cells causes increased synthesis of proteoglycans,64 172 including LDL-binding proteoglycans,173 and possibly LpL132 133 (cf Reference 146146 ). Thus, retained lipoproteins can directly or indirectly provoke all known features of early lesions and, by stimulating local synthesis of proteoglycans and LpL, can accelerate further lipoprotein retention and aggregation.
Lesion development may be altered by local cellular expression of apoE within the arterial wall. As macrophages become foam cells in situ, they appear to increase their synthesis of apoE,148 174 a molecule that has been shown in vitro to release lipoproteins from the extracellular matrix175 (see Reference 137137 ). The ultimate fate of these released lipoproteins, however, is unclear. They could leave the lesion, or they could be taken up by arterial cells, particularly through apoE-mediated binding.
The atherogenic nature of Lp(a) may originate from its extensive propensity for intramural retention.41 136 176 177 178 Despite plasma concentrations of Lp(a) that are far lower than those of other apoB-rich lipoproteins, Lp(a) may account for most of the apoB in human lesions.179 180 In vitro, Lp(a) binds to arterial proteoglycans with greater affinity176 and capacity176 181 than does LDL. Avid cellular uptake of Lp(a) by at least four processes may then occur: through scavenger receptors after oxidation86 ; through the heparan sulfateproteoglycan pathway in the presence of intramural LpL122 123 ; by phagocytosis following aggregation and cross-linking by LpL, SMase, and proteoglycans127 ; and by a specific Lp(a)/apo(a) receptor on cholesterol-enriched macrophages.182 183 After Lp(a) retention, many other biological effects occur, including enhanced LDL retention,184 stimulation of smooth muscle cell proliferation,185 and, possibly, local inhibition of lysis of microthrombi186 187 188 189 (cf References 190 through 192190 191 192 ).
| Future Directions |
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Tools now exist or can be developed to assess the roles of proteoglycans and arterial wall enzymes in very early atherogenesis. Many proteoglycan core proteins of endothelial194 195 196 and smooth muscle194 195 197 198 199 200 201 202 cells have been cloned and sequenced, which would allow linkage studies in animals and humans and direct genetic manipulation, particularly at lesion-susceptible branch points. Enzymes that are involved in proteoglycan side-chain assembly are still being characterized,203 204 205 206 but we suggest that polymorphisms might play a role in atherosclerosis susceptibility (see References 207 and 208207 208 ). To establish a causal role for LpL in atherogenesis in vivo, direct stimulation and especially suppression of intramural arterial LpL must be done, followed by an examination of lesion progression (see Reference 140140 ). Because several functional domains within LpL have already been characterized,209 specific constructs can be engineered to separately examine in vivo the atherogenicity of its enzymatic121 versus structural122 123 125 127 actions. Two decades ago, lesions were shown to be enriched with SMase, but detailed enzymatic or molecular characterization of this lipase activity is still lacking, thus preventing linkage studies or genetic manipulation. The mechanism of SMase-induced aggregation in vitro has been shown to depend on the generation of ceramide.130 Thus, to implicate SMase in atherogenesis, lesional lipoproteins will have to be shown to be enriched in ceramide.
Investigation into the local roles of apoproteins and other molecules in very early atherogenesis can also be performed. Transgenic mice that overexpress apoE in the arterial wall, among other sites, have shown reduced atherosclerosis in one preliminary report,210 consistent with the hypothesis of a local protective role for this molecule in vivo.175 211 Transgenic mice that overexpress apoA-I show reduced lesion development,212 213 214 perhaps because of accelerated reverse cholesterol transport, but possibly because of the local inhibitory effects that apoA-I particles exert on aggregation215 216 and oxidation77 80 84 215 217 of atherogenic lipoproteins. It will be interesting to develop animal models in which overexpression of apoE or apoA-I is cleanly confined to the arterial wall. The physical characteristics of LDL, including its size,218 219 apoB conformation,220 or sialic acid content,221 may affect binding affinity to arterial proteoglycans135 219 221 and subsequent oxidation.220 222 Apo(a) polymorphisms177 should also be examined.
