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Volume 28, Issue 1; January 1, 2008
Editorials
Brief Reviews
Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Retraction
Letters to the Editor
Clinical and Population Studies
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Editorials
Protective Signaling Pathways of Activated Protein C in Endothelial Cells
Matthias Riewald and Reto A. Schuepbach
Arterioscler Thromb Vasc Biol. 2008;28:1-3, doi:10.1161/ATVBAHA.107.157321
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Angiotensin II and New Vessel Formation: Aiming for the Right Oxidative Window
Juan C. Velasquez-Castano and W. Robert Taylor
Arterioscler Thromb Vasc Biol. 2008;28:4-5, doi:10.1161/ATVBAHA.107.155978
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Twin Layers of Lightning: A New Role for the Chaperone Hsp90 in Angiogenesis
Xinchun Pi and Cam Patterson
Arterioscler Thromb Vasc Biol. 2008;28:6-7; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.156786
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Brief Reviews
MCAT Elements and the TEF-1 Family of Transcription Factors in Muscle Development and Disease
Tadashi Yoshida
Arterioscler Thromb Vasc Biol. 2008;28:8-17; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.155788
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This article summarizes the role of MCAT elements and the transcriptional enhancer factor-1 family of transcription factors in cardiac, smooth, and skeletal muscle development and disease, and reviews recent progress in our understanding of the transcriptional regulatory mechanisms involved in MCAT element-dependent muscle-specific gene expression.
VAP-1 and CD73, Endothelial Cell Surface Enzymes in Leukocyte Extravasation
Sirpa Jalkanen and Marko Salmi
Arterioscler Thromb Vasc Biol. 2008;28:18-26; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.153130
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Leukocyte extravasation from the blood into tissues is crucial for normal immune surveillance and in inflammation. Emerging evidence suggests that enzymes expressed on the surface of endothelial cells and leukocytes contribute to the leukocyte extravasation cascade. They also provide new possibilities to inhibit inappropriate inflammations.
Fatty Liver: A Novel Component of the Metabolic Syndrome
Anna Kotronen and Hannele Yki-Järvinen
Arterioscler Thromb Vasc Biol. 2008;28:27-38; published online before print August 9 2007, doi:10.1161/ATVBAHA.107.147538
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Fat accumulation in the liver characterizes subjects who develop the metabolic syndrome. Liver fat also predicts, independent of obesity, the increased risk of type 2 diabetes, CVD, and liver disease, which accompany the metabolic syndrome.
Is There a Role for Fibrates in the Management of Dyslipidemia in the Metabolic Syndrome?
Philip J. Barter and Kerry-Anne Rye
Arterioscler Thromb Vasc Biol. 2008;28:39-46; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.148817
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Features of the metabolic syndrome identify people who have a disproportionately large reduction in cardiovascular events when treated with fibrates. The protection in these people is largely independent of changes in plasma lipids, raising questions about the mechanism of the protection.
Integrative Physiology/Experimental Medicine
Increased Smooth Muscle Cell Activation and Neointima Formation in Response to Injury in AIF-1 Transgenic Mice
Laura J. Sommerville, Sheri E. Kelemen, and Michael V. Autieri
Arterioscler Thromb Vasc Biol. 2008;28:47-53; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.156794
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A transgenic mouse in which AIF-1 expression was driven by a VSMC-specific SM22{alpha} promoter was generated. Injured arteries from this mouse demonstrate a significant increase in neointimal area in response to ligation injury. In vivo and ex vivo, transgenic VSMCs demonstrate increased migration, proliferation, and activation of signal transduction proteins.
Late-Outgrowth Endothelial Cells Attenuate Intimal Hyperplasia Contributed by Mesenchymal Stem Cells After Vascular Injury
Chao-Hung Wang, Wen-Jin Cherng, Ning-I Yang, Li-Tang Kuo, Chia-Ming Hsu, Hung-I Yeh, Yii-Jenq Lan, Chi-Hsiao Yeh, and William L. Stanford
Arterioscler Thromb Vasc Biol. 2008;28:54-60; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.147256
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Mesenchymal stem cells (MSCs) are one of the cell types being used for cardiac regeneration therapy. MSCs exhibited a strong adhesive capacity and contributed to vascular remodeling of diseased vessels, such as intimal hyperplasia. Combining MSC therapy with outgrowth endothelial cells significantly modulated and attenuated this MSC-related adverse effect.
