Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [1])

About This Cover

Volume 25, Issue 1; January 1, 2005

Announcement
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Corrections
Acknowledgment of Reviewers

To see an article, click its "Full Text" or "PDF" link. To review many abstracts, check the boxes to the left of the titles you want, and click the "Get All Checked Abstract(s)" button. To see one abstract at a time, click its "Abstract" link.

button_lock_image article is free immediately upon publication

	Announcement
	New Investigator Awards Arterioscler Thromb Vasc Biol. 2005;25:1, doi:10.1161/01.ATV.0000153738.88475.f7 Full Text \| PDF
	Editorials
	Arteriosclerosis, Thrombosis, and Vascular Biology, 2005 Donald D. Heistad Arterioscler Thromb Vasc Biol. 2005;25:2-4, doi:10.1161/01.ATV.0000151931.91737.00 Full Text \| PDF
	Plasma Plant Sterol Levels: Another Coronary Heart Disease Risk Factor? Ephraim Sehayek and Jan L. Breslow Arterioscler Thromb Vasc Biol. 2005;25:5-6, doi:10.1161/01.ATV.0000151984.34920.aa Full Text \| PDF
	ACAT Inhibition: Bad for Macrophages, Good for Smooth Muscle Cells? Sergio Fazio, Dwayne E. Dove, and MacRae F. Linton Arterioscler Thromb Vasc Biol. 2005;25:7-9, doi:10.1161/01.ATV.0000153086.46231.8c Full Text \| PDF
	Lesion Macrophages Are a Key Target for the Antiatherogenic Effects of LXR Agonists Michelle N. Bradley and Peter Tontonoz Arterioscler Thromb Vasc Biol. 2005;25:10-11, doi:10.1161/01.ATV.0000152727.69018.61 Full Text \| PDF
	The ADAMTS Proteases, Extracellular Matrix, and Vascular Disease: Waking the Sleeping Giant(s)! Thomas N. Wight Arterioscler Thromb Vasc Biol. 2005;25:12-14, doi:10.1161/01.ATV.0000150043.43083.aa Full Text \| PDF
	Beyond the G Protein: The Saga of the Type 2 Angiotensin II Receptor E.J. Landon and T. Inagami Arterioscler Thromb Vasc Biol. 2005;25:15-16, doi:10.1161/01.ATV.0000153047.93274.5c Full Text \| PDF
	Brief Reviews
	ATVB In Focus: Immunity and Atherosclerosis Göran K. Hansson Arterioscler Thromb Vasc Biol. 2005;25:17, doi:10.1161/01.ATV.0000153139.83149.a2 Full Text \| PDF
	Immunomodulation of Atherosclerosis: Implications for Vaccine Development Jan Nilsson, Göran K. Hansson, and Prediman K. Shah Arterioscler Thromb Vasc Biol. 2005;25:18-28; published online before print October 28 2004, doi:10.1161/01.ATV.0000149142.42590.a2 Abstract \| Full Text \| PDF The immune system is actively involved in development of atherosclerosis, mounting inflammatory responses promoting disease as well as specific protective responses. This review summarizes recent studies suggesting that influencing these responses by vaccines and means of immunomodulation may represent a novel therapy for prevention and treatment of atherosclerosis.
	Oxidative Stress and Vascular Disease Nageswara R. Madamanchi, Aleksandr Vendrov, and Marschall S. Runge Arterioscler Thromb Vasc Biol. 2005;25:29-38; published online before print November 11 2004, doi:10.1161/01.ATV.0000150649.39934.13 Abstract \| Full Text \| PDF Antioxidants are ineffective in reducing cardiovascular death despite evidence for oxidative stress (OS) in cardiovascular diseases (CVD) from animal and human investigations. A better understanding of cellular redox reactions, development of targeted antioxidants and phenotype-genotype linkage analysis for OS are necessary for broader use of pharmacological and regenerative therapies for CVD.
	Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries P.E. Norman and J.T. Powell Arterioscler Thromb Vasc Biol. 2005;25:39-46; published online before print October 21 2004, doi:10.1161/01.ATV.0000148450.56697.4a Abstract \| Full Text \| PDF Vitamin D influences a wide range of metabolic systems through both genomic and nongenomic pathways that have an impact on the properties of peripheral arteries. Although some vitamin D is essential for cardiovascular health, excess may have detrimental effects, including calcification, inflammation, and impaired elastogenesis in the arterial wall.
	Tissue Factor–Factor VIIa Signaling L. Vijaya Mohan Rao and Usha R. Pendurthi Arterioscler Thromb Vasc Biol. 2005;25:47-56; published online before print November 29 2004, doi:10.1161/01.ATV.0000151624.45775.13 Abstract \| Full Text \| PDF Recent studies show that tissue factor-factor VIIa, whose primary function is to initiate the clotting cascade, transduces cell signaling in various cell types. This brief review summarizes recent literature on potential mechanisms by which tissue factor-factor VIIa activates cell signaling, and how tissue factor-factor VIIa-induced cell signaling may affect various pathophysiological processes.