Tools exist as well to investigate the proposed sequence of events in early atherogenesis, subsequent to lipoprotein retention. For example, on the basis of the apparent sequence of events in vivo, we predict that massive retention of LDL or Lp(a) by smooth muscle cells or matrix127 will stimulate nearby endothelial and possibly smooth muscle cells127 152 223 to express cell adhesion molecules, chemoattractants, and growth factors (see "Competing Hypotheses"). A likely mechanism would be oxidation of the retained lipoproteins, followed by release of biologically active components, such as lysophosphatidylcholine, which is known to stimulate the expression of VCAM-1, platelet-derived growth factor, and other molecules by otherwise-normal endothelium.224 The prediction can be tested by coculture in vitro,84 with specific emphasis on the search for lipoprotein retention as an initial event. In addition, we predict that one key atherogenic effect of turbulent blood flow on prelesional sites in vivo is the locally enhanced expression of apoB-retaining molecules, particularly by vascular smooth muscle cells. A search for these molecules in susceptible versus resistant prelesional arterial sites could be undertaken, the molecules genetically manipulated if already cloned, and the effects on atherogenesis examined. Possible mechanisms for altered expression of these molecules would include direct effects of hemodynamic forces acting through sheer stress responseelements in underlying smooth muscle cells18 or through endothelium-dependent effects,63 including direct electrical communication between the endothelium and smooth muscle18 225 or humoral signals.63 For example, transforming growth factorß is expressed by the endothelium under control of a shear stressresponsive element57 and is known to stimulate synthesis of chondroitin sulfate proteoglycans by smooth muscle cells.226 227
Finally, the search for additional molecules or mechanisms that may be important in vivo to lipoprotein retention and responses to retention should continue. For example, collagen,114 fibrin,115 116 fibronectin,117 118 119 and matrix-bound phospholipase A2228 229 have been implicated in several studies. Also, the LDL receptorrelated protein, which binds LpL230 and apoE231 on ligand blots in vitro, has recently been reported to be present in normal and lesional arteries.232 233 Of particular interest is how an arterial segment might remain healthy after the entry of lipoproteins (see Reference 9292 ). For example, there is substantial and well-documented evidence for the egress of atherogenic lipoproteins from the normal arterial wall,27 36 which has generally been assumed to be passive, though it may not be. Other processes that could blunt or enhance oxidative and inflammatory responses to retained lipoproteins show genetic variability in mice234 and merit further study in humans.
Arterial retention of atherogenic lipoproteins is a logical target for therapeutic intervention. So far, three strategies specifically directed against lipoprotein retention have been proposed in the literature. The first strategy is the local use of molecules that interfere with adherence of apoB or apo(a)-apoB to arterial proteoglycans. As noted before, apoE is a promising candidate, in vitro137 175 and possibly in mice.210 Boosting local expression of apoE in human arterial segments, however, would be difficult at present and may require gene therapy, an approach still in its infancy. Other potential candidates include apoB fragments137 or other proteoglycan-binding peptides.235 236 237 The second strategy proposed in the literature is inhibition of intra-arterial SMase activity.129 The effects of SMase, unlike the effect of LpL, involve its enzymatic action.130 Specific enzymatic inhibitors could test its role in vivo and might provide therapeutic benefit. A third strategy to reduce arterial retention of LDL is the use of nifedipine,238 a calcium-channel blocker that alters many cellular functions,239 including arterial retention of autologous, but not human, LDL in normocholesterolemic rabbits.238 Note, however, that calcium-channel blockers do not appear to affect atherogenesis in LDL receptordeficient rabbits, which exhibit nondietary hyperlipidemia.240 Other novel targets to consider would be inhibition of intramural production of proteoglycans or LpL, alteration of cytokine expression, such as transforming growth factorß, and perhaps stimulation of ceramidase production.
| Concluding Remarks |
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| Acknowledgments |
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Received December 5, 1994; accepted February 21, 1995.
