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Volume 24, Issue 12; December 1, 2004
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
Corrections
Author Index
Subject Index
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Editorials
Glimpse of the Secret Life of the Plaque
Göran K. Hansson
Arterioscler Thromb Vasc Biol. 2004;24:2203-2204, doi:10.1161/01.ATV.0000149672.83911.5b.
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Proteolysis of Pericellular Matrix: A Process Linking Inflammation to Plaque Destabilization and Rupture
Ken A. Lindstedt and Petri T. Kovanen
Arterioscler Thromb Vasc Biol. 2004;24:2205-2206, doi:10.1161/01.ATV.0000149753.74793.88.
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Propagation of Arterial Thrombi: Local and Remote Contributory Factors
Shinya Goto
Arterioscler Thromb Vasc Biol. 2004;24:2207-2208, doi:10.1161/01.ATV.0000149144.86175.03.
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24(S),25-EpoxycholesterolA Potential Friend
Ingemar Bjorkhem and Ulf Diczfalusy
Arterioscler Thromb Vasc Biol. 2004;24:2209-2210, doi:10.1161/01.ATV.0000148704.72481.28.
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Brief Reviews
Molecular Interactions Leading to Lipoprotein Retention and the Initiation of Atherosclerosis
Maged F. Khalil, William D. Wagner, and Ira J. Goldberg
Arterioscler Thromb Vasc Biol. 2004;24:2211-2218; published online before print October 7 2004, doi:10.1161/01.ATV.0000147163.54024.70.
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Atherosclerosis is initiated by the accumulation of lipoprotein lipid within the artery wall. This process is thought to involve an ionic interaction between apoB and proteoglycans. Lipoprotein aggregation and association with other matrix proteins are likely additional routes to lipoprotein retention.
Lipoprotein(a): An Elusive Cardiovascular Risk Factor
Lars Berglund and Rajasekhar Ramakrishnan
Arterioscler Thromb Vasc Biol. 2004;24:2219-2226; published online before print September 2 2004, doi:10.1161/01.ATV.0000144010.55563.63.
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Lp(a) is present in humans and primates. Apo(a) affects Lp(a) properties, variation in apo(a) size, and an upstream pentanucleotide repeat number influences Lp(a) levels. Lp(a) is a risk factor for coronary artery disease, and smaller size apo(a) is associated with coronary artery disease. The physiological role of Lp(a) is unknown.
Potential Role of Endotoxin as a Proinflammatory Mediator of Atherosclerosis
Lynn L. Stoll, Gerene M. Denning, and Neal L. Weintraub
Arterioscler Thromb Vasc Biol. 2004;24:2227-2236; published online before print October 7 2004, doi:10.1161/01.ATV.0000147534.69062.dc.
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Bacterial endotoxin is a potential source of vascular inflammation and may be an important risk factor for atherosclerosis. Here, we discuss the endotoxin signaling pathway, vascular proinflammatory effects of endotoxin and their relevance to atherogenesis, interactions between endotoxin and serum lipoproteins, and possible immunomodulatory effects of statins.
Vascular Biology
Molecular Evaluation of Endothelial Progenitor Cells in Patients With Ischemic Limbs: Therapeutic Effect by Stem Cell Transplantation
Koji Yamamoto, Takahisa Kondo, Satoshi Suzuki, Hideo Izawa, Masayoshi Kobayashi, Nobuhiko Emi, Kimihiro Komori, Tomoki Naoe, Junki Takamatsu, and Toyoaki Murohara
Arterioscler Thromb Vasc Biol. 2004;24:e192-e196; published online before print October 14 2004, doi:10.1161/01.ATV.0000147730.78953.60.
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The gene expression of EPC-specific molecules in bone marrow-derived and peripheral blood-derived mononuclear cells, analyzed by real-time RT-PCR, was lower in patients with ischemic limbs than in healthy subjects. Therapeutic angiogenesis by autologous stem cell transplantation was effective for the patients and increased circulating EPCs.