	Vascular Biology
	Regulation of Transport of the Angiotensin AT2 Receptor by a Novel Membrane-Associated Golgi Protein Christoph J. Wruck, Heiko Funke-Kaiser, Thomas Pufe, Heike Kusserow, Mario Menk, Jan H. Schefe, Marie L. Kruse, Monika Stoll, and Thomas Unger Arterioscler Thromb Vasc Biol. 2005;25:57-64; published online before print November 11 2004, doi:10.1161/01.ATV.0000150662.51436.14 Abstract \| Full Text \| PDF \| Data Supplement We identified a Golgi membrane-associated protein termed ATBP50 that binds to the cytoplasmatic terminus of the angiotensin AT2 receptor. We also cloned ATBP60 and ATBP135 encoded by the same gene. Downregulation of ATBP50 leads to retention of AT2R in inner compartments, reduced cell surface expression, and decreased antiproliferative effects of AT2R.
	Dual Effect of Angiotensin-Converting Enzyme Inhibition on Angiogenesis in Type 1 Diabetic Mice Téni G. Ebrahimian, Radia Tamarat, Michel Clergue, Micheline Duriez, Bernard I. Levy, and Jean-Sébastien Silvestre Arterioscler Thromb Vasc Biol. 2005;25:65-70; published online before print November 4 2004, doi:10.1161/01.ATV.0000149377.90852.d8 Abstract \| Full Text \| PDF \| Data Supplement ACE inhibition improved neovascularization in the diabetic ischemic leg through activation of bradykinin signaling, whereas it reduced vessel growth in the diabetic retina through inhibition of overacting Ang II pathway. ACEI may constitute a novel therapeutic strategy for the treatment of macrovascular and microvascular diseases in the setting of diabetes.
	Antiangiogenic Activity of Semisynthetic Biotechnological Heparins: Low-Molecular-Weight-Sulfated Escherichia coli K5 Polysaccharide Derivatives as Fibroblast Growth Factor Antagonists Marco Presta, Pasqua Oreste, Giorgio Zoppetti, Mirella Belleri, Elena Tanghetti, Daria Leali, Chiara Urbinati, Antonella Bugatti, Roberto Ronca, Stefania Nicoli, Emanuela Moroni, Helena Stabile, Maura Camozzi, German Andrés Hernandez, Stefania Mitola, Patrizia Dell’Era, Marco Rusnati, and Domenico Ribatti Arterioscler Thromb Vasc Biol. 2005;25:71-76; published online before print October 28 2004, doi:10.1161/01.ATV.0000148863.24445.b4 Abstract \| Full Text \| PDF \| Data Supplement Low-molecular-weight compounds from a N,O-sulfated derivative of Escherichia coli K5 polysaccharide bind fibroblast growth factor-2, thus inhibiting its receptor interactions. They also inhibit endothelial cell proliferation and sprouting and angiogenesis in vivo. These semisynthetic biotechnological heparin-like compounds may provide the basis for the design of novel angiostatic molecules.
	Vascular Injury Induces Expression of Periostin: Implications for Vascular Cell Differentiation and Migration Volkhard Lindner, Qiaozeng Wang, Barbara A. Conley, Robert E. Friesel, and Calvin P.H. Vary Arterioscler Thromb Vasc Biol. 2005;25:77-83; published online before print October 28 2004, doi:10.1161/01.ATV.0000149141.81230.c6 Abstract \| Full Text \| PDF Periostin is an abundant sequence induced on vascular injury arteries. We find that periostin is associated with smooth muscle cell differentiation and that it functions as a migratory stimulus. In addition, inability to downregulate periostin expression with FGF-2 may be a useful criterion to discriminate between smooth muscle and fibroblast lineages.
	Differential Effects of Vasodilatory Prostaglandins on Focal Adhesions, Cytoskeletal Architecture, and Migration in Human Aortic Smooth Muscle Cells C. Bulin, U. Albrecht, J.G. Bode, A.-A. Weber, K. Schrör, B. Levkau, and J.W. Fischer Arterioscler Thromb Vasc Biol. 2005;25:84-89; published online before print September 30 2004, doi:10.1161/01.ATV.0000146814.81581.68 Abstract \| Full Text \| PDF \| Data Supplement The present study identifies focal adhesions (FAs) as a target of prostaglandin signaling in human vascular smooth muscle cells. Specifically, it is demonstrated that vasodilatory prostaglandins inhibit in a cAMP-dependent manner FA-kinase phosphorylation, which is associated with disassembly of FA, actin cytoskeleton, and reduced VSMC migration.