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M. Rahmani, R. P. Cruz, D. J. Granville, and B. M. McManus Allograft Vasculopathy Versus Atherosclerosis Circ. Res., October 13, 2006; 99(8): 801 - 815. [Abstract] [Full Text] [PDF] |
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L. A. Cuniberti, P. G. Stutzbach, E. Guevara, G. G. Yannarelli, R. P. Laguens, and R. R. Favaloro Development of Mild Aortic Valve Stenosis in a Rabbit Model of Hypertension J. Am. Coll. Cardiol., June 6, 2006; 47(11): 2303 - 2309. [Abstract] [Full Text] [PDF] |
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J. Dong, J. Liu, B. Lou, Z. Li, X. Ye, M. Wu, and X.-C. Jiang Adenovirus-mediated overexpression of sphingomyelin synthases 1 and 2 increases the atherogenic potential in mice J. Lipid Res., June 1, 2006; 47(6): 1307 - 1314. [Abstract] [Full Text] [PDF] |
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K. J. Williams and I. Tabas Letter by Williams and Tabas Regarding Article "Atherosclerosis 2005: Recent Discoveries and Novel Hypotheses" Circulation, May 30, 2006; 113(21): e782 - e782. [Full Text] [PDF] |
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J. Nigro, N. Osman, A. M. Dart, and P. J. Little Insulin Resistance and Atherosclerosis Endocr. Rev., May 1, 2006; 27(3): 242 - 259. [Abstract] [Full Text] [PDF] |
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L. M. Wilson, C. L. L. Pham, A. J. Jenkins, J. D. Wade, A. F. Hill, M. A. Perugini, and G. J. Howlett High density lipoproteins bind A{beta} and apolipoprotein C-II amyloid fibrils J. Lipid Res., April 1, 2006; 47(4): 755 - 760. [Abstract] [Full Text] [PDF] |
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M. Y. Chang, C.-Y. Han, T. N. Wight, and A. Chait Antioxidants Inhibit the Ability of Lysophosphatidylcholine to Regulate Proteoglycan Synthesis Arterioscler. Thromb. Vasc. Biol., March 1, 2006; 26(3): 494 - 500. [Abstract] [Full Text] [PDF] |
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R. Oksjoki, P. T. Kovanen, K. A. Lindstedt, B. Jansson, and M. O. Pentikainen OxLDL-IgG Immune Complexes Induce Survival of Human Monocytes Arterioscler. Thromb. Vasc. Biol., March 1, 2006; 26(3): 576 - 583. [Abstract] [Full Text] [PDF] |
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L. D. Adams, R. L. Geary, J. Li, A. Rossini, and S. M. Schwartz Expression Profiling Identifies Smooth Muscle Cell Diversity Within Human Intima and Plaque Fibrous Cap: Loss of RGS5 Distinguishes the Cap Arterioscler. Thromb. Vasc. Biol., February 1, 2006; 26(2): 319 - 325. [Abstract] [Full Text] [PDF] |
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C. Qin, T. Nagao, I. Grosheva, F. R. Maxfield, and L. M. Pierini Elevated Plasma Membrane Cholesterol Content Alters Macrophage Signaling and Function Arterioscler. Thromb. Vasc. Biol., February 1, 2006; 26(2): 372 - 378. [Abstract] [Full Text] [PDF] |
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M. Rodriguez-Lee, G. Ostergren-Lunden, B. Wallin, J. Moses, G. Bondjers, and G. Camejo Fatty Acids Cause Alterations of Human Arterial Smooth Muscle Cell Proteoglycans That Increase the Affinity for Low-Density Lipoprotein Arterioscler. Thromb. Vasc. Biol., January 1, 2006; 26(1): 130 - 135. [Abstract] [Full Text] [PDF] |
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C. Edelstein, M. Yousef, and A. M. Scanu Elements in the C terminus of apolipoprotein [a] responsible for the binding to the tenth type III module of human fibronectin J. Lipid Res., December 1, 2005; 46(12): 2673 - 2680. [Abstract] [Full Text] [PDF] |
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M. Sneck, P. T. Kovanen, and K. Oorni Decrease in pH Strongly Enhances Binding of Native, Proteolyzed, Lipolyzed, and Oxidized Low Density Lipoprotein Particles to Human Aortic Proteoglycans J. Biol. Chem., November 11, 2005; 280(45): 37449 - 37454. [Abstract] [Full Text] [PDF] |
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I. Tabas Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis: The Importance of Lesion Stage and Phagocytic Efficiency Arterioscler. Thromb. Vasc. Biol., November 1, 2005; 25(11): 2255 - 2264. [Abstract] [Full Text] [PDF] |