Induction of Angiogenesis by Heat Shock Protein 90 Mediated by Protein Kinase Akt and Endothelial Nitric Oxide Synthase
Jianxin Sun and James K. Liao
Arterioscler Thromb Vasc Biol. 2004;24:2238-2244; published online before print October 14 2004, doi:10.1161/01.ATV.0000147894.22300.4c.
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We showed that inhibition of Hsp90 leads not only to decreased Akt and eNOS phosphorylation but also to decreased eNOS gene transcription. This correlated with decrease VEGF-induced endothelial cell migration and angiogenesis. These findings indicate that inhibition of Hsp90 may be an important target for antitumor and anti-angiogenesis therapy.
Granzyme B Induces Smooth Muscle Cell Apoptosis in the Absence of Perforin: Involvement of Extracellular Matrix Degradation
Jonathan C. Choy, Vivian H.Y. Hung, Arwen L. Hunter, Paul K. Cheung, Bruce Motyka, Ing Swie Goping, Tracy Sawchuk, R. Chris Bleackley, Thomas J. Podor, Bruce M. McManus, and David J. Granville
Arterioscler Thromb Vasc Biol. 2004;24:2245-2250; published online before print October 7 2004, doi:10.1161/01.ATV.0000147162.51930.b7.
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We studied the mechanisms of granzyme B-induced smooth muscle cell (SMC) death. In the absence of perforin, granzyme B induced SMC apoptosis. Internalization of granzyme B was not required for SMC death, and this protease induced the cleavage of several extracellular proteins, including fibronectin.
Promotion of Leukocyte Adhesion by a Novel Interaction Between Vitronectin and the ß
2
Integrin Mac-1 (
M
ß
2
, CD11b/CD18)
Sandip M. Kanse, Rachel L. Matz, Klaus T. Preissner, and Karlheinz Peter
Arterioscler Thromb Vasc Biol. 2004;24:2251-2256; published online before print September 30 2004, doi:10.1161/01.ATV.0000146529.68729.8b.
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Vitronectin promotes cell adhesion by binding to ß1, ß3, and ß5 integrins and the urokinase receptor. We now demonstrate that vitronectin also binds directly to the leukocyte ß2 integrin, Mac-1 ({alpha}Mß2, CD11b/CD18), and this interaction mediates leukocyte adhesion and migration.
Intracellular Labile Iron Modulates Adhesion of Human Monocytes to Human Endothelial Cells
Apriliana E.R. Kartikasari, Niki A. Georgiou, Frank L.J. Visseren, Henny van Kats-Renaud, B. Sweder van Asbeck, and Joannes J.M. Marx
Arterioscler Thromb Vasc Biol. 2004;24:2257-2262; published online before print October 14 2004, doi:10.1161/01.ATV.0000147406.00871.b3.
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An increase in the level of intracellular labile iron induced monocyte adhesion to endothelium, an initial event in atherosclerotic plaque formation. A concordant increase in the cell adhesion molecule expression was observed. Furthermore, only inclusion of membrane-permeable iron chelators and radical scavengers resulted in a complete inhibition of these effects of iron.
Interaction of Monocytes With Vascular Smooth Muscle Cells Regulates Monocyte Survival and Differentiation Through Distinct Pathways
Qiangjun Cai, Linda Lanting, and Rama Natarajan
Arterioscler Thromb Vasc Biol. 2004;24:2263-2270; published online before print September 30 2004, doi:10.1161/01.ATV.0000146552.16943.5e.
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We investigated the impact of vascular smooth muscle cell (VSMC)/monocyte interactions on monocyte functions. We observed that VSMC/monocyte interactions led to antiapoptotic effects and increased scavenger receptor CD36 expression in monocytes through distinct signaling pathways. These data provide evidence for a novel VSMC-dependent local regulation of monocyte survival, retention, and differentiation in atherosclerosis.
Angiotensin IIInduced Protein Kinase D Activation Is Regulated by Protein Kinase C
and Mediated via the Angiotensin II Type 1 Receptor in Vascular Smooth Muscle Cells
Mingqi Tan, Xuemin Xu, Motoi Ohba, and Mei-Zhen Cui
Arterioscler Thromb Vasc Biol. 2004;24:2271-2276; published online before print October 21 2004, doi:10.1161/01.ATV.0000148449.92035.3a.
