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About This Cover
Volume 28, Issue 5; May 1, 2008
Editorials
Brief Reviews
Integrative Physiology/Experimental Medicine
Integrated Physiology/Experimental Medicine
Cell Biology and Signaling
Clinical and Population Studies
Corrections
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Key:  
VB = Vascular Biology
  
AL = Atherosclerosis/Lipoproteins
  
TH = Thrombosis
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article is free immediately upon publication
Editorials
Recipients of the 2008 New Investigator Awards
Connie Melsha
Arterioscler Thromb Vasc Biol. 2008;28:799-800, doi:10.1161/ATVBAHA.108.166447
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Nanomedicine Captures Cardiovascular Disease
Willem J.M. Mulder and Zahi A. Fayad
Arterioscler Thromb Vasc Biol. 2008;28:801-802, doi:10.1161/ATVBAHA.108.165332
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The Adult Epicardium: Realizing the Potential for Neovascular Therapy
Paul R. Riley
Arterioscler Thromb Vasc Biol. 2008;28:803-804, doi:10.1161/ATVBAHA.108.165191
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Cysteinyl-Leukotrienes in Cerebrovascular Disease: Angels and Demons?
Magnus Bäck
Arterioscler Thromb Vasc Biol. 2008;28:805-806, doi:10.1161/ATVBAHA.108.164459
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Expanding the Concept of Telomere Dysfunction in Cardiovascular Disease
Pim van der Harst, Dirk J. van Veldhuisen, and Nilesh J. Samani
Arterioscler Thromb Vasc Biol. 2008;28:807-808, doi:10.1161/ATVBAHA.108.164434
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HDL, PTX3, and Vascular Protection
Ziad Mallat and Alain Tedgui
Arterioscler Thromb Vasc Biol. 2008;28:809-811, doi:10.1161/ATVBAHA.108.163204
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Brief Reviews
Role of Smooth Muscle Cells in the Initiation and Early Progression of Atherosclerosis
Amanda C. Doran, Nahum Meller, and Coleen A. McNamara
Arterioscler Thromb Vasc Biol. 2008;28:812-819; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.159327
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Smooth muscle cells (SMCs) play a key role in fibrous cap formation and plaque stability in advanced atherosclerosis; however, less is known about the role of SMCs in the initiation and progression of atherosclerosis. This review summarizes the present data implicating SMCs in the development of early atherogenesis.
Integrative Physiology/Experimental Medicine
Angiopoietin-Related Growth Factor Enhances Blood Flow Via Activation of the ERK1/2-eNOS-NO Pathway in a Mouse Hind-Limb Ischemia Model
Takashi Urano, Yasuhiro Ito, Masaki Akao, Tomohiro Sawa, Keishi Miyata, Mitsuhisa Tabata, Tohru Morisada, Tai Hato, Masato Yano, Tsuyoshi Kadomatsu, Kunio Yasunaga, Rei Shibata, Toyoaki Murohara, Takaaki Akaike, Hidenobu Tanihara, Toshio Suda, and Yuichi Oike
Arterioscler Thromb Vasc Biol. 2008;28:827-834; published online before print February 7 2008, doi:10.1161/ATVBAHA.107.149674
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We sought to determine whether AGF enhances blood flow in a mouse hind-limb ischemia model and to define its molecular mechanisms. Activation of an ERK1/2-eNOS-NO pathway is crucial for AGF-induced angiogenesis and arteriogenesis. AGF signaling pathway may contribute to develop a new clinical strategy for ischemic vascular diseases.
Sequential Activation of Matrix Metalloproteinase 9 and Transforming Growth Factor β in Arterial Elastocalcinosis
Céline Bouvet, Simon Moreau, Joannie Blanchette, Denis de Blois, and Pierre Moreau
Arterioscler Thromb Vasc Biol. 2008;28:856-862; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.153056
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The objective was to determine the importance and timing of matrix degradation in relation to elastocalcinosis associated with enhanced vascular stiffness. Matrix degradation and its cellular signaling are essential to elastocalcinosis and precede elastin fragmentation, overt calcification, and enhanced vascular stiffness. These early events could represent means to limit stiffening of large arteries.