	Ceramide-Induced Impairment of Endothelial Function Is Prevented by CuZn Superoxide Dismutase Overexpression Sean P. Didion and Frank M. Faraci Arterioscler Thromb Vasc Biol. 2005;25:90-95; published online before print November 4 2004, doi:10.1161/01.ATV.0000149868.74075.5d Abstract \| Full Text \| PDF Ceramide, an important intracellular second messenger, has been found to increase superoxide. The results of the present study indicate that ceramide-induced increases in superoxide impairs endothelium-dependent relaxation and that select overexpression of the CuZn isoform of superoxide dismutase is very effective in preventing ceramide-induced oxidative stress in vessels.
	Loss of Redox Factor 1 Decreases NF- ${kappa}$ B Activity and Increases Susceptibility of Endothelial Cells to Apoptosis Zhanjun Guan, David Basi, Qinglu Li, Ami Mariash, Yi-Feng Xia, Jian-Guo Geng, Esther Kao, and Jennifer L. Hall Arterioscler Thromb Vasc Biol. 2005;25:96-101; published online before print November 11 2004, doi:10.1161/01.ATV.0000150418.14698.75 Abstract \| Full Text \| PDF \| Data Supplement We assessed the role of Ref-1 as an upstream determinant governing NF-{kappa}B survival pathways in the vessel. NF-{kappa}B binding and A20 were downregulated in aortas of Ref-1+/- mice. Further studies defined the region(s) of Ref-1 regulating NF-{kappa}B and survival.
	Uterine Spiral Artery Remodeling Involves Endothelial Apoptosis Induced by Extravillous Trophoblasts Through Fas/FasL Interactions Sandra V. Ashton, Guy St. J. Whitley, Philip R. Dash, Mark Wareing, Ian P. Crocker, Philip N. Baker, and Judith E. Cartwright Arterioscler Thromb Vasc Biol. 2005;25:102-108; published online before print October 21 2004, doi:10.1161/01.ATV.0000148547.70187.89 Abstract \| Full Text \| PDF \| Data Supplement Remodeling of uterine spiral arteries occurs in the first trimester of pregnancy, with failed remodeling a characteristic of preeclampsia. This study gives the first insights into the possible mechanisms involved in this remodeling and suggests that trophoblast induction of endothelial apoptosis through Fas/FasL interactions may be important.
	Enhanced Cellular Adenosine Uptake Limits Adenosine Receptor Stimulation in Patients With Hyperhomocysteinemia Niels P. Riksen, Gerard A. Rongen, Godfried H.J. Boers, Henk J. Blom, Petra H.H. van den Broek, and Paul Smits Arterioscler Thromb Vasc Biol. 2005;25:109-114; published online before print November 11 2004, doi:10.1161/01.ATV.0000150651.85907.69 Abstract \| Full Text \| PDF We postulate that a homocysteine-induced fall in extracellular adenosine contributes to the cardiovascular complications of hyperhomocysteinemia. In patients with severe hyperhomocysteinemia, we demonstrated impaired adenosine-induced vasodilation, which was restored by coinfusion of the adenosine uptake inhibitor dipyridamole. In conclusion, cellular adenosine uptake in hyperhomocysteinemia is enhanced, thereby limiting adenosine receptor stimulation.
	Hyperhomocysteinemia Is Inversely Related With Left Ventricular Ejection Fraction and Predicts Cardiovascular Mortality in High-Risk Coronary Artery Disease Hypertensives Maurizio Cesari, Mario Zanchetta, Alberto Burlina, Luigi Pedon, Giuseppe Maiolino, Daniele Sticchi, Achille C. Pessina, and Gian Paolo Rossi Arterioscler Thromb Vasc Biol. 2005;25:115-121; published online before print November 4 2004, doi:10.1161/01.ATV.0000149674.62430.e7 Abstract \| Full Text \| PDF \| Data Supplement The purpose of this study was to investigate the relationship of plasma homocysteine (tHcy) levels with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) in high-risk patients undergoing coronary angiography for suspected CAD. In arterial hypertensive but not in normotensive patients, HHcy predicts cardiovascular mortality and a low LVEF, independent of CAD and history of myocardial infarction.
	Atherosclerosis and Lipoproteins
	Acyl-CoenzymeA (CoA):Cholesterol Acyltransferase Inhibition in Rat and Human Aortic Smooth Muscle Cells Is Nontoxic and Retards Foam Cell Formation James X. Rong, Jun Kusunoki, Peter Oelkers, Stephen L. Sturley, and Edward A. Fisher Arterioscler Thromb Vasc Biol. 2005;25:122-127; published online before print October 21 2004, doi:10.1161/01.ATV.0000148202.49842.3b Abstract \| Full Text \| PDF \| Data Supplement Aortic smooth muscle foam cell formation was induced with cholesterol-cyclodextrin complexes. Compared with current and published data in macrophages, simultaneous cholesterol-loading and ACAT inhibition led to little cytotoxicity in SMCs. Therefore, the potential for adverse consequences of ACAT inhibitors used therapeutically may be related to dose and the cell type.