The Mechanistic Basis for the Disparate Effects of Angiotensin II on Coronary Collateral Growth
Ryan Reed, Christopher Kolz, Barry Potter, and Petra Rocic
Arterioscler Thromb Vasc Biol. 2008;28:61-67; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.154294
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Ang II regulates repetitive ischemia (RI)-induced coronary collateral growth (CCG) via ROS generation and redox-sensitive signaling. In normal oxidative stress, AT1R blockade decreases CCG; in elevated oxidative stress (metabolic syndrome), AT1R blockade rescues CCG by normalizing oxidative stress and activating p38 and Akt.
Phosphoinositide 3-Kinase
Gene Knockout Impairs Postischemic Neovascularization and Endothelial Progenitor Cell Functions
Paolo Madeddu, Nicolle Kraenkel, Luciola S. Barcelos, Mauro Siragusa, Paola Campagnolo, Atsuhiko Oikawa, Andrea Caporali, Andrew Herman, Ornella Azzolino, Laura Barberis, Alessia Perino, Federico Damilano, Costanza Emanueli, and Emilio Hirsch
Arterioscler Thromb Vasc Biol. 2008;28:68-76; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.145573
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We demonstrated that PI3K{gamma} is fundamental for reparative neovascularization and EPC function. PI3K{gamma} is upregulated in ischemic limb muscles and hypoxic EPCs. After limb ischemia, PI3K{gamma}-deficient mice show impaired revascularization and blood flow recovery, attributable to reduced EC proliferation and enhanced apoptosis. PI3K{gamma} deficiency impairs EPC growth, survival, migration, and adhesion.
Magnetic Resonance Imaging of Endothelial Adhesion Molecules in Mouse Atherosclerosis Using Dual-Targeted Microparticles of Iron Oxide
Martina A. McAteer, Jurgen E. Schneider, Ziad A. Ali, Nicholas Warrick, Christina A. Bursill, Constantin von zur Muhlen, David R. Greaves, Stefan Neubauer, Keith M. Channon, and Robin P. Choudhury
Arterioscler Thromb Vasc Biol. 2008;28:77-83; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.145466
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Microparticles of iron oxide (MPIO) were conjugated with monoclonal antibodies targeting VCAM-1 and P-selectin. After in vivo intravenous injection, dual-targeted MPIO binding to aortic root plaque endothelium in apolipoprotein E knockout mice was detected by high-resolution ex vivo MRI.
Accumulation of Myeloperoxidase-Positive Neutrophils in Atherosclerotic Lesions in LDLR
–/–
Mice
Marcella van Leeuwen, Marion J.J. Gijbels, Adriaan Duijvestijn, Marjan Smook, Marie José van de Gaar, Peter Heeringa, Menno P.J. de Winther, and Jan Willem Cohen Tervaert
Arterioscler Thromb Vasc Biol. 2008;28:84-89; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.154807
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We identified myeloperoxidase-positive neutrophils in mouse atherosclerotic lesions. Although neutrophils were not detected in early lesions, they were abundantly present in more advanced stages. In addition, circulating myeloperoxidase levels were strongly increased by high-fat feeding of the mice. Therefore, neutrophils should be considered as a potential important cellular mediator in atherogenesis.
Critical Role of Bone Marrow Angiotensin II Type 1 Receptor in the Pathogenesis of Atherosclerosis in Apolipoprotein E–Deficient Mice
Daiju Fukuda, Masataka Sata, Nobukazu Ishizaka, and Ryozo Nagai
Arterioscler Thromb Vasc Biol. 2008;28:90-96; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.152363
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We demonstrated potential contribution of angiotensin II type 1 receptor (AT1R) in bone marrow (BM) to the pathogenesis of atherosclerotic lesions, at least in part. Therefore, blockade of AT1R not only in vascular cells but also in BM could be an important strategy to prevent atherosclerosis.