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The results of our study reveal for the first time that Ang II-induced PKD activation is mediated via AT1 and regulated by PKC{delta} in living cells. These data may provide new insights into molecular mechanisms involved in Ang II-induced physiological and pathological events.
Vein Graft Neointimal Hyperplasia Is Exacerbated by Tumor Necrosis Factor Receptor-1 Signaling in Graft-Intrinsic Cells
Lisheng Zhang, Karsten Peppel, Leigh Brian, Lynn Chien, and Neil J. Freedman
Arterioscler Thromb Vasc Biol. 2004;24:2277-2283; published online before print October 14 2004, doi:10.1161/01.ATV.0000147766.68987.0d.
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In surgical mouse chimeras, TNF receptor-1 (p55)-deficient vein grafts (compared with WT grafts) demonstrated less ICAM-1, VCAM-1, and MCP-1 expression, accelerated endothelialization, and reduced neointimal hyperplasia. However, vein graft medial thickness was unaffected. SMC chemokine expression and DNA synthesis in response to TNF, but not PDGF, was abrogated by p55 deficiency.
Essential Role of Vascular Endothelial Growth Factor and Flt-1 Signals in Neointimal Formation After Periadventitial Injury
Qingwei Zhao, Kensuke Egashira, Ken-ichi Hiasa, Minako Ishibashi, Shujiro Inoue, Kisho Ohtani, Chunyan Tan, Masabumi Shibuya, Akira Takeshita, and Kenji Sunagawa
Arterioscler Thromb Vasc Biol. 2004;24:2284-2289; published online before print October 7 2004, doi:10.1161/01.ATV.0000147161.42956.80.
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We examined the role of vascular endothelial growth factor (VEGF) in the pathogenesis of neointimal formation after cuff-induced periadventitial injury in mice. Blockade of VEGF by transfecting mice with the sFlt-1 gene inhibited neointimal formation associated with reduced expression of various inflammation-promoting factors. Therefore, VEGF might promote neointimal formation by acting as a proinflammatory cytokine after cuff-induced periadventitial injury.
Inhibitory Effect of High Concentration of Glucose on Relaxations to Activation of ATP-Sensitive K
+
Channels in Human Omental Artery
Hiroyuki Kinoshita, Toshiharu Azma, Katsutoshi Nakahata, Hiroshi Iranami, Yoshiki Kimoto, Mayuko Dojo, Osafumi Yuge, and Yoshio Hatano
Arterioscler Thromb Vasc Biol. 2004;24:2290-2295; published online before print October 14 2004, doi:10.1161/01.ATV.0000148006.78179.c7.
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Our results regarding the acute effects of high glucose on the human omental artery indicate that in the human visceral artery, acute hyperglycemia modulates vasodilation mediated by ATP-sensitive K+ channels via the production of superoxide, possibly mediated by the activation of protein kinase C.
7-Ketocholesterol Induces Protein Ubiquitination, Myelin Figure Formation, and Light Chain 3 Processing in Vascular Smooth Muscle Cells
Wim Martinet, Martine De Bie, Dorien M. Schrijvers, Guido R.Y. De Meyer, Arnold G. Herman, and Mark M. Kockx
Arterioscler Thromb Vasc Biol. 2004;24:2296-2301; published online before print September 30 2004, doi:10.1161/01.ATV.0000146266.65820.a1.
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7-Ketocholesterol induces a complex mode of cell death in human aortic smooth muscle cells associated with accumulation of ubiquitinated proteins in the cytoplasm, myelin figure formation, and LC3 processing, evocating autophagic processes.