	ACAT1 Deficiency Disrupts Cholesterol Efflux and Alters Cellular Morphology in Macrophages Dwayne E. Dove, Yan Ru Su, Wenwu Zhang, W. Gray Jerome, Larry L. Swift, MacRae F. Linton, and Sergio Fazio Arterioscler Thromb Vasc Biol. 2005;25:128-134; published online before print October 21 2004, doi:10.1161/01.ATV.0000148323.94021.e5 Abstract \| Full Text \| PDF To elucidate the mechanism of the increased atherosclerosis caused by the deletion of macrophage acyl-coenzyme A: cholesterol acyltransferase (ACAT1), studies of cholesterol storage and efflux were performed using ACAT1(-/-) macrophages. These studies show that ACAT1 influences the efflux of cellular and lipoprotein-derived cholesterol and causes a pro-atherogenic transformation of macrophages.
	Macrophage Liver X Receptor Is Required for Antiatherogenic Activity of LXR Agonists Nancy Levin, Eric D. Bischoff, Chris L. Daige, Diane Thomas, Calvin T. Vu, Richard A. Heyman, Rajendra K. Tangirala, and Ira G. Schulman Arterioscler Thromb Vasc Biol. 2005;25:135-142; published online before print November 11 2004, doi:10.1161/01.ATV.0000150044.84012.68 Abstract \| Full Text \| PDF LXR agonist treatment increases ATP-binding cassette transporter expression within preexisting atherosclerotic lesions, resulting in lesion regression, remodeling from vulnerable to stable lesions, and a reduction in lesion macrophage content. Using bone marrow transplantation, we provide the first evidence that macrophage LXR expression is necessary for the atheroprotective actions of an LXR agonist.
	Scavenger Receptor Class B Type I Mediates the Selective Uptake of High-Density Lipoprotein–Associated Cholesteryl Ester by the Liver in Mice May Brundert, Anne Ewert, Joerg Heeren, Barbara Behrendt, Rajasekhar Ramakrishnan, Heiner Greten, Martin Merkel, and Franz Rinninger Arterioscler Thromb Vasc Biol. 2005;25:143-148; published online before print November 4 2004, doi:10.1161/01.ATV.0000149381.16166.c6 Abstract \| Full Text \| PDF \| Data Supplement In mice with a targeted mutation in the SR-BI gene (knockout), no HDL-selective CE uptake is detected in the liver. This result is contrast to results found with wild-type animals. SR-BI has a physiological role in selective HDL CE uptake in vivo.
	Differential Additive Effects of Endothelial Lipase and Scavenger Receptor-Class B Type I on High-Density Lipoprotein Metabolism in Knockout Mouse Models Ke Ma, Trudy Forte, James D. Otvos, and Lawrence Chan Arterioscler Thromb Vasc Biol. 2005;25:149-154; published online before print November 11 2004, doi:10.1161/01.ATV.0000150414.89591.6a Abstract \| Full Text \| PDF \| Data Supplement We created EL and SR-BI single- and double-null mice and compared their effects on HDL concentration, composition, and structure. We demonstrated that EL and SR-BI display additive effects on plasma HDL in vivo with evident gene dosage effects. The 2 genes use different mechanisms to regulate HDL concentration and composition.
	Bilirubin From Heme Oxygenase-1 Attenuates Vascular Endothelial Activation and Dysfunction Keiichi Kawamura, Kazunobu Ishikawa, Youichiro Wada, Satoshi Kimura, Hayato Matsumoto, Takahide Kohro, Hiroyuki Itabe, Tatsuhiko Kodama, and Yukio Maruyama Arterioscler Thromb Vasc Biol. 2005;25:155-160; published online before print October 21 2004, doi:10.1161/01.ATV.0000148405.18071.6a Abstract \| Full Text \| PDF \| Data Supplement Vascular endothelial expression of heme oxygenase-1 (HO-1) attenuated the productions of proinflammatory cytokines and growth factors. HO-1 overexpression also alleviated the attenuated expression of endothelial-type NO synthase. These effects of HO-1 were predominantly mediated by one of its reaction products, bilirubin.
	Effect of Low Dose Atorvastatin Versus Diet-Induced Cholesterol Lowering on Atherosclerotic Lesion Progression and Inflammation in Apolipoprotein E3–Leiden Transgenic Mice Lars Verschuren, Robert Kleemann, Erik H. Offerman, Alexander J. Szalai, Sjef J. Emeis, Hans M. G. Princen, and Teake Kooistra Arterioscler Thromb Vasc Biol. 2005;25:161-167; published online before print October 28 2004, doi:10.1161/01.ATV.0000148866.29829.19 Abstract \| Full Text \| PDF \| Data Supplement We evaluated whether low-dose atorvastatin suppresses atherosclerotic lesion progression and inflammation independent of its cholesterol-lowering effect in apoE3-Leiden mice carrying preexisting mild lesions. Atorvastatin tended to retard atherogenesis in the aortic arch beyond cholesterol lowering and reduced inflammation (ie, VCAM-1 expression and monocyte adhesion) independently of cholesterol lowering.