Integrated Physiology/Experimental Medicine
Intramural Delivery of Rapamycin With
v
β
3
-Targeted Paramagnetic Nanoparticles Inhibits Stenosis After Balloon Injury
Tillmann Cyrus, Huiying Zhang, John S. Allen, Todd A. Williams, Grace Hu, Shelton D. Caruthers, Samuel A. Wickline, and Gregory M. Lanza
Arterioscler Thromb Vasc Biol. 2008;28:820-826; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.156281
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Femoral arteries of 48 atherosclerotic rabbits underwent balloon stretch injury and were treated locally with either: (1) {alpha}vβ3-targeted rapamycin nanoparticles, (2) {alpha}vβ3-targeted nanoparticles without rapamycin, (3) nontargeted rapamycin nanoparticles, or (4) saline. Intramural delivery of {alpha}vβ3-targeted rapamycin nanoparticles inhibited stenosis at 2 weeks without delaying endothelial healing following balloon injury over 4 weeks.
Suppression of the Raf/MEK/ERK Signaling Cascade and Inhibition of Angiogenesis by the Carboxyl Terminus of Angiopoietin-Like Protein 4
Ying-Hua Yang, Yu Wang, Karen S.L. Lam, Ming-Hon Yau, Kenneth K.Y. Cheng, Jialiang Zhang, Weidong Zhu, Donghai Wu, and Aimin Xu
Arterioscler Thromb Vasc Biol. 2008;28:835-840; published online before print March 13 2008, doi:10.1161/ATVBAHA.107.157776
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This study comprehensively investigated the structural and cellular basis underlying the antiangiogenic activities of angiopoietin-like protein-4 (Angptl4). We found that the carboxyl terminus of Angptl4 alone is sufficient to suppress neovascularization in an N-glycosylation-dependent manner. Furthermore, our results showed that Angplt4 inhibits the Raf-1/ERK1/2 MAPK pathway in endothelial cells.
Prokineticin Receptor-1 Induces Neovascularization and Epicardial-Derived Progenitor Cell Differentiation
Kyoji Urayama, Célia Guilini, Gulen Turkeri, Selcuk Takir, Hitoshi Kurose, Nadia Messaddeq, Andrée Dierich, and Canan G. Nebigil
Arterioscler Thromb Vasc Biol. 2008;28:841-849, doi:10.1161/ATVBAHA.108.162404
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Prokineticins are secreted bioactive proteins that bind to 2 GPCRs, PKR1 and PKR2. Using transgenic mice, coculture cell models, EPDC, and PKR1-null mutants, we showed that cardiomyocyte-PKR1 signaling upregulates its own ligand prokineticin-2 as a paracrine factor, trigerring pluripotency of EPDCs, to promote neovascularization.
Site-Specific Atherogenic Gene Expression Correlates With Subsequent Variable Lesion Development in Coronary and Peripheral Vasculature
Emile R. Mohler, III, Lea Sarov-Blat, Yi Shi, Damir Hamamdzic, Andrew Zalewski, Colin MacPhee, Raul Llano, Dan Pelchovitz, Sumeet K. Mainigi, Hashim Osman, Troy Hallman, Klaudia Steplewski, Zachary Gertz, Min Min Lu, and Robert L Wilensky
Arterioscler Thromb Vasc Biol. 2008;28:850-855; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.154534
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Differential development of advanced atherosclerosis in 3 arterial beds of diabetic and hypercholesterolemic pigs was associated with differential gene expression in cholesterol metabolism, insulin, and inflammation signaling related pathways. The results provide insight into the arterial-specific and time-dependent variability of vascular gene expression.
Adiponectin Protects Against Angiotensin II–Induced Cardiac Fibrosis Through Activation of PPAR-
Koichi Fujita, Norikazu Maeda, Mina Sonoda, Koji Ohashi, Toshiyuki Hibuse, Hitoshi Nishizawa, Makoto Nishida, Aki Hiuge, Akifumi Kurata, Shinji Kihara, Iichiro Shimomura, and Tohru Funahashi
Arterioscler Thromb Vasc Biol. 2008;28:863-870; published online before print February 28 2008, doi:10.1161/ATVBAHA.107.156687
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Adiponectin-deficient mice revealed severe angiotensin II-induced cardiac fibrosis and its phenotype were reversed by adiponectin supplementation. However, adiponectin treatment failed to ameliorate cardiac fibrosis in angiotensin II-infused PPAR-{alpha}-deficient mice. In vivo and in vitro experiments suggested that adiponectin protects against angiotensin II-induced cardiac fibrosis possibly through AMPK-dependent PPAR-{alpha} activation.