Cell Biology/Signaling
Regulation of Endothelial Cell Proliferation by Primary Monocytes
Shai Y. Schubert, Alejandro Benarroch, Janne Ostvang, and Elazer R. Edelman
Arterioscler Thromb Vasc Biol. 2008;28:97-104; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.157537
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After direct contact with primary unactivated monocytes, endothelial cells enter S-phase through a mechanism mediated in part by contact-dependent activation of endothelial Met. Monocyte-induced endothelial cell proliferation is accompanied by prolonged ERK activation, it is specific to endothelial cells, and does not occur with vascular smooth muscle cells.
Dominant-Negative Hsp90 Reduces VEGF-Stimulated Nitric Oxide Release and Migration in Endothelial Cells
Robert Q. Miao, Jason Fontana, David Fulton, Michelle I. Lin, Kenneth D. Harrison, and William C. Sessa
Arterioscler Thromb Vasc Biol. 2008;28:105-111; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.155499
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To explore functions of Hsp90 in endothelial cells (ECs), a dominant-negative Hsp90 (D88N-Hsp90beta) was generated that could not bind ATP. Adenovirus-mediated transduction of ECs with D88N-Hsp90beta suppressed VEGF-induced phosphorylation of Akt and eNOS and inhibited VEGF-stimulated NO release, stress fiber formation, and VEGF-induced chemotaxis.
FOXO3a Turns the Tumor Necrosis Factor Receptor Signaling Towards Apoptosis Through Reciprocal Regulation of c-Jun N-Terminal Kinase and NF-
B
Hae-Young Lee, Seock-Won Youn, Ju-Young Kim, Kyung-Woo Park, Chang-Il Hwang, Woong-Yang Park, Byung-Hee Oh, Young-Bae Park, Kenneth Walsh, Jeong-Sun Seo, and Hyo-Soo Kim
Arterioscler Thromb Vasc Biol. 2008;28:112-120; published online before print November 21 2007, doi:10.1161/ATVBAHA.107.153304
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The effects of FOXO3a on endothelial cells were evaluated by microarray analysis. The activation of FOXO3a promotes apoptosis through activation of JNK and suppression of NF-{kappa}B. This study identifies a novel role of FOXO3a in directing TNF receptor signaling to a proapoptotic JNK-dependent pathway.
Peripheral Circadian Clock Rhythmicity Is Retained in the Absence of Adrenergic Signaling
Dermot F. Reilly, Anne M. Curtis, Yan Cheng, Elizabeth J. Westgate, Radu D. Rudic, Georgios Paschos, Jacqueline Morris, Ming Ouyang, Steven A. Thomas, and Garret A. FitzGerald
Arterioscler Thromb Vasc Biol. 2008;28:121-126; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.152538
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We have examined the impact of adrenergic signaling on circadian timing in vascular tissues. Using vascular smooth muscle cells and dopamine β hydroxylase knockout mice we found that adrenergic signaling can influence circadian gene expression in vitro, but peripheral circadian rhythmicity is retained despite its ablation in vivo.
Activation of Thromboxane Receptor Upregulates Interleukin (IL)-1β–Induced VCAM-1 Expression Through JNK Signaling
Hossein Bayat, Shanqin Xu, David Pimentel, Richard A. Cohen, and Bingbing Jiang
Arterioscler Thromb Vasc Biol. 2008;28:127-134; published online before print November 21 2007, doi:10.1161/ATVBAHA.107.150250
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Activation of thromboxane receptors (TPr) is implicated in atherosclerosis and inflammation. This study demonstrated that in vascular smooth muscle cells, activation of TPr with U46619 alone does not induce vascular cell adhesion molecule (VCAM)-1 expression, but enhances IL-1β-induced VCAM-1 expression through enhancing JNK-dependent AP-1 activation, which enhances monocyte adhesion.