	Low-Density Lipoprotein From Apolipoprotein E-Deficient Mice Induces Macrophage Lipid Accumulation in a CD36 and Scavenger Receptor Class A-Dependent Manner Zhenze Zhao, Maria C. de Beer, Lei Cai, Reto Asmis, Frederick C. de Beer, Willem J.S. de Villiers, and Deneys R. van der Westhuyzen Arterioscler Thromb Vasc Biol. 2005;25:168-173; published online before print October 28 2004, doi:10.1161/01.ATV.0000149145.00865.d9 Abstract \| Full Text \| PDF \| Data Supplement We investigated the atherogenic capability of circulating LDL from apoE-deficient mice and found that it functions in a proatherogenic manner, even without any further modification in vascular wall, through its uptake by scavenger receptors CD36 and SR-A.
	Reduced Macrophage Apoptosis Is Associated With Accelerated Atherosclerosis in Low-Density Lipoprotein Receptor-Null Mice June Liu, Douglas P. Thewke, Yan Ru Su, MacRae F. Linton, Sergio Fazio, and Michael S. Sinensky Arterioscler Thromb Vasc Biol. 2005;25:174-179; published online before print October 21 2004, doi:10.1161/01.ATV.0000148548.47755.22 Abstract \| Full Text \| PDF Bone marrow transplantation was performed to study the pathogenic role of macrophage apoptosis in atherogenesis. We found the atherosclerotic lesions in the aortic roots of low-density lipoprotein receptor-null mice reconstituted with Bax-/- bone marrow were increased by 49.2% compared with those in wild-type group, indicating macrophage apoptosis suppresses the development of atherosclerosis.
	Role of ADAMTS-1 in Atherosclerosis: Remodeling of Carotid Artery, Immunohistochemistry, and Proteolysis of Versican Ann-Cathrine Jönsson-Rylander, Tina Nilsson, Regina Fritsche-Danielson, Anette Hammarström, Margareta Behrendt, Jan-Olof Andersson, Kerstin Lindgren, Ann-Katrin Andersson, Pia Wallbrandt, Birgitta Rosengren, Peter Brodin, Anders Thelin, Annika Westin, Eva Hurt-Camejo, and Chung-Hyun Lee-Søgaard Arterioscler Thromb Vasc Biol. 2005;25:180-185; published online before print November 11 2004, doi:10.1161/01.ATV.0000150045.27127.37 Abstract \| Full Text \| PDF \| Data Supplement We investigated the potential role of ADAMTS-1 in atherogenesis. We show that ADAMTS-1 is differentially expressed in human plaques and VSMCs and that overexpression increased intimal hyperplasia in a mouse model for arterial remodeling. We hypothesize that ADAMTS-1 promotes VSMC migration and formation of neointima.
	Protein Kinase C Pathway Is Involved in Transcriptional Regulation of C-Reactive Protein Synthesis in Human Hepatocytes Yuri Ivashchenko, Frank Kramer, Stefan Schäfer, Andrea Bucher, Kerstin Veit, Vinzenz Hombach, Andreas Busch, Olaf Ritzeler, Jürgen Dedio, and Jan Torzewski Arterioscler Thromb Vasc Biol. 2005;25:186-192; published online before print November 11 2004, doi:10.1161/01.ATV.0000150041.81963.68 Abstract \| Full Text \| PDF We identify the PKC pathway as a novel pathway in the regulation of CRP synthesis in primary human hepatocytes. Stable transfection of HepG2 cells with the 1kb CRP promoter results in a cell line strongly inducible by IL-1ß/IL-6. Using this cell line, we show that PKC-mediated CRP transcription is NF-{kappa}B dependent. Moreover, this cell line may be useful for high throughput screening to identify inhibitors of CRP synthesis.
	Association Between Elevated Liver Enzymes and C-Reactive Protein: Possible Hepatic Contribution to Systemic Inflammation in the Metabolic Syndrome Arthur Kerner, Ophir Avizohar, Ron Sella, Peter Bartha, Oren Zinder, Walter Markiewicz, Yishai Levy, Gerald J. Brook, and Doron Aronson Arterioscler Thromb Vasc Biol. 2005;25:193-197; published online before print October 21 2004, doi:10.1161/01.ATV.0000148324.63685.6a Abstract \| Full Text \| PDF Elevated liver enzymes secondary to hepatic steatosis are frequent in subjects with the metabolic syndrome. We show a direct independent association between elevated liver enzymes and C-reactive protein concentrations. Thus, inflammatory processes that accompany hepatic steatosis may contribute to the systemic inflammation observed in subjects with the metabolic syndrome.