2-Chlorohexadecanal Derived From Hypochlorite-Modified High-Density LipoproteinAssociated Plasmalogen Is a Natural Inhibitor of Endothelial Nitric Oxide Biosynthesis
Gunther Marsche, Regine Heller, Günter Fauler, Alenka Kovacevic, Alexander Nuszkowski, Wolfgang Graier, Wolfgang Sattler, and Ernst Malle
Arterioscler Thromb Vasc Biol. 2004;24:2302-2306; published online before print October 28 2004, doi:10.1161/01.ATV.0000148703.43429.25.
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Modification of HDL by HOCl (generated in vivo by the myeloperoxidase-H2O2 system) promotes dislocalization of eNOS from the plasma membrane and perinuclear location of endothelial cells, and attenuates eNOS expression and NO biosynthesis. The component mediating this proatherogenic effect was identified as 2-chlorohexadecanal formed during HOCl-mediated attack of lipoprotein-associated plasmalogen.
Atherosclerosis and Lipoproteins
Reduced In Vivo Aortic Uptake of Radiolabeled Oxidation-Specific Antibodies Reflects Changes in Plaque Composition Consistent With Plaque Stabilization
Michael Torzewski, Peter X. Shaw, Kyoo-Rok Han, Brian Shortal, Karl J. Lackner, Joseph L. Witztum, Wulf Palinski, and Sotirios Tsimikas
Arterioscler Thromb Vasc Biol. 2004;24:2307-2312; published online before print November 4 2004, doi:10.1161/01.ATV.0000149378.98458.fe.
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In vivo plaque uptake of radiolabeled oxidation-specific antibodies (Ox-AB) was found to be significantly diminished in regressing lesions with reductions in OxLDL and macrophages and increases in smooth muscle cells and collagen. Thus, labeled Ox-AB may be useful to detect lipid-rich, oxidation-rich plaques and assess stabilization of pre-existing lesions.
Overexpression of IL-18 Decreases Intimal Collagen Content and Promotes a Vulnerable Plaque Phenotype in Apolipoprotein-EDeficient Mice
R. de Nooijer, J.H. von der Thüsen, C.J.N. Verkleij, J. Kuiper, J.W. Jukema, E.E. van der Wall, Th.J.C. van Berkel, and E.A.L. Biessen
Arterioscler Thromb Vasc Biol. 2004;24:2313-2319; published online before print October 7 2004, doi:10.1161/01.ATV.0000147126.99529.0a.
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The effect of IL-18 overexpression on the stability of preexisting advanced atherosclerotic lesions was studied in apoE-deficient mice. A marked decrease in intimal collagen content and an increase in the incidence of vulnerable plaque morphology were observed. It is suggested that IL-18 increases extracellular matrix degradation.
Increased Expression of the DNA-Binding Cytokine HMGB1 in Human Atherosclerotic Lesions: Role of Activated Macrophages and Cytokines
N. Kalinina, A. Agrotis, Y. Antropova, G. DiVitto, P. Kanellakis, G. Kostolias, O. Ilyinskaya, E. Tararak, and A. Bobik
Arterioscler Thromb Vasc Biol. 2004;24:2320-2325; published online before print September 16 2004, doi:10.1161/01.ATV.0000145573.36113.8a.
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The expression and regulation of high-mobility group box 1 (HMGB1) proinflammatory cytokine in human atherosclerosis were examined. HMGB1 is mostly expressed by macrophages and its expression increases during atherogenesis. Inflammatory cytokines upregulate HMGB1 expression and secretion. HMGB1 is a common mediator of inflammation and may contribute to atherosclerotic lesion progression.
No Association Between Plasma Levels of Plant Sterols and Atherosclerosis in Mice and Men
Kenneth R. Wilund, Liqing Yu, Fang Xu, Gloria L. Vega, Scott M. Grundy, Jonathan C. Cohen, and Helen H. Hobbs
Arterioscler Thromb Vasc Biol. 2004;24:2326-2332; published online before print October 28 2004, doi:10.1161/01.ATV.0000149140.00499.92.
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The effect of sitosterolemia on aortic lesion development in genetically modified mice was examined. Elevated plasma levels of plant sterols were not associated with aortic atherosclerosis, nor was a significant association found between plasma plant sterol levels and the presence of coronary artery calcium in 2542 middle-aged men and women.