TF/FVIIa Transactivate PDGFRβ to Regulate PDGF-BB–Induced Chemotaxis in Different Cell Types: Involvement of Src And PLC
Agneta Siegbahn, Matilda Johnell, Anna Nordin, Mikael Åberg, and Teet Velling
Arterioscler Thromb Vasc Biol. 2008;28:135-141; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.155754
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TF/FVIIa was found to selectively potentiate the PDGF-BB-induced chemotaxis of 3 principally different cell types. We provide data concerning the signaling pathways involved in this potentiation, and describe the TF/FVIIa-induced, PAR-2, c-Src, and c-Yes-dependent transactivation of PDGFRβ as a likely mechanism of its regulation.
Retraction
Correction
Arterioscler Thromb Vasc Biol. 2008;28:e1, doi:10.1161/ATVBAHA.107.158881
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Letters to the Editor
Choice of Anticoagulant Critically Affects Measurement of Circulating Platelet-Leukocyte Complexes
Stylianos Bournazos, Jillian Rennie, Simon P. Hart, and Ian Dransfield
Arterioscler Thromb Vasc Biol. 2008;28:e2-e3; published online before print January 1 2008, doi:10.1161/ATVBAHA.107.153387
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Clinical and Population Studies
Inflammation, Statin Therapy, and Risk of Stroke After an Acute Coronary Syndrome in the MIRACL Study
Scott Kinlay, Gregory G. Schwartz, Anders G. Olsson, Nader Rifai, Michael Szarek, David D. Waters, Peter Libby, Peter Ganz for the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study Investigators
Arterioscler Thromb Vasc Biol. 2008;28:142-147; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.151787
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We measured baseline CRP, SAA, and IL-6 in 2926 subjects in the MIRACL study, a randomized trial of atorvastatin versus placebo in acute coronary syndromes. Greater levels of inflammatory markers were related to stroke, and atorvastatin abrogated this risk providing a novel rationale for statins in acute coronary syndromes.
Inhibition of CETP by Torcetrapib Attenuates the Atherogenicity of Postprandial TG-Rich Lipoproteins in Type IIB Hyperlipidemia
Maryse Guerin, Wilfried Le Goff, Emilie Duchene, Zélie Julia, Tu Nguyen, Tom Thuren, Charles L. Shear, and M. John Chapman
Arterioscler Thromb Vasc Biol. 2008;28:148-154; published online before print October 19 2007, doi:10.1161/ATVBAHA.107.151688
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CETP inhibition via torcetrapib, on a background of atorvastatin, reduces the postprandial accumulation of atherogenic triglyceride-rich subspecies including chylomicrons and VLDL-1 in type IIB hyperlipidemia, but equally attenuates their atherogenicity by reducing core CE content.
Differential Impact of Age, Sex, and Hypertension on Aortic Atherosclerosis: The Framingham Heart Study
Noriko Oyama, Philimon Gona, Carol J. Salton, Michael L. Chuang, Rahul R. Jhaveri, Susan J. Blease, Anya R. Manning, Marc Lahiri, René M. Botnar, Daniel Levy, Martin G. Larson, Christopher J. ODonnell, and Warren J. Manning
Arterioscler Thromb Vasc Biol. 2008;28:155-159; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.153544
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In a free-living cohort, subclinical aortic plaque was seen in nearly half of subjects and increased with age. Hypertension was associated with increased aortic plaque burden. Among nonhypertensive subjects, women had greater plaque burden than men. The data underline the importance of focusing on preventive measures in both sexes.
Are Serum Carcinoembryonic Antigen Levels Associated With Carotid Atherosclerosis in Japanese Men?