	Decreased Binding of Annexin V to Endothelial Cells: A Potential Mechanism in Atherothrombosis of Patients With Systemic Lupus Erythematosus Anna Cederholm, Elisabet Svenungsson, Kerstin Jensen-Urstad, Christina Trollmo, Ann-Kristin Ulfgren, Jesper Swedenborg, Guo-Zhong Fei, and Johan Frostegård Arterioscler Thromb Vasc Biol. 2005;25:198-203; published online before print November 11 2004, doi:10.1161/01.ATV.0000150415.18759.36 Abstract \| Full Text \| PDF Plasma from Systemic Lupus Erythematosus (SLE) patients with a history of atherothrombosis-induced decreased annexin V binding to endothelial cells as compared with SLE patients without and population controls. This effect was caused by antibodies. Immunohistochemistry revealed presence of antithrombotic annexin V in advanced human plaques. Inhibition of annexin V binding may promote atherothrombosis.
	Quantitative Trait Locus Mapping of Genetic Modifiers of Metabolic Syndrome and Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice: Identification of a Locus for Metabolic Syndrome and Increased Atherosclerosis on Chromosome 4 Sara Bretschger Seidelmann, Carl De Luca, Rudolph L. Leibel, Jan L. Breslow, Alan R. Tall, and Carrie L. Welch Arterioscler Thromb Vasc Biol. 2005;25:204-210; published online before print October 28 2004, doi:10.1161/01.ATV.0000149146.32385.1b Abstract \| Full Text \| PDF The purpose of this study was to examine genetic factors responsible for metabolic syndrome and atherosclerosis in a setting of LDL receptor deficiency in a cross between C57BL/6J and PERA/Ei (PERA) inbred mouse strains. The PERA strain is highly susceptible to the development of metabolic syndrome after feeding a Western-type diet, because of a locus on murine chromosome 4 in which PERA alleles predispose to adiposity, increased insulin, and accelerated atherogenesis in the absence of marked hyperlipidemia.
	Phenotype of Heterozygotes for Low-Density Lipoprotein Receptor Mutations Identified in Different Background Populations Anne Tybjærg-Hansen, Henrik Kjærulf Jensen, Marianne Benn, Rolf Steffensen, Gorm Jensen, and Børge G. Nordestgaard Arterioscler Thromb Vasc Biol. 2005;25:211-215; published online before print November 4 2004, doi:10.1161/01.ATV.0000149380.94984.f0 Abstract \| Full Text \| PDF \| Data Supplement We determined the relative importance of background population and type of mutation for cholesterol phenotype in 10 262 individuals. The phenotype associated with a given mutation should not be determined in patients, but rather in unselected individuals in the general population.
	Association of Lipoprotein-Associated Phospholipase A₂ Mass and Activity With Calcified Coronary Plaque in Young Adults: The CARDIA Study Carlos Iribarren, Myron D. Gross, Jeanne A. Darbinian, David R. Jacobs, Jr, Stephen Sidney, and Catherine M. Loria Arterioscler Thromb Vasc Biol. 2005;25:216-221; published online before print October 21 2004, doi:10.1161/01.ATV.0000148322.89911.44 Abstract \| Full Text \| PDF This nested case-control study among CARDIA participants at the year 15 examination (2000 to 01, 33 to 45 years old) demonstrates an independent association of Lp-PLA2 mass (but not its activity) with presence and amount of calcified coronary plaque. Therefore, Lp-PLA2 mass may be a useful marker of sub-clinical cardiovascular risk.
	Polymorphisms of the Interleukin-1ß Gene Affect the Risk of Myocardial Infarction and Ischemic Stroke at Young Age and the Response of Mononuclear Cells to Stimulation In Vitro L. Iacoviello, A. Di Castelnuovo, M. Gattone, A. Pezzini, D. Assanelli, R. Lorenzet, E. Del Zotto, M. Colombo, E. Napoleone, C. Amore, A. D’Orazio, A. Padovani, G. de Gaetano, P. Giannuzzi, M.B. Donati on behalf of IGIGI Investigators Arterioscler Thromb Vasc Biol. 2005;25:222-227; published online before print November 11 2004, doi:10.1161/01.ATV.0000150039.60906.02 Abstract \| Full Text \| PDF \| Data Supplement The T allele of the -511C/T polymorphism of the IL-1ß gene reduced the risk of premature MI and stroke. Mononuclear cells from carriers of the T allele showed decreased IL-1ß release and TF expression. Our findings support a role of inflammation in the pathogenesis of ischemic vascular disease.
	Mercury, Fish Oils, and Risk of Acute Coronary Events and Cardiovascular Disease, Coronary Heart Disease, and All-Cause Mortality in Men in Eastern Finland Jyrki K. Virtanen, Sari Voutilainen, Tiina H. Rissanen, Jaakko Mursu, Tomi-Pekka Tuomainen, Maarit J. Korhonen, Veli-Pekka Valkonen, Kari Seppänen, Jari A. Laukkanen, and Jukka T. Salonen Arterioscler Thromb Vasc Biol. 2005;25:228-233; published online before print November 11 2004, doi:10.1161/01.ATV.0000150040.20950.61 Abstract \| Full Text \| PDF Mercury may increase the risk of cardiovascular diseases. In this study, high mercury content in hair increased the risk of cardiovascular morbidity and mortality in middle-aged Finnish men and attenuated the beneficial effects of fish oils on cardiovascular health. Regular consumption of fish with high mercury content should be avoided.