Effects of Statins on Adipose Tissue Inflammation: Their Inhibitory Effect on MyD88-Independent IRF3/IFN-β Pathway in Macrophages
Manabu Abe, Morihiro Matsuda, Hironori Kobayashi, Yugo Miyata, Yuki Nakayama, Ryutaro Komuro, Atsunori Fukuhara, and Iichiro Shimomura
Arterioscler Thromb Vasc Biol. 2008;28:871-877; published online before print March 6 2008, doi:10.1161/ATVBAHA.107.160663
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We investigated the effects of HMG CoA reductase inhibitors (statins) on adipose tissue inflammation and macrophages. We found that treatment of obese mice with statins partially attenuated the development of adipose tissue inflammation, and that statins had an inhibitory effect on MyD88-independent IRF3/IFN-β pathway in macrophages.
Cell Biology and Signaling
AP-1–Dependent Transcriptional Regulation of NADPH Oxidase in Human Aortic Smooth Muscle Cells: Role of p22
phox
Subunit
Adrian Manea, Simona A. Manea, Anca V. Gafencu, Monica Raicu, and Maya Simionescu
Arterioscler Thromb Vasc Biol. 2008;28:878-885; published online before print February 28 2008, doi:10.1161/ATVBAHA.108.163592
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Gas6–Axl Receptor Signaling Is Regulated by Glucose in Vascular Smooth Muscle Cells
Megan E. Cavet, Elaine M. Smolock, Oktay H. Ozturk, Cameron World, Jinjiang Pang, Atsushi Konishi, and Bradford C. Berk
Arterioscler Thromb Vasc Biol. 2008;28:886-891; published online before print February 21 2008, doi:10.1161/ATVBAHA.108.162693
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This study demonstrates a role for glucose in altering Axl signaling through coupling to binding partners. Specifically, binding of Axl to the p85 subunit of PI3-kinase was increased in low glucose, whereas binding to SHP-2 was increased in high glucose. The data suggest that Axl contributes to VSMC dysfunction in diabetes.
GIT1 Mediates HDAC5 Activation by Angiotensin II in Vascular Smooth Muscle Cells
Jinjiang Pang, Chen Yan, Kanchana Natarajan, Megan E. Cavet, Michael P. Massett, Guoyong Yin, and Bradford C. Berk
Arterioscler Thromb Vasc Biol. 2008;28:892-898; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.161349
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Adiponectin Protects Against Angiotensin II or Tumor Necrosis Factor
–Induced Endothelial Cell Monolayer Hyperpermeability: Role of cAMP/PKA Signaling
Shi-Qiong Xu, Kalyankar Mahadev, Xiangdong Wu, Lauren Fuchsel, Sylvia Donnelly, Rosario G. Scalia, and Barry J. Goldstein
Arterioscler Thromb Vasc Biol. 2008;28:899-905; published online before print February 21 2008, doi:10.1161/ATVBAHA.108.163634
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Full-length and globular adiponectin abrogated the hyperpermeability of an endothelial monolayer elicited by TNF-{alpha} or Ang II, measured by electric resistance or albumin diffusion. Hyperpermeability correlated with actin stress fiber development, intercellular gap formation, and β-tubulin disassembly, which were all suppressed by adiponectin. Adiponectin increased cellular cAMP, and its effects were blocked by inhibition of cAMP/PKA signaling.
Human Stanniocalcin-1 Blocks TNF-
–Induced Monolayer Permeability in Human Coronary Artery Endothelial Cells
Changyi Chen, Md Saha Jamaluddin, Shaoyu Yan, David Sheikh-Hamad, and Qizhi Yao
Arterioscler Thromb Vasc Biol. 2008;28:906-912; published online before print February 28 2008, doi:10.1161/ATVBAHA.108.163667
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CNGA2 Channels Mediate Adenosine-Induced Ca
2+
Influx in Vascular Endothelial Cells
Kwong-Tai Cheng, Yuk-Ki Leung, Bing Shen, Yuk-Chi Kwok, Ching-On Wong, Hiu-Yee Kwan, Yu-Bun Man, Xin Ma, Yu Huang, and Xiaoqiang Yao
Arterioscler Thromb Vasc Biol. 2008;28:913-918; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.148338
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Differential Regulation of VEGF Signaling by PKC-
and PKC-
in Endothelial Cells
Christian Rask-Madsen and George L. King
Arterioscler Thromb Vasc Biol. 2008;28:919-924; published online before print March 6 2008, doi:10.1161/ATVBAHA.108.162842
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Downregulation of PKC{epsilon} with siRNA decreased Akt, eNOS, and Erk1/2 phosphorylation, NO synthase activity, and DNA synthesis stimulated by VEGF, likely through a dramatic decrease in VEGF receptor-2 (VEGFR2) tyrosine phosphorylation, and VEGFR2 protein and mRNA expression. In contrast, PKC-{alpha} knockdown increased VEGFR2 phosphorylation, VEGFR2 expression, and downstream signaling.