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B. B. Boyanovsky, D. R. van der Westhuyzen, and N. R. Webb Group V Secretory Phospholipase A2-modified Low Density Lipoprotein Promotes Foam Cell Formation by a SR-A- and CD36-independent Process That Involves Cellular Proteoglycans J. Biol. Chem., September 23, 2005; 280(38): 32746 - 32752. [Abstract] [Full Text] [PDF] |
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V. Fuster, P. R. Moreno, Z. A. Fayad, R. Corti, and J. J. Badimon Atherothrombosis and High-Risk Plaque: Part I: Evolving Concepts J. Am. Coll. Cardiol., September 20, 2005; 46(6): 937 - 954. [Abstract] [Full Text] [PDF] |
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A. Daugherty, N. R. Webb, D. L. Rateri, and V. L. King Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis J. Lipid Res., September 1, 2005; 46(9): 1812 - 1822. [Abstract] [Full Text] [PDF] |
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X. Zeng, J. Chen, Y. I. Miller, K. Javaherian, and K. S. Moulton Endostatin binds biglycan and LDL and interferes with LDL retention to the subendothelial matrix during atherosclerosis J. Lipid Res., September 1, 2005; 46(9): 1849 - 1859. [Abstract] [Full Text] [PDF] |
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P. Davidsson, J. Hulthe, B. Fagerberg, B.-M. Olsson, C. Hallberg, B. Dahllof, and G. Camejo A proteomic study of the apolipoproteins in LDL subclasses in patients with the metabolic syndrome and type 2 diabetes J. Lipid Res., September 1, 2005; 46(9): 1999 - 2006. [Abstract] [Full Text] [PDF] |
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P. Talusan, S. Bedri, S. Yang, T. Kattapuram, N. Silva, P. J. Roughley, and J. R. Stone Analysis of Intimal Proteoglycans in Atherosclerosis-prone and Atherosclerosis-resistant Human Arteries by Mass Spectrometry Mol. Cell. Proteomics, September 1, 2005; 4(9): 1350 - 1357. [Abstract] [Full Text] [PDF] |
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J. Tian, K. Ishibashi, K. Ishibashi, K. Reiser, R. Grebe, S. Biswal, P. Gehlbach, and J. T. Handa Advanced glycation endproduct-induced aging of the retinal pigment epithelium and choroid: A comprehensive transcriptional response PNAS, August 16, 2005; 102(33): 11846 - 11851. [Abstract] [Full Text] [PDF] |
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K. J. Williams and I. Tabas Lipoprotein Retention--and Clues for Atheroma Regression Arterioscler. Thromb. Vasc. Biol., August 1, 2005; 25(8): 1536 - 1540. [Abstract] [Full Text] [PDF] |
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K. Oorni, P. Posio, M. Ala-Korpela, M. Jauhiainen, and P. T. Kovanen 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., August 1, 2005; 25(8): 1678 - 1683. [Abstract] [Full Text] [PDF] |
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K. Reifenberg, H.-A. Lehr, D. Baskal, E. Wiese, S. C. Schaefer, S. Black, D. Samols, M. Torzewski, K. J. Lackner, M. Husmann, et al. Role of C-Reactive Protein in Atherogenesis: Can the Apolipoprotein E Knockout Mouse Provide the Answer? Arterioscler. Thromb. Vasc. Biol., August 1, 2005; 25(8): 1641 - 1646. [Abstract] [Full Text] [PDF] |
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C.-M. Li, B. H. Chung, J. B. Presley, G. Malek, X. Zhang, N. Dashti, L. Li, J. Chen, K. Bradley, H. S. Kruth, et al. Lipoprotein-like Particles and Cholesteryl Esters in Human Bruch's Membrane: Initial Characterization Invest. Ophthalmol. Vis. Sci., July 1, 2005; 46(7): 2576 - 2586. [Abstract] [Full Text] [PDF] |
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C.-M. Li, J. B. Presley, X. Zhang, N. Dashti, B. H. Chung, N. E. Medeiros, C. Guidry, and C. A. Curcio Retina expresses microsomal triglyceride transfer protein: implications for age-related maculopathy J. Lipid Res., April 1, 2005; 46(4): 628 - 640. [Abstract] [Full Text] [PDF] |
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K. Hashimura, K. Sudhir, J. Nigro, S. Ling, M. R. I. Williams, P. A. Komesaroff, and P. J. Little Androgens Stimulate Human Vascular Smooth Muscle Cell Proteoglycan Biosynthesis and Increase Lipoprotein Binding Endocrinology, April 1, 2005; 146(4): 2085 - 2090. [Abstract] [Full Text] [PDF] |