	Quantitative Evaluation of Carotid Plaque Composition by In Vivo MRI T. Saam, M.S. Ferguson, V.L. Yarnykh, N. Takaya, D. Xu, N.L. Polissar, T.S. Hatsukami, and C. Yuan Arterioscler Thromb Vasc Biol. 2005;25:234-239; published online before print November 4 2004, doi:10.1161/01.ATV.0000149867.61851.31 Abstract \| Full Text \| PDF In vivo MR images of carotid plaques from 31 subjects scheduled for carotid endarterectomy were matched with corresponding histology sections. MRI measurements of plaque composition as percentage of the vessel wall corresponded to those of histology. This study demonstrates the potential of multicontrast MRI in the quantitative characterization of the main components of human atherosclerotic plaque.
	Thrombosis
	MRI of Atherothrombosis Associated With Plaque Rupture Jason Viereck, Frederick L. Ruberg, Ye Qiao, Alexandra S. Perez, Kara Detwiller, Michael Johnstone, and James A. Hamilton Arterioscler Thromb Vasc Biol. 2005;25:240-245; published online before print November 4 2004, doi:10.1161/01.ATV.0000149673.00564.0a Abstract \| Full Text \| PDF Excised aortas from atherosclerotic New Zealand rabbits after triggered plaque rupture were analyzed by MRI and histology. Platelet/fibrin-rich atherothrombi yielded imaging characteristics distinct from red cell-rich thrombi and were well resolved from the vessel wall by diffusion-weighted imaging. This technique has potential application for characterization of atherothrombosis.
	Helicobacter Pylori Infection Causes Persistent Platelet Activation In Vivo Through Enhanced Lipid Peroxidation Giovanni Davì, Matteo Neri, Angela Falco, Davide Festi, Tea Taraborelli, Giovanni Ciabattoni, Stefania Basili, Franco Cuccurullo, and Carlo Patrono Arterioscler Thromb Vasc Biol. 2005;25:246-251; published online before print October 7 2004, doi:10.1161/01.ATV.0000147128.10278.99 Abstract \| Full Text \| PDF Urinary excretion of 8-iso-PGF2a and 11-dehydro-TXB2 was significantly higher in Helicobacter pylori-positive individuals than in controls, with direct correlations between the degree of positivity to the 13C-urea breath test and urinary 8-iso-PGF2{alpha} and between the 2 metabolites. Successful H pylori eradication led to a reduction in these indexes of lipid peroxidation and platelet activation. We suggest a novel mechanism by which an infectious agent could contribute to atherothrombosis.
	Dimorphism in the P2Y1 ADP Receptor Gene Is Associated With Increased Platelet Activation Response to ADP Simon L. Hetherington, Ravi K. Singh, David Lodwick, John R. Thompson, Alison H. Goodall, and Nilesh J. Samani Arterioscler Thromb Vasc Biol. 2005;25:252-257; published online before print October 28 2004, doi:10.1161/01.ATV.0000148708.44691.27 Abstract \| Full Text \| PDF \| Data Supplement ADP is an important mediator of platelet aggregation. In this study, we show that a polymorphism (1622A>G) in the P2Y1 ADP receptor gene is associated with a significant effect on platelet ADP response. This genotype effect explains some of the interindividual variability in platelet reactivity and may influence thrombotic risk.
	Sulfatides Activate Platelets Through P-Selectin and Enhance Platelet and Platelet–Leukocyte Aggregation Michael Merten, Christian Beythien, Kai Gutensohn, Peter Kühnl, Thomas Meinertz, and Perumal Thiagarajan Arterioscler Thromb Vasc Biol. 2005;25:258-263; published online before print November 4 2004, doi:10.1161/01.ATV.0000149675.83552.83 Abstract \| Full Text \| PDF \| Data Supplement Sulfatides, sulfated glycosphingolipids, activated platelets via P-selectin as determined by an increase in activation of platelet GPIIb/IIIa and P-selectin. Therefore, sulfatides provide a positive feedback loop that can potentiate platelet aggregation. Furthermore, sulfatides aggregated washed platelets in a dose-dependent manner. In an ex vivo thrombosis model, sulfatides enhanced platelet and platelet-leukocyte aggregation.
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2005;25:264, doi:10.1161/01.ATV.0000165504.53303.9c Full Text \| PDF
	Acknowledgment of Reviewers
	Acknowledgment of Reviewers Arterioscler Thromb Vasc Biol. 2005;25:e1-e6, doi:10.1161/01.ATV.0000154200.48568.9a Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 1; January 1, 2005