Stem Cell Transplantation Reveals That Absence of Macrophage CD36 Is Protective Against Atherosclerosis
Maria Febbraio, Ella Guy, and Roy L. Silverstein
Arterioscler Thromb Vasc Biol. 2004;24:2333-2338; published online before print October 14 2004, doi:10.1161/01.ATV.0000148007.06370.68.
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To determine whether absence of macrophage CD36 alone was protective against atherosclerosis, mice were lethally irradiated and reconstituted with CD36 wild-type or null stem cells in the context of Apo E-null mice lacking CD36 in macrophages alone were profoundly protected against atherosclerosis (88.1% reduction of lesion area).
Differential Expression Patterns of Proinflammatory and Antiinflammatory Mediators During Atherogenesis in Mice
Niels R. Veillard, Sabine Steffens, Fabienne Burger, Graziano Pelli, and François Mach
Arterioscler Thromb Vasc Biol. 2004;24:2339-2344; published online before print September 30 2004, doi:10.1161/01.ATV.0000146532.98235.e6.
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Despite further increase of atherosclerotic lesion size in ApoE-/- mice after 10 weeks of diet, expression of important pro- and antiinflammatory mediators did not further increase or even decreased. These results could be correlated with the amount of inflammatory cells present within atherosclerotic lesions.
Probucol Inhibits ABCA1-Mediated Cellular Lipid Efflux
Elda Favari, Ilaria Zanotti, Francesca Zimetti, Nicoletta Ronda, Franco Bernini, and George H. Rothblat
Arterioscler Thromb Vasc Biol. 2004;24:2345-2350; published online before print October 28 2004, doi:10.1161/01.ATV.0000148706.15947.8a.
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This study characterized probucol effect on ABCA1-mediated lipid efflux. Probucol inhibits ABCA1-mediated efflux but not SR-BI-mediated efflux by affecting the ABCA1 translocation to the plasma membrane, the membrane cholesterol pool, and the 125I-apo-AI binding.
Quantitative and Qualitative Differences in Proatherogenic NKT Cells in Apolipoprotein EDeficient Mice
Amy S. Major, Michael T. Wilson, Jennifer L. McCaleb, Yan Ru Su, Aleksandar K. Stanic, Sebastian Joyce, Luc Van Kaer, Sergio Fazio, and MacRae F. Linton
Arterioscler Thromb Vasc Biol. 2004;24:2351-2357; published online before print October 7 2004, doi:10.1161/01.ATV.0000147112.84168.87.
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Natural killer T (NKT) cells have characteristics of both T and NK cells and recognize glycolipid antigens. We show that NKT cell-deficiency in male apoE0 mice results in decreased atherosclerosis whereas activation of NKT cells resulted in a 2-fold increase in atherosclerosis. NKT cell numbers and functions are affected by the hyperlipidemia state.
Transcription Factor Sterol Regulatory Element Binding Protein 2 Regulates Scavenger Receptor Cla-1 Gene Expression
Morgan Tréguier, Chantal Doucet, Martine Moreau, Christiane Dachet, Joëlle Thillet, M. John Chapman, and Thierry Huby
Arterioscler Thromb Vasc Biol. 2004;24:2358-2364; published online before print October 14 2004, doi:10.1161/01.ATV.0000147896.69299.85.
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The putative regulation of the expression of the human scavenger receptor Cla-1 gene by intracellular cholesterol content and SREBP transcription factors was evaluated. Transient transfection, site-directed mutation, and electrophoretic mobility shift assay allowed identification of a functional SRE in the Cla-1 promoter. SREBP-stably transfected cells provided strong evidence of the implication of SREBP-2 in Cla-1 gene expression.
Statins Inhibit Synthesis of an Oxysterol Ligand for the Liver X Receptor in Human Macrophages With Consequences for Cholesterol Flux
Jenny Wong, Carmel M. Quinn, and Andrew J. Brown
Arterioscler Thromb Vasc Biol. 2004;24:2365-2371; published online before print October 28 2004, doi:10.1161/01.ATV.0000148707.93054.7d.