Long Pentraxin 3, a Key Component of Innate Immunity, Is Modulated by High-Density Lipoproteins in Endothelial Cells
Giuseppe Danilo Norata, Patrizia Marchesi, Angela Pirillo, Patrizia Uboldi, Giulia Chiesa, Virginia Maina, Cecilia Garlanda, Alberto Mantovani, and Alberico Luigi Catapano
Arterioscler Thromb Vasc Biol. 2008;28:925-931; published online before print January 24 2008, doi:10.1161/ATVBAHA.107.160606
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Here we report that HDL modulate the expression of PTX3, a member of the acute phase proteins superfamily, in vitro and in vivo. Our data suggest that part of the atheroprotective effects of HDL could result from the modulation of molecules that act as sensors of the immuno-inflammatory balance in the vascular wall.
Induction of CXCR2 Receptor by Peroxisome Proliferator-Activated Receptor
in Human Macrophages
Elena Rigamonti, Coralie Fontaine, Bruno Lefebvre, Christian Duhem, Philippe Lefebvre, Nikolaus Marx, Bart Staels, and Giulia Chinetti-Gbaguidi
Arterioscler Thromb Vasc Biol. 2008;28:932-939; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.161679
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IL-8 recruits and activates phagocytes acting through CXCR1 and CXCR2 receptors. Regulation of these genes by PPAR-{gamma} was studied in macrophages. PPAR-{gamma} induces CXCR2 expression, leading to an acquired induction of ROS production in response to IL-8 and Groβ. These results provide a novel role for PPAR-{gamma} in macrophage immune response.
Clinical and Population Studies
Dilation-Dependent Activation of Platelets and Prothrombin in Human Thoracic Ascending Aortic Aneurysm
Ziad Touat, Laurent Lepage, Véronique Ollivier, Patrick Nataf, Ulrich Hvass, Julien Labreuche, Martine Jandrot-Perrus, Jean-Baptiste Michel, and Guillaume Jondeau
Arterioscler Thromb Vasc Biol. 2008;28:940-946; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.158576
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Platelet activation and thrombin formation were evidenced in Marfan patients with ascending aortic dilatation above 45 mm (but not below 45 mm), and in patients with large aneurysm of other aetiologies. Thrombin (susceptible to activate MMPs) present within the aortic wall suggests that it could participate in aortic dilatation.
Tissue Factor in Patients With Acute Coronary Syndromes: Expression in Platelets, Leukocytes, and Platelet-Leukocyte Aggregates
Marta Brambilla, Marina Camera, Deborah Colnago, Giancarlo Marenzi, Monica De Metrio, Peter L. Giesen, Alessandra Balduini, Fabrizio Veglia, Karl Gertow, Paolo Biglioli, and Elena Tremoli
Arterioscler Thromb Vasc Biol. 2008;28:947-953; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.161471
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In ACS patients the number of TF-positive platelets and platelet-monocyte aggregates as well as the platelet-associated TF mRNA levels are significantly greater than in SA or Controls, strengthening the link between platelet activation, blood coagulation, and thrombus formation, and may further contribute to the hypercoagulability associated with the disease.
Impact of Asymmetric Dimethylarginine on Mortality After Acute Myocardial Infarction
Marianne Zeller, Claudia Korandji, Jean-Claude Guilland, Pierre Sicard, Catherine Vergely, Luc Lorgis, Jean-Claude Beer, Laurence Duvillard, Anne-Cécile Lagrost, Daniel Moreau, Philippe Gambert, Yves Cottin, and Luc Rochette
Arterioscler Thromb Vasc Biol. 2008;28:954-960; published online before print February 14 2008, doi:10.1161/ATVBAHA.108.162768
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From patients with acute myocardial infarction (MI), we analyzed the levels of circulating asymmetrical dimethylarginine (ADMA). High ADMA was a predictor for mortality, even when adjusted for potential confounders. Our study suggests that ADMA has a prognostic value for mortality after MI, beyond traditional risk factors and biomarkers.