Nobukazu Ishizaka, Yuko Ishizaka, Ei-Ichi Toda, Kazuhiko Koike, Minoru Yamakado, and Ryozo Nagai
Arterioscler Thromb Vasc Biol. 2008;28:160-165; published online before print October 19 2007, doi:10.1161/ATVBAHA.107.155465
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Association between serum levels of carcinoembryonic antigen (CEA) and carotid atherosclerosis was investigated by analyzing the cross-sectional data of 4181 Japanese men undergoing general health screening. Multivariate analysis showed that serum CEA levels were associated with carotid atherosclerosis that was independent of white blood cell count and hsCRP.
Serum Total Bilirubin Level and Prevalent Lower-Extremity Peripheral Arterial Disease: National Health and Nutrition Examination Survey (NHANES) 1999 to 2004
Todd S. Perlstein, Reena L. Pande, Joshua A. Beckman, and Mark A. Creager
Arterioscler Thromb Vasc Biol. 2008;28:166-172; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.153262
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Bilirubin has antiinflammatory, antioxidant, and possibly atheroprotective properties. Among 7075 adults in the NHANES 1999 to 2004, we found that bilirubin was inversely associated with PAD prevalence independent of traditional and novel PAD risk factors. Higher bilirubin levels may therefore be associated with lessened susceptibility to PAD.
Association of Gene Variants With Incident Myocardial Infarction in the Cardiovascular Health Study
Dov Shiffman, Ellen S. OMeara, Lance A. Bare, Charles M. Rowland, Judy Z. Louie, Andre R. Arellano, Thomas Lumley, Kenneth Rice, Olga Iakoubova, May M. Luke, Bradford A. Young, Mary J. Malloy, John P. Kane, Stephen G. Ellis, Russell P. Tracy, James J. Devlin, and Bruce M. Psaty
Arterioscler Thromb Vasc Biol. 2008;28:173-179; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.153981
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We identified 4 SNPs (in KIF6, VAMP8, LPA, and TAS2R50) that are associated with increased risk of incident MI in CHS, a prospective study of adults aged 65 years or older.
Genetic Variation in
ABCA1
Predicts Ischemic Heart Disease in the General Population
Ruth Frikke-Schmidt, Børge G. Nordestgaard, Gorm B. Jensen, Rolf Steffensen, and Anne Tybjærg-Hansen
Arterioscler Thromb Vasc Biol. 2008;28:180-186; published online before print October 19 2007, doi:10.1161/ATVBAHA.107.153858
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We tested whether nonsynonymous SNPs in ABCA1 affect risk of IHD in the general population. We show that 3 of 6 nonsynonymous SNPs in ABCA1 predict risk of IHD in the general population.
Association Between Plasma LDL Particle Size, Valvular Accumulation of Oxidized LDL, and Inflammation in Patients With Aortic Stenosis
Dania Mohty, Philippe Pibarot, Jean-Pierre Després, Claude Côté, Benoit Arsenault, Amélie Cartier, Pierre Cosnay, Christian Couture, and Patrick Mathieu
Arterioscler Thromb Vasc Biol. 2008;28:187-193; published online before print November 1 2007, doi:10.1161/ATVBAHA.107.154989
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In 102 aortic valves explanted for a stenosis, we found that valves with a higher content of oxidized LDL had more pronounced inflammation and tissue remodeling. The proportion of circulating small dense LDL particles was associated with valvular accumulation of oxidized LDL and faster progression of stenosis.
Arterial Stiffness Is Associated With Regional Ventricular Systolic and Diastolic Dysfunction: The Multi-Ethnic Study of Atherosclerosis
Verônica Rolim S. Fernandes, Joseph F. Polak, Susan Cheng, Boaz D. Rosen, Benilton Carvalho, Khurram Nasir, Robyn McClelland, Gregory Hundley, Greg Pearson, Daniel H. OLeary, David A. Bluemke, and João A.C. Lima
Arterioscler Thromb Vasc Biol. 2008;28:194-201; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.156950
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We sought to determine whether or not arterial compliance is related to regional myocardial function among participants of the Multi-Ethnic Study of Atherosclerosis. We found a significant association between arterial compliance and regional myocardial function (SRS and SRE). Arterial stiffness is associated with early and asymptomatic impairment of regional myocardial function.
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