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We show that statins downregulate key genes involved in cholesterol efflux from nonloaded human macrophages. Furthermore, statin treatment drastically reduced cholesterol efflux from these cells. Moreover, we identify a likely mechanism as inhibition of the synthesis of 24(S),25-epoxycholesterol, an oxysterol ligand for the liver X receptor.
Ultrasensitive Confocal Fluorescence Microscopy of C-Reactive Protein Interacting With Fc
RIIa
Dimitar E. Manolov, Carlheinz Röcker, Vinzenz Hombach, G. Ulrich Nienhaus, and Jan Torzewski
Arterioscler Thromb Vasc Biol. 2004;24:2372-2377; published online before print October 14 2004, doi:10.1161/01.ATV.0000147407.17137.02.
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We have studied CRP binding to Fc{gamma}RIIa using the novel method of ultrasensitive confocal fluorescence microscopy. We unambiguously show that CRP interacts with Fc{gamma}RIIa and characterize this interaction quantitatively. We also provide explanations as to why controversial results were obtained previously.
Induction of the Paraoxonase-1 Gene Expression by Resveratrol
Cédric Gouédard, Robert Barouki, and Yannick Morel
Arterioscler Thromb Vasc Biol. 2004;24:2378-2383; published online before print September 30 2004, doi:10.1161/01.ATV.0000146530.24736.ce.
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The human paraoxonase-1 (PON-1) is a high-density lipoprotein-associated enzyme displaying protective properties toward cardiovascular disease. We show that resveratrol, a wine component, increases the PON-1 gene expression in human hepatocytes and in the HuH7 hepatoma cell line by an unusual AhR-mediated transcriptional mechanism.
Quantification and 3D Reconstruction of Atherosclerotic Plaque Components in Apolipoprotein E Knockout Mice Using Ex Vivo High-Resolution MRI
Martina A. McAteer, Jürgen E. Schneider, Kieran Clarke, Stefan Neubauer, Keith M. Channon, and Robin P. Choudhury
Arterioscler Thromb Vasc Biol. 2004;24:2384-2390; published online before print September 30 2004, doi:10.1161/01.ATV.0000146811.19029.fb.
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We tested the ability of high-resolution MRI to quantify mouse atherosclerotic plaque components ex vivo. MRI accurately quantified lipid-rich/necrotic core and cell-rich cap components, as confirmed by histopathology. Three-dimensional reconstruction of brachiocephalic arteries enabled more sensitive volumetric quantification of differences in plaque and lipid-rich/necrotic cores than 2D analysis.
Decorin Promotes Aortic Smooth Muscle Cell Calcification and Colocalizes to Calcified Regions in Human Atherosclerotic Lesions
Jens W. Fischer, Susie A. Steitz, Pamela Y. Johnson, Allen Burke, Frank Kolodgie, Renu Virmani, Cecilia Giachelli, and Thomas N. Wight
Arterioscler Thromb Vasc Biol. 2004;24:2391-2396; published online before print October 7 2004, doi:10.1161/01.ATV.0000147029.63303.28.
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Calcification of atherosclerotic plaques is positively correlated with plaque burden and cardiovascular mortality. The present study demonstrates that decorin expression enhances calcification of arterial smooth muscle cells in vitro and that decorin colocalizes with calcium deposits in human atherosclerotic plaques, suggesting that decorin is a promoter of vascular calcification.
Insulin Resistance Is Independently Associated With Postprandial Alterations of Triglyceride-Rich Lipoproteins in Type 2 Diabetes Mellitus
Giovanni Annuzzi, Claudia De Natale, Ciro Iovine, Lidia Patti, Lucrezia Di Marino, Silvana Coppola, Stefano Del Prato, Gabriele Riccardi, and Angela A. Rivellese
Arterioscler Thromb Vasc Biol. 2004;24:2397-2402; published online before print September 30 2004, doi:10.1161/01.ATV.0000146267.71816.30.