Asymmetric Dimethylarginine Independently Predicts Fatal and Nonfatal Myocardial Infarction and Stroke in Women: 24-Year Follow-Up of the Population Study of Women in Gothenburg
Tora Leong, Dimitri Zylberstein, Ian Graham, Lauren Lissner, Deirdre Ward, Jane Fogarty, Calle Bengtsson, Cecilia Björkelund, Dag Thelle for The Swedish-Irish-Norwegian (SIN) Collaboration
Arterioscler Thromb Vasc Biol. 2008;28:961-967; published online before print February 21 2008, doi:10.1161/ATVBAHA.107.156596
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Baseline ADMA in the Population Study of Women in Gothenburg was associated with approximately 30% increase (adjusted) in incident cardiovascular events per 0.15 {micro}mol/L (1 SD) increase in ADMA after 24 years of follow-up. ADMA >=0.71 {micro}mol/L can enhance both the SCORE and Framingham systems of cardiovascular risk assessment.
Telomere Gap Between Granulocytes and Lymphocytes Is a Determinant for Hematopoetic Progenitor Cell Impairment in Patients With Previous Myocardial Infarction
Ioakim Spyridopoulos, Young Erben, Tim H. Brummendorf, Judith Haendeler, Klaus Dietz, Florian Seeger, Christine K. Kissel, Hans Martin, Jedrzej Hoffmann, Birgit Assmus, Andreas M. Zeiher, and Stefanie Dimmeler
Arterioscler Thromb Vasc Biol. 2008;28:968-974; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.160846
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In patients with CAD, telomere shortening is already present in mononuclear bone marrow cells. Telomere length depends on both age and the extent of CAD and correlates with bone marrow cell functionality. The telomere length difference between granulocytes and lymphocytes is the most sensitive determinant for telomere-associated bone marrow impairment.
Variants of the Interferon Regulatory Factor 5 Gene Regulate Expression of IRF5 mRNA in Atherosclerotic Tissue But Are Not Associated With Myocardial Infarction
Anders Mälarstig, Snaevar Sigurdsson, Per Eriksson, Gabrielle Paulsson-Berne, Ulf Hedin, Lars Wallentin, Agneta Siegbahn, Anders Hamsten, and Ann-Christine Syvänen
Arterioscler Thromb Vasc Biol. 2008;28:975-982; published online before print March 6 2008, doi:10.1161/ATVBAHA.108.163733
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Association Analysis of Allelic Variants of USF1 in Coronary Atherosclerosis
Kati Kristiansson, Erkki Ilveskoski, Terho Lehtimäki, Leena Peltonen, Markus Perola, and Pekka J. Karhunen
Arterioscler Thromb Vasc Biol. 2008;28:983-989; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.156463
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USF1 is well established as a gene associated with familial combined hyperlipidemia. Our findings in a unique autopsy series of middle-aged men provide evidence that USF1 contributes to coronary atherosclerosis, the pathological arterial wall phenotype resulting in CHD and in its most dramatic consequence--sudden cardiac death.
Promotor Polymorphisms in Leukotriene C
4
Synthase and Risk of Ischemic Cerebrovascular Disease
Jacob J. Freiberg, Anne Tybjærg-Hansen, Henrik Sillesen, Gorm B. Jensen, and Børge G. Nordestgaard
Arterioscler Thromb Vasc Biol. 2008;28:990-996; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.158873
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Leukotrienes are involved in innate immunity and inflammation. We tested the hypothesis that the -1072 G/A and -444 A/C polymorphisms of the leukotriene C4 synthase associate with risk of ischemic cerebrovascular disease. These leukotriene C4 synthase genotypes predicted 3-fold increased and 40% reduced risk of ischemic cerebrovascular disease.