Announcement

New Investigator Awards

Editorials

Arteriosclerosis, Thrombosis, and Vascular Biology, 2005

Plasma Plant Sterol Levels: Another Coronary Heart Disease Risk Factor?

ACAT Inhibition: Bad for Macrophages, Good for Smooth Muscle Cells?

Lesion Macrophages Are a Key Target for the Antiatherogenic Effects of LXR Agonists

The ADAMTS Proteases, Extracellular Matrix, and Vascular Disease: Waking the Sleeping Giant(s)!

Beyond the G Protein: The Saga of the Type 2 Angiotensin II Receptor

Brief Reviews

ATVB In Focus: Immunity and Atherosclerosis

Immunomodulation of Atherosclerosis: Implications for Vaccine Development

Oxidative Stress and Vascular Disease

Vitamin D, Shedding Light on the Development of Disease in Peripheral Arteries

Tissue Factor–Factor VIIa Signaling

Vascular Biology

Regulation of Transport of the Angiotensin AT2 Receptor by a Novel Membrane-Associated Golgi Protein

Dual Effect of Angiotensin-Converting Enzyme Inhibition on Angiogenesis in Type 1 Diabetic Mice

Antiangiogenic Activity of Semisynthetic Biotechnological Heparins: Low-Molecular-Weight-Sulfated Escherichia coli K5 Polysaccharide Derivatives as Fibroblast Growth Factor Antagonists

Vascular Injury Induces Expression of Periostin: Implications for Vascular Cell Differentiation and Migration

Differential Effects of Vasodilatory Prostaglandins on Focal Adhesions, Cytoskeletal Architecture, and Migration in Human Aortic Smooth Muscle Cells

Ceramide-Induced Impairment of Endothelial Function Is Prevented by CuZn Superoxide Dismutase Overexpression

Loss of Redox Factor 1 Decreases NF-B Activity and Increases Susceptibility of Endothelial Cells to Apoptosis

Uterine Spiral Artery Remodeling Involves Endothelial Apoptosis Induced by Extravillous Trophoblasts Through Fas/FasL Interactions

Enhanced Cellular Adenosine Uptake Limits Adenosine Receptor Stimulation in Patients With Hyperhomocysteinemia

Hyperhomocysteinemia Is Inversely Related With Left Ventricular Ejection Fraction and Predicts Cardiovascular Mortality in High-Risk Coronary Artery Disease Hypertensives

Atherosclerosis and Lipoproteins

Acyl-CoenzymeA (CoA):Cholesterol Acyltransferase Inhibition in Rat and Human Aortic Smooth Muscle Cells Is Nontoxic and Retards Foam Cell Formation

ACAT1 Deficiency Disrupts Cholesterol Efflux and Alters Cellular Morphology in Macrophages

Macrophage Liver X Receptor Is Required for Antiatherogenic Activity of LXR Agonists

Scavenger Receptor Class B Type I Mediates the Selective Uptake of High-Density Lipoprotein–Associated Cholesteryl Ester by the Liver in Mice

Differential Additive Effects of Endothelial Lipase and Scavenger Receptor-Class B Type I on High-Density Lipoprotein Metabolism in Knockout Mouse Models

Bilirubin From Heme Oxygenase-1 Attenuates Vascular Endothelial Activation and Dysfunction

Effect of Low Dose Atorvastatin Versus Diet-Induced Cholesterol Lowering on Atherosclerotic Lesion Progression and Inflammation in Apolipoprotein E*3–Leiden Transgenic Mice

Low-Density Lipoprotein From Apolipoprotein E-Deficient Mice Induces Macrophage Lipid Accumulation in a CD36 and Scavenger Receptor Class A-Dependent Manner

Reduced Macrophage Apoptosis Is Associated With Accelerated Atherosclerosis in Low-Density Lipoprotein Receptor-Null Mice

Role of ADAMTS-1 in Atherosclerosis: Remodeling of Carotid Artery, Immunohistochemistry, and Proteolysis of Versican

Protein Kinase C Pathway Is Involved in Transcriptional Regulation of C-Reactive Protein Synthesis in Human Hepatocytes

Association Between Elevated Liver Enzymes and C-Reactive Protein: Possible Hepatic Contribution to Systemic Inflammation in the Metabolic Syndrome

Decreased Binding of Annexin V to Endothelial Cells: A Potential Mechanism in Atherothrombosis of Patients With Systemic Lupus Erythematosus

Quantitative Trait Locus Mapping of Genetic Modifiers of Metabolic Syndrome and Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice: Identification of a Locus for Metabolic Syndrome and Increased Atherosclerosis on Chromosome 4

Phenotype of Heterozygotes for Low-Density Lipoprotein Receptor Mutations Identified in Different Background Populations

Association of Lipoprotein-Associated Phospholipase A2 Mass and Activity With Calcified Coronary Plaque in Young Adults: The CARDIA Study

Polymorphisms of the Interleukin-1ß Gene Affect the Risk of Myocardial Infarction and Ischemic Stroke at Young Age and the Response of Mononuclear Cells to Stimulation In Vitro

Mercury, Fish Oils, and Risk of Acute Coronary Events and Cardiovascular Disease, Coronary Heart Disease, and All-Cause Mortality in Men in Eastern Finland

Quantitative Evaluation of Carotid Plaque Composition by In Vivo MRI

Thrombosis

MRI of Atherothrombosis Associated With Plaque Rupture

Helicobacter Pylori Infection Causes Persistent Platelet Activation In Vivo Through Enhanced Lipid Peroxidation

Dimorphism in the P2Y1 ADP Receptor Gene Is Associated With Increased Platelet Activation Response to ADP

Sulfatides Activate Platelets Through P-Selectin and Enhance Platelet and Platelet–Leukocyte Aggregation

Corrections

Correction

Acknowledgment of Reviewers

Acknowledgment of Reviewers

Spotlight

Loss of Redox Factor 1 Decreases NF- ${kappa}$ B Activity and Increases Susceptibility of Endothelial Cells to Apoptosis

Association of Lipoprotein-Associated Phospholipase A₂ Mass and Activity With Calcified Coronary Plaque in Young Adults: The CARDIA Study