Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [10])

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Volume 25, Issue 10; October 1, 2005

Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Corrections

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	Editorials
	Fat, Fit, and Leading the Charge: The Evolution of Measuring High-Density Lipoprotein Subpopulations Vijay Nambi and Christie M. Ballantyne Arterioscler Thromb Vasc Biol. 2005;25:2013-2015, doi:10.1161/01.ATV.0000186043.86570.4f Extract \| Full Text \| PDF
	A Role for the Pregnane X Receptor in High-Density Lipoprotein Metabolism Gregory S. Shelness and Lawrence L. Rudel Arterioscler Thromb Vasc Biol. 2005;25:2016-2017, doi:10.1161/01.ATV.0000186042.94668.2b Extract \| Full Text \| PDF
	Gain-of-Function Mutations and Therapeutic Implications: Lipoprotein Lipase S447X to the Rescue Daniel J. Rader Arterioscler Thromb Vasc Biol. 2005;25:2018-2019, doi:10.1161/01.ATV.0000183606.81315.85 Extract \| Full Text \| PDF
	Brief Reviews
	The Farnesoid X Receptor: A Molecular Link Between Bile Acid and Lipid and Glucose Metabolism Thierry Claudel, Bart Staels, and Folkert Kuipers Arterioscler Thromb Vasc Biol. 2005;25:2020-2030; published online before print July 21 2005, doi:10.1161/01.ATV.0000178994.21828.a7 Abstract \| Full Text \| PDF The Farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids. FXR regulates bile acid synthesis, conjugation, and transport, as well as various aspects of lipid and glucose metabolism that are summarized in this review. Finally, we discussed the potential of FXR as a pharmacological target.
	An Unsuspected Metabolic Role for Atrial Natriuretic Peptides: The Control of Lipolysis, Lipid Mobilization, and Systemic Nonesterified Fatty Acids Levels in Humans Max Lafontan, Cédric Moro, Coralie Sengenes, Jean Galitzky, François Crampes, and Michel Berlan Arterioscler Thromb Vasc Biol. 2005;25:2032-2042; published online before print August 25 2005, doi:10.1161/01.ATV.0000183728.14712.d8 Abstract \| Full Text \| PDF Natriuretic peptides (NPs) are novel factors which may open promising research pathways to explain the control of lipid mobilization in physiological and pathological conditions. The metabolic impact of altered production and circulation of NPs remains to be established. The potential influence of NPs on the development of lipid disorders, obesity-related cardiovascular events, and cardiac cachexia will be discussed in this review.
	Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events David Feinbloom and Kenneth A. Bauer Arterioscler Thromb Vasc Biol. 2005;25:2043-2053; published online before print August 11 2005, doi:10.1161/01.ATV.0000181762.31694.da Abstract \| Full Text \| PDF
	Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage Renu Virmani, Frank D. Kolodgie, Allen P. Burke, Aloke V. Finn, Herman K. Gold, Thomas N. Tulenko, Steven P. Wrenn, and Jagat Narula Arterioscler Thromb Vasc Biol. 2005;25:2054-2061; published online before print July 21 2005, doi:10.1161/01.ATV.0000178991.71605.18 Abstract \| Full Text \| PDF \| Data Supplement Intraplaque hemorrhage is a major contributor to coronary lesion progression. The formation of immature blood vessels within a plaque promotes red blood cell leakage, an important source of free cholesterol. This review discusses the potential role of angiogenesis in lesion instability as it relates to plaque rupture.
	Vascular Biology
	A Paracrine Loop Between Adipocytes and Macrophages Aggravates Inflammatory Changes: Role of Free Fatty Acids and Tumor Necrosis Factor ${alpha}$ Takayoshi Suganami, Junko Nishida, and Yoshihiro Ogawa Arterioscler Thromb Vasc Biol. 2005;25:2062-2068; published online before print August 25 2005, doi:10.1161/01.ATV.0000183883.72263.13 Abstract \| Full Text \| PDF \| Data Supplement We developed an in vitro coculture system composed of adipocytes and macrophages to elucidate the functional interaction between these cells. The data suggest that a paracrine loop involving FFAs and TNF-{alpha} derived from adipocytes and macrophages, respectively, establishes a vicious cycle that aggravates inflammatory changes in the adipose tissue
	The Effects of Leukocyte-Type 12/15-Lipoxygenase on Id3-Mediated Vascular Smooth Muscle Cell Growth Angela M. Taylor, Ross Hanchett, Rama Natarajan, Catherine C. Hedrick, Scott Forrest, Jerry L. Nadler, and Coleen A. McNamara Arterioscler Thromb Vasc Biol. 2005;25:2069-2074; published online before print July 21 2005, doi:10.1161/01.ATV.0000178992.40088.f2 Abstract \| Full Text \| PDF 12/15-Lipoxygenase (12/15-LO) has been implicated in the pathogenesis of vascular disease. Id3 has been shown to regulate growth in various cell types and is expressed in VSMCs within atherosclerotic and restenotic lesions. The growth-promoting effects of 12/15-LO are at least partially mediated through induction of Id3 transcription.
	Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors Lijun Li, Ann-Cathrine Jönsson-Rylander, Ken Abe, and Zofia Zukowska Arterioscler Thromb Vasc Biol. 2005;25:2075-2080; published online before print July 28 2005, doi:10.1161/01.ATV.0000179601.19888.19 Abstract \| Full Text \| PDF \| Data Supplement Cold-stress or exogenous neuropeptide Y (NPY) induces rapid occlusion of angioplasty injured carotid artery with an atherosclerotic-like lesion, both of which are prevented after infusion of an NPY Y1 receptor antagonist. Thus, NPY Y1 receptor antagonist treatment could represent a future therapeutic target to treat atherosclerosis and restenosis.
	Regulation of Vein Graft Hyperplasia by Survivin, an Inhibitor of Apoptosis Protein Grace J. Wang, Xin Xin Sui, Hector F. Simosa, Mukesh K. Jain, Dario C. Altieri, and Michael S. Conte Arterioscler Thromb Vasc Biol. 2005;25:2081-2087; published online before print August 25 2005, doi:10.1161/01.ATV.0000183885.66153.8a Abstract \| Full Text \| PDF \| Data Supplement Vein graft remodeling is incompletely understood. Survivin (SVV) is a unique inhibitor of apoptosis protein that has been implicated in cancer and vascular injury. We investigated the role of SVV in vein graft healing and demonstrate that SVV regulates several processes, including proliferation, apoptosis, and angiogenesis, that determine vein graft remodeling
	Rho/Rho-Kinase Pathway Contributes to C-Reactive Protein–Induced Plasminogen Activator Inhibitor-1 Expression in Endothelial Cells Tetsuya Nakakuki, Masaaki Ito, Hitoshi Iwasaki, Yasuko Kureishi, Ryuji Okamoto, Nobuyuki Moriki, Mariko Kongo, Shinya Kato, Norikazu Yamada, Naoki Isaka, and Takeshi Nakano Arterioscler Thromb Vasc Biol. 2005;25:2088-2093; published online before print August 25 2005, doi:10.1161/01.ATV.0000183607.50230.9f Abstract \| Full Text \| PDF
	Estrogen Treatment Abrogates Neointima Formation in Human C-Reactive Protein Transgenic Mice Dajun Wang, Suzanne Oparil, Yiu-Fai Chen, Mark A. McCrory, Gregory A. Skibinski, Wenguang Feng, and Alexander J. Szalai Arterioscler Thromb Vasc Biol. 2005;25:2094-2099; published online before print July 28 2005, doi:10.1161/01.ATV.0000179602.85797.3f Abstract \| Full Text \| PDF We tested whether estrogen could modulate the exaggerated vascular response to injury seen in C-reactive protein (CRP) transgenic mice. Estrogen treatment reduced carotid artery ligation-induced expression of CRP (protein and mRNA) in the neointima, and lessened CRP-mediated exacerbation of injury. These data suggest that estrogen is vasoprotective.
	${alpha}$ -Lipoic Acid–Induced Heme Oxygenase-1 Expression Is Mediated by Nuclear Factor Erythroid 2-Related Factor 2 and p38 Mitogen-Activated Protein Kinase in Human Monocytic Cells Richard M. Ogborne, Stuart A. Rushworth, and Maria A. O’Connell Arterioscler Thromb Vasc Biol. 2005;25:2100-2105; published online before print August 25 2005, doi:10.1161/01.ATV.0000183745.37161.6e Abstract \| Full Text \| PDF \| Data Supplement The effect of {alpha}-lipoic acid (ALA) on heme oxygenase-1 (HO-1) expression was investigated in THP-1 monocytic cells. ALA induced HO-1 expression via Nrf2 and p38. Further studies are required to investigate whether the protective effects of ALA in monocytes are mediated by HO-1.
	Reduced Vascular Remodeling, Endothelial Dysfunction, and Oxidative Stress in Resistance Arteries of Angiotensin II–Infused Macrophage Colony-Stimulating Factor–Deficient Mice: Evidence for a Role in Inflammation in Angiotensin-Induced Vascular Injury Carolina De Ciuceis, Farhad Amiri, Pascal Brassard, Dierk H. Endemann, Rhian M. Touyz, and Ernesto L. Schiffrin Arterioscler Thromb Vasc Biol. 2005;25:2106-2113; published online before print August 11 2005, doi:10.1161/01.ATV.0000181743.28028.57 Abstract \| Full Text \| PDF \| Data Supplement Ang II-induced vascular damage and remodeling, which is partially mediated by ROS generation and inflammation, was investigated in a model of reduced inflammation (m-CSF-deficient mice). We demonstrated that vascular proinflammatory mediators play a crucial role in Ang II-induced endothelial dysfunction and vascular remodeling.