Gender Differences in Endothelial Progenitor Cells and Cardiovascular Risk Profile: The Role of Female Estrogens
Gian Paolo Fadini, Saula de Kreutzenberg, Mattia Albiero, Anna Coracina, Elisa Pagnin, Ilenia Baesso, Andrea Cignarella, Chiara Bolego, Mario Plebani, Giovanni B. Nardelli, Saverio Sartore, Carlo Agostini, and Angelo Avogaro
Arterioscler Thromb Vasc Biol. 2008;28:997-1004; published online before print February 14 2008, doi:10.1161/ATVBAHA.107.159558
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We provide evidence that fertile women have a larger pool of circulating endothelial progenitors than men. This may be attributed to the cyclic bone marrow mobilization during menstrual cycle. Thanks to estrogens, female EPCs also display better function and higher vasculogenic properties than male EPCs.
A Potential Role of the CXC Chemokine GRO
in Atherosclerosis and Plaque Destabilization: Downregulatory Effects of Statins
Unni M. Breland, Bente Halvorsen, Johanna Hol, Erik Øie, Gabrielle Paulsson-Berne, Arne Yndestad, Camilla Smith, Kari Otterdal, Ulf Hedin, Torgun Wæhre, Wiggo J. Sandberg, Stig S. Frøland, Guttorm Haraldsen, Lars Gullestad, Jan K. Damås, Gøran K. Hansson, and Pål Aukrust
Arterioscler Thromb Vasc Biol. 2008;28:1005-1011; published online before print February 14 2008, doi:10.1161/ATVBAHA.108.162305
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The involvement of CXCR2 in atherogenesis is well recognized, thought to reflect interaction with interleukin-8. In the present study we found another CXCR2 ligand (ie, GRO{alpha}) to be significantly upregulated in human atherosclerosis both in circulating leukocytes and within the atherosclerotic lesion, potentially promoting matrix degradation, lipid accumulation, and inflammation.
Associations of Dyslipidemias From Childhood to Adulthood With Carotid Intima-Media Thickness, Elasticity, and Brachial Flow-Mediated Dilatation in Adulthood: The Cardiovascular Risk in Young Finns Study
Markus Juonala, Jorma S.A. Viikari, Tapani Rönnemaa, Jukka Marniemi, Antti Jula, Britt-Marie Loo, and Olli T. Raitakari
Arterioscler Thromb Vasc Biol. 2008;28:1012-1017; published online before print February 28 2008, doi:10.1161/ATVBAHA.108.163329
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Dyslipidemias are the major cause for atherosclerosis. In the present study, we examined the effects of dyslipidemias from childhood to adulthood and their interaction with nonlipid risk factors on markers of subclinical atherosclerosis. Our findings suggest that type IIb dyslipidemia has deleterious effects on vasculature already since childhood.
Coffee Consumption and Coronary Calcification: The Rotterdam Coronary Calcification Study
Geertruida J. van Woudenbergh, Rozemarijn Vliegenthart, Frank J.A. van Rooij, Albert Hofman, Matthijs Oudkerk, Jacqueline C.M. Witteman, and Johanna M. Geleijnse
Arterioscler Thromb Vasc Biol. 2008;28:1018-1023; published online before print March 6 2008, doi:10.1161/ATVBAHA.107.160457
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The relation of coffee intake with coronary calcification was examined in 1570 older Dutch subjects. In smoking and nonsmoking women, coffee intake was strongly inversely related to severe coronary calcification. In smoking men, however, a direct relationship was observed. The effect of coffee on coronary calcification, and the interaction with gender and smoking, warrant further study.
Accumulation of Zinc in Human Atherosclerotic Lesions Correlates With Calcium Levels But Does Not Protect Against Protein Oxidation
Nadina Stadler, Naomi Stanley, Sylvia Heeneman, Vladimir Vacata, Mat J.A.P. Daemen, Paul G. Bannon, Johannes Waltenberger, and Michael J. Davies
Arterioscler Thromb Vasc Biol. 2008;28:1024-1030; published online before print February 28 2008, doi:10.1161/ATVBAHA.108.162735
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Oxidation of lipids and proteins has been linked to the development of atherosclerosis; zinc has been proposed as a protective agent. Zinc levels are elevated in advanced lesions but correlate positively with iron concentrations and do not correlate with protein oxidation markers, indicating that zinc does not prevent protein oxidation.
Corrections
Correction
Arterioscler Thromb Vasc Biol. 2008;28:e31, doi:10.1161/ATVBAHA.108.123456
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