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K. D. O'Brien, T. O. McDonald, V. Kunjathoor, K. Eng, E. A. Knopp, K. Lewis, R. Lopez, E. A. Kirk, A. Chait, T. N. Wight, et al. Serum Amyloid A and Lipoprotein Retention in Murine Models of Atherosclerosis Arterioscler. Thromb. Vasc. Biol., April 1, 2005; 25(4): 785 - 790. [Abstract] [Full Text] [PDF] |
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M. Rahmani, J. T. Read, J. M. Carthy, P. C. McDonald, B. W. Wong, M. Esfandiarei, X. Si, Z. Luo, H. Luo, P. S. Rennie, et al. Regulation of the Versican Promoter by the {beta}-Catenin-T-cell Factor Complex in Vascular Smooth Muscle Cells J. Biol. Chem., April 1, 2005; 280(13): 13019 - 13028. [Abstract] [Full Text] [PDF] |
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A. Chait, C. Y. Han, J. F. Oram, and J. W. Heinecke Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease? J. Lipid Res., March 1, 2005; 46(3): 389 - 403. [Abstract] [Full Text] [PDF] |
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S. A. I. Ghesquiere, M. J. J. Gijbels, M. Anthonsen, P. J. J. van Gorp, I. van der Made, B. Johansen, M. H. Hofker, and M. P. J. de Winther Macrophage-specific overexpression of group IIa sPLA2 increases atherosclerosis and enhances collagen deposition J. Lipid Res., February 1, 2005; 46(2): 201 - 210. [Abstract] [Full Text] [PDF] |
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M. B. Kahn, K. Boesze-Battaglia, D. W. Stepp, A. Petrov, Y. Huang, R. P. Mason, and T. N. Tulenko Influence of serum cholesterol on atherogenesis and intimal hyperplasia after angioplasty: inhibition by amlodipine Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H591 - H600. [Abstract] [Full Text] [PDF] |
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Z. Zhao, M. C. de Beer, L. Cai, R. Asmis, F. C. de Beer, W. J.S. de Villiers, and D. R. van der Westhuyzen Low-Density Lipoprotein From Apolipoprotein E-Deficient Mice Induces Macrophage Lipid Accumulation in a CD36 and Scavenger Receptor Class A-Dependent Manner Arterioscler. Thromb. Vasc. Biol., January 1, 2005; 25(1): 168 - 173. [Abstract] [Full Text] [PDF] |
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M. F. Khalil, W. D. Wagner, and I. J. Goldberg Molecular Interactions Leading to Lipoprotein Retention and the Initiation of Atherosclerosis Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2211 - 2218. [Abstract] [Full Text] [PDF] |
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T.-S. Park, R. L. Panek, S. B. Mueller, J. C. Hanselman, W. S. Rosebury, A. W. Robertson, E. K. Kindt, R. Homan, S. K. Karathanasis, and M. D. Rekhter Inhibition of Sphingomyelin Synthesis Reduces Atherogenesis in Apolipoprotein E-Knockout Mice Circulation, November 30, 2004; 110(22): 3465 - 3471. [Abstract] [Full Text] [PDF] |
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C. Verseyden, S. Meijssen, and M. C. Cabezas Effects of Atorvastatin on Fasting Plasma and Marginated Apolipoproteins B48 and B100 in Large, Triglyceride-Rich Lipoproteins in Familial Combined Hyperlipidemia J. Clin. Endocrinol. Metab., October 1, 2004; 89(10): 5021 - 5029. [Abstract] [Full Text] [PDF] |
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R. Stocker and J. F. Keaney Jr. Role of Oxidative Modifications in Atherosclerosis Physiol Rev, October 1, 2004; 84(4): 1381 - 1478. [Abstract] [Full Text] [PDF] |
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R. K. Vikramadithyan, Y. Kako, G. Chen, Y. Hu, E. Arikawa-Hirasawa, Y. Yamada, and I. J. Goldberg Atherosclerosis in perlecan heterozygous mice J. Lipid Res., October 1, 2004; 45(10): 1806 - 1812. [Abstract] [Full Text] [PDF] |
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K. Oorni, M. Sneck, D. Bromme, M. O. Pentikainen, K. A. Lindstedt, M. Mayranpaa, H. Aitio, and P. T. Kovanen Cysteine Protease Cathepsin F Is Expressed in Human Atherosclerotic Lesions, Is Secreted by Cultured Macrophages, and Modifies Low Density Lipoprotein Particles in Vitro J. Biol. Chem., August 13, 2004; 279(33): 34776 - 34784. [Abstract] [Full Text] [PDF] |
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K. E. Lewis, E. A. Kirk, T. O. McDonald, S. Wang, T. N. Wight, K. D. O'Brien, and A. Chait Increase in Serum Amyloid A Evoked by Dietary Cholesterol Is Associated With Increased Atherosclerosis in Mice Circulation, August 3, 2004; 110(5): 540 - 545. [Abstract] [Full Text] [PDF] |
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T. N. Wight and M. J. Merrilees Proteoglycans in Atherosclerosis and Restenosis: Key Roles for Versican Circ. Res., May 14, 2004; 94(9): 1158 - 1167. [Abstract] [Full Text] [PDF] |
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A. E. Cozen, H. Moriwaki, M. Kremen, M. B. DeYoung, H. L. Dichek, K. I. Slezicki, S. G. Young, M. Veniant, and D. A. Dichek Macrophage-Targeted Overexpression of Urokinase Causes Accelerated Atherosclerosis, Coronary Artery Occlusions, and Premature Death Circulation, May 4, 2004; 109(17): 2129 - 2135. [Abstract] [Full Text] [PDF] |
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C. Flood, M. Gustafsson, R. E. Pitas, L. Arnaboldi, R. L. Walzem, and J. Boren 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., March 1, 2004; 24(3): 564 - 570. [Abstract] [Full Text] |
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E. F LaBelle and T. N Tulenko LDL, IGF-1, and VSMC apoptosis: linking atherogenesis to plaque rupture in vulnerable lesions Cardiovasc Res, February 1, 2004; 61(2): 204 - 205. [Full Text] [PDF] |
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M. Formato, M. Farina, R. Spirito, M. Maggioni, A. Guarino, G. M. Cherchi, P. Biglioli, C. Edelstein, and A. M. Scanu Evidence for a Proinflammatory and Proteolytic Environment in Plaques From Endarterectomy Segments of Human Carotid Arteries Arterioscler. Thromb. Vasc. Biol., January 1, 2004; 24(1): 129 - 135. [Abstract] [Full Text] [PDF] |
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X.-C. Jiang, T. P. Beyer, Z. Li, J. Liu, W. Quan, R. J. Schmidt, Y. Zhang, W. R. Bensch, P. I. Eacho, and G. Cao Enlargement of High Density Lipoprotein in Mice via Liver X Receptor Activation Requires Apolipoprotein E and Is Abolished by Cholesteryl Ester Transfer Protein Expression J. Biol. Chem., December 5, 2003; 278(49): 49072 - 49078. [Abstract] [Full Text] [PDF] |
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F. E. Thorngate, P. G. Yancey, G. Kellner-Weibel, L. L. Rudel, G. H. Rothblat, and D. L. Williams Testing the role of apoA-I, HDL, and cholesterol efflux in the atheroprotective action of low-level apoE expression J. Lipid Res., December 1, 2003; 44(12): 2331 - 2338. [Abstract] [Full Text] [PDF] |
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M. Patel, J. Morrow, F. R. Maxfield, D. K. Strickland, S. Greenberg, and I. Tabas The Cytoplasmic Domain of the Low Density Lipoprotein (LDL) Receptor-related Protein, but Not That of the LDL Receptor, Triggers Phagocytosis J. Biol. Chem., November 7, 2003; 278(45): 44799 - 44807. [Abstract] [Full Text] [PDF] |
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C. D. Meyers, L. R. Tannock, T. N. Wight, and A. Chait Statin-exposed vascular smooth muscle cells secrete proteoglycans with decreased binding affinity for LDL J. Lipid Res., November 1, 2003; 44(11): 2152 - 2160. [Abstract] [Full Text] [PDF] |
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W. Cao, Y. V Bobryshev, R. S.A Lord, R. E.I Oakley, S. H Lee, and J. Lu Dendritic cells in the arterial wall express C1q: potential significance in atherogenesis Cardiovasc Res, October 15, 2003; 60(1): 175 - 186. [Abstract] [Full Text] [PDF] |
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B. OSTERUD and E. BJORKLID Role of Monocytes in Atherogenesis Physiol Rev, October 1, 2003; 83(4): 1069 - 1112. [Abstract] [Full Text] [PDF] |
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G McGwin Jr, C Owsley, C A Curcio, and R J Crain The association between statin use and age related maculopathy Br. J. Ophthalmol., September 1, 2003; 87(9): 1121 - 1125. [Abstract] [Full Text] [PDF] |