	Oxidative Stress Promotes Endothelial Cell Apoptosis and Loss of Microvessels in the Spontaneously Hypertensive Rats Nobuhiko Kobayashi, Frank A. DeLano, and Geert W. Schmid-Schönbein Arterioscler Thromb Vasc Biol. 2005;25:2114-2121; published online before print July 21 2005, doi:10.1161/01.ATV.0000178993.13222.f2 Abstract \| Full Text \| PDF \| Data Supplement Loss of microvessels contributes to the development of hypertensive disease. Antioxidants suppressed endothelial cell apoptosis in microvessels and preserved vessel length density in the spontaneously hypertensive rats. Oxidative stress seems to promote endothelial cell apoptosis and loss of microvessels during the development of hypertension.
	Bradycardia Stimulates Vascular Growth During Gradual Coronary Occlusion Kathryn G. Lamping, Wei Zheng, Dezhi Xing, Lance P. Christensen, James Martins, and Robert J. Tomanek Arterioscler Thromb Vasc Biol. 2005;25:2122-2127; published online before print July 28 2005, doi:10.1161/01.ATV.0000179598.57819.77 Abstract \| Full Text \| PDF \| Data Supplement We tested the hypothesis that chronic bradycardia stimulates growth of the collateral circulation. During coronary artery occlusion, bradycardia enhanced maximal conductance, indices of vascular density, and release of growth factors and their receptors in collateral-dependent myocardium. We conclude that bradycardia facilitates angiogenesis/arteriogenesis to preserve myocardial perfusion.
	Targeted Delivery of Bone Marrow Mononuclear Cells by Ultrasound Destruction of Microbubbles Induces Both Angiogenesis and Arteriogenesis Response Takanobu Imada, Tetsuya Tatsumi, Yasukiyo Mori, Takashi Nishiue, Masayuki Yoshida, Hiroya Masaki, Mitsuhiko Okigaki, Hiroyuki Kojima, Yoshihisa Nozawa, Yasunobu Nishiwaki, Noriko Nitta, Toshiji Iwasaka, and Hiroaki Matsubara Arterioscler Thromb Vasc Biol. 2005;25:2128-2134; published online before print July 28 2005, doi:10.1161/01.ATV.0000179768.06206.cb Abstract \| Full Text \| PDF \| Data Supplement Ultrasound (US)-targeted microbubble destruction combined with transplantation of bone marrow mononuclear cells (BM-MNCs) enhances blood flow restoration by stimulating both angiogenesis and arteriogenesis. Release of proinflammatory factors from platelets activated by Bubble+US play a key role for adhesion of BM-MNCs on endothelium. This cell delivery system is efficient for therapeutic angiogenesis and arteriogenesis.
	Atherosclerosis and Lipoproteins
	Proteomic and Metabolomic Analyses of Atherosclerotic Vessels From Apolipoprotein E-Deficient Mice Reveal Alterations in Inflammation, Oxidative Stress, and Energy Metabolism Manuel Mayr, Yuen-Li Chung, Ursula Mayr, Xiaoke Yin, Lucy Ly, Helen Troy, Salim Fredericks, Yanhua Hu, John R. Griffiths, and Qingbo Xu Arterioscler Thromb Vasc Biol. 2005;25:2135-2142; published online before print August 25 2005, doi:10.1161/01.ATV.0000183928.25844.f6 Abstract \| Full Text \| PDF \| Data Supplement Our study is a first attempt to show how changes in the proteome and the metabolome are reciprocally connected during atherogenesis and provides evidence that attenuated lesion formation in apolipoprotein E-/- mice is associated with reduced oxidative stress and successful recovery of the vascular energy pool.
	Complete Rescue of Lipoprotein Lipase–Deficient Mice by Somatic Gene Transfer of the Naturally Occurring LPL^S447X Beneficial Mutation Colin J.D. Ross, Guoqing Liu, Jan Albert Kuivenhoven, Jaap Twisk, Jaap Rip, Willemijn van Dop, Katherine J.D. Ashbourne Excoffon, Suzanne M.E. Lewis, John J. Kastelein, and Michael R. Hayden Arterioscler Thromb Vasc Biol. 2005;25:2143-2150; published online before print July 7 2005, doi:10.1161/01.ATV.0000176971.27302.b0 Abstract \| Full Text \| PDF We investigated the in vivo mechanism by which naturally occurring LPLS447X variant improves the lipid profile of S447X carriers by comparing human LPLS447X to LPLWT in newborn LPL-/- mice. LPLWT prolonged newborn survival to 21 days. In contrast, the increased catalytic activity of LPLS447X completely rescued LPL-/- mice to adulthood.