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In an experimental setting, taking care of the effects of hyperglycemia and hyperinsulinemia (hyperinsulinemic glycemic clamp,) insulin-resistant type 2 diabetic patients showed higher postprandial levels of lipids and apoB in large VLDL compared with controls, indicating that insulin resistance is a proper target to correct postprandial dyslipidemia in type 2 diabetes.
Cardiovascular Risk in Type 2 Diabetes Is Associated With Variation at the
PPARG
Locus: A Go-DARTS Study
Alex S.F. Doney, Bettina Fischer, Graham Leese, Andrew D. Morris, and Colin N.A. Palmer
Arterioscler Thromb Vasc Biol. 2004;24:2403-2407; published online before print October 14 2004, doi:10.1161/01.ATV.0000147897.57527.e4.
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Variants of PPARG may influence cardiovascular risk. The association of the linked Pro12Ala and C1431T variants with myocardial infarction was investigated in a large cohort of patients with type 2 diabetes. Ala12 was associated with a significantly decreased risk and T1431 a significantly increased risk.
Intimal Thickness Is not Associated With Wall Shear Stress Patterns in the Human Right Coronary Artery
Anil K. Joshi, Richard L. Leask, Jerry G. Myers, Matadial Ojha, Jagdish Butany, and C. Ross Ethier
Arterioscler Thromb Vasc Biol. 2004;24:2408-2413; published online before print October 7 2004, doi:10.1161/01.ATV.0000147118.97474.4b.
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To determine whether low wall shear stress causes intimal thickening in the human right coronary artery, we compared postmortem histological data with computed wall shear stresses in 4 patients. We found no consistent correlation between intimal thickness and wall shear stress.
Low-Grade Inflammation and Microalbuminuria in Hypertension
Roberto Pedrinelli, Giulia DellOmo, Vitantonio Di Bello, Giovanni Pellegrini, Laura Pucci, Stefano Del Prato, and Giuseppe Penno
Arterioscler Thromb Vasc Biol. 2004;24:2414-2419; published online before print October 14 2004, doi:10.1161/01.ATV.0000147415.40692.7f.
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Microalbuminuria accompanied by high hs-CRP was characterized by higher 24-hour SBP, postload glucose, BMI, lower HDL cholesterol, more frequent metabolic syndrome, concentric LVH, and active smoking indicating that this phenotypic pattern is a strong correlate of metabolic abnormalities in essential hypertension and identifies a patient subset at very high cardiovascular risk.
Thrombosis
Increased Vascular Wall Thrombogenicity Combined With Reduced Blood Flow Promotes Occlusive Thrombus Formation in Rabbit Femoral Artery
Atsushi Yamashita, Eiji Furukoji, Kousuke Marutsuka, Kinta Hatakeyama, Hiroshi Yamamoto, Shozo Tamura, Yasuo Ikeda, Akinobu Sumiyoshi, and Yujiro Asada
Arterioscler Thromb Vasc Biol. 2004;24:2420-2424; published online before print October 14 2004, doi:10.1161/01.ATV.0000147767.61336.de.
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We demonstrated in an animal model that increased vascular wall thrombogenicity combined with a blood flow reduction (>75%) promoted occlusive thrombus formation that was prevented by inhibiting plasma vWF. Reduced blood flow at plaque disruption sites might contribute to thrombus propagation and lead to acute coronary syndromes.
Letters to the Editor
Lower Doses of Estrogen Replacement Therapy and the Risk of Cardiovascular Disease
Akihiko Wakatsuki, Kwang Kon Koh, Eak Kyun Shin, and Ichiro Sakuma
Arterioscler Thromb Vasc Biol. 2004;24:e197, doi:10.1161/01.ATV.0000148203.03346.b5.
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Corrections
Correction
Arterioscler Thromb Vasc Biol. 2004;24:2425, doi:10.1161/01.ATV.0000150446.71767.67.
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Author Index
Arterioscler Thromb Vasc Biol. 2004;24:2426-2433.
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Subject Index
Arterioscler Thromb Vasc Biol. 2004;24:2434-2467.
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