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G. Camejo Hydrolytic Enzymes Released From Resident Macrophages and Located in the Intima Extracellular Matrix as Agents That Modify Retained Apolipoprotein B Lipoproteins Arterioscler. Thromb. Vasc. Biol., August 1, 2003; 23(8): 1312 - 1313. [Full Text] [PDF] |
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T. B. Twickler, M. J. M. Cramer, G. M. Dallinga-Thie, M. J. Chapman, D. W. Erkelens, and H. P. F. Koppeschaar Adult-Onset Growth Hormone Deficiency: Relation of Postprandial Dyslipidemia to Premature Atherosclerosis J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2479 - 2488. [Full Text] [PDF] |
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M. Y. Chang, C. Tsoi, T. N. Wight, and A. Chait Lysophosphatidylcholine Regulates Synthesis of Biglycan and the Proteoglycan Form of Macrophage Colony Stimulating Factor Arterioscler. Thromb. Vasc. Biol., May 1, 2003; 23(5): 809 - 815. [Abstract] [Full Text] [PDF] |
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Z. Chen, R. L. Fitzgerald, J. E. Saffitz, C. F. Semenkovich, and G. Schonfeld Amino Terminal 38.9% of Apolipoprotein B-100 Is Sufficient to Support Cholesterol-Rich Lipoprotein Production and Atherosclerosis Arterioscler. Thromb. Vasc. Biol., April 1, 2003; 23(4): 668 - 674. [Abstract] [Full Text] [PDF] |
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T. Nassar, B. S. Sachais, S.'e. Akkawi, M. A. Kowalska, K. Bdeir, E. Leitersdorf, E. Hiss, L. Ziporen, M. Aviram, D. Cines, et al. Platelet Factor 4 Enhances the Binding of Oxidized Low-density Lipoprotein to Vascular Wall Cells J. Biol. Chem., February 14, 2003; 278(8): 6187 - 6193. [Abstract] [Full Text] [PDF] |
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G. Malek, C.-M. Li, C. Guidry, N. E. Medeiros, and C. A. Curcio Apolipoprotein B in Cholesterol-Containing Drusen and Basal Deposits of Human Eyes with Age-Related Maculopathy Am. J. Pathol., February 1, 2003; 162(2): 413 - 425. [Abstract] [Full Text] [PDF] |
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K. Olin-Lewis, R. M. Krauss, M. La Belle, P. J. Blanche, P. H. R. Barrett, T. N. Wight, and A. Chait ApoC-III content of apoB-containing lipoproteins is associated with binding to the vascular proteoglycan biglycan J. Lipid Res., November 1, 2002; 43(11): 1969 - 1977. [Abstract] [Full Text] [PDF] |
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A. Zalewski, Y. Shi, and A. G. Johnson Diverse Origin of Intimal Cells: Smooth Muscle Cells, Myofibroblasts, Fibroblasts, and Beyond? Circ. Res., October 18, 2002; 91(8): 652 - 655. [Full Text] [PDF] |
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I. GOUNI-BERTHOLD and A. SACHINIDIS Does the coronary risk factor low density lipoprotein alter growth and signaling in vascular smooth muscle cells? FASEB J, October 1, 2002; 16(12): 1477 - 1487. [Abstract] [Full Text] [PDF] |
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F. D. Kolodgie, A. P. Burke, A. Farb, D. K. Weber, R. Kutys, T. N. Wight, and R. Virmani Differential Accumulation of Proteoglycans and Hyaluronan in Culprit Lesions: Insights Into Plaque Erosion Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1642 - 1648. [Abstract] [Full Text] [PDF] |
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C. Flood, M. Gustafsson, P. E. Richardson, S. C. Harvey, J. P. Segrest, and J. Boren Identification of the Proteoglycan Binding Site in Apolipoprotein B48 J. Biol. Chem., August 23, 2002; 277(35): 32228 - 32233. [Abstract] [Full Text] [PDF] |
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M. Falkenberg, C. Tom, M. B. DeYoung, S. Wen, R. Linnemann, and D. A. Dichek Increased expression of urokinase during atherosclerotic lesion development causes arterial constriction and lumen loss, and accelerates lesion growth PNAS, August 6, 2002; 99(16): 10665 - 10670. [Abstract] [Full Text] [PDF] |
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W. Huang, I. Ishii, W.-Y. Zhang, M. Sonobe, and H. S. Kruth PMA activation of macrophages alters macrophage metabolism of aggregated LDL J. Lipid Res., August 1, 2002; 43(8): 1275 - 1282. [Abstract] [Full Text] [PDF] |
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