	Lack of the Cysteine Protease Inhibitor Cystatin C Promotes Atherosclerosis in Apolipoprotein E–Deficient Mice Eva Bengtsson, Fong To, Katarina Håkansson, Anders Grubb, Lena Brånén, Jan Nilsson, and Stefan Jovinge Arterioscler Thromb Vasc Biol. 2005;25:2151-2156; published online before print July 28 2005, doi:10.1161/01.ATV.0000179600.34086.7d Abstract \| Full Text \| PDF Cystatin C inhibits collagen- and elastin-degrading cysteine proteases of cathepsins. We crossed cystatin C-deficient (cysC-/-) and apolipoprotein E-deficient (apoE-/-) mice. CysC-/-apoE-/- mice had larger plaques with increased macrophage content compared with cysC+/+apoE-/- mice. Bone marrow transplantations suggest that the protective role of cystatin C is dependent on its expression in nonhematopoietic cells.
	Advanced Glycosylation End Products Might Promote Atherosclerosis Through Inducing the Immune Maturation of Dendritic Cells Junbo Ge, Qingzhe Jia, Chun Liang, Yukun Luo, Dong Huang, Aijun Sun, Keqiang Wang, Yunzeng Zou, and Haozhu Chen Arterioscler Thromb Vasc Biol. 2005;25:2157-2163; published online before print August 11 2005, doi:10.1161/01.ATV.0000181744.58265.63 Abstract \| Full Text \| PDF We studied the effects of AGE-BSA on the maturation of DCs and the expressions of SR-A and RAGE on DCs. AGE-BSA-induced maturation of DCs and augmented their capacity to stimulate T-cell proliferation and cytokine secretions. These findings might explain in part the interactive roles of AGEs and DCs in the processes of atherosclerosis.
	Expression of the Pregnane X Receptor in Mice Antagonizes the Cholic Acid–Mediated Changes in Plasma Lipoprotein Profile David Masson, Laurent Lagrost, Anne Athias, Philippe Gambert, Cynthia Brimer-Cline, Lubin Lan, John D. Schuetz, Erin G. Schuetz, and Mahfoud Assem Arterioscler Thromb Vasc Biol. 2005;25:2164-2169; published online before print August 25 2005, doi:10.1161/01.ATV.0000183674.88817.fb Abstract \| Full Text \| PDF \| Data Supplement To determine the contribution of PXR to the effect of bile acids on plasma lipoproteins, wild-type mice, PXR-deficient mice, and Pxr-null mice expressing human PXR were fed a cholic acid-containing diet. Mouse and human PXR were found to antagonize the cholic acid-mediated decreases in plasma HDL cholesterol and apoA-I.
	Extracellular Signal-Regulated Kinase–Dependent Stabilization of Hepatic Low-Density Lipoprotein Receptor mRNA by Herbal Medicine Berberine Parveen Abidi, Yue Zhou, Jian-Dong Jiang, and Jingwen Liu Arterioscler Thromb Vasc Biol. 2005;25:2170-2176; published online before print August 11 2005, doi:10.1161/01.ATV.0000181761.16341.2b Abstract \| Full Text \| PDF \| Data Supplement \| Data Supplement Our recent studies identified berberine (BBR) as a novel cholesterol-lowering drug that upregulates low-density lipoprotein (LDL) receptor expression through mRNA stabilization. Here, we investigated mechanisms underlying regulatory effects of BBR on LDL receptor (LDLR) messenger. These new findings demonstrate that the BBR-induced stabilization of LDLR mRNA is mediated by the ERK signaling pathway through interactions of cis-regulatory sequences of 3'UTR and mRNA binding proteins that are downstream effectors of this signaling cascade.
	Cholesteryl Ester Transfer Protein Directly Mediates Selective Uptake of High Density Lipoprotein Cholesteryl Esters by the Liver Andre Gauthier, Paulina Lau, Xiaohui Zha, Ross Milne, and Ruth McPherson Arterioscler Thromb Vasc Biol. 2005;25:2177-2184; published online before print August 25 2005, doi:10.1161/01.ATV.0000183613.13929.13 Abstract \| Full Text \| PDF \| Data Supplement These studies demonstrate that cholesteryl ester transfer protein (CETP) mediates the selective uptake of IIDL-derived cholesteryl esters by hepatocytes both in vitro and in vivo by a mechanism that is independent of other lipoprotein receptors and which is only partially sensitive to inhibition by torcetrapib.
	Value of High-Density Lipoprotein (HDL) Subpopulations in Predicting Recurrent Cardiovascular Events in the Veterans Affairs HDL Intervention Trial Bela F. Asztalos, Dorothea Collins, L. Adrienne Cupples, Serkalem Demissie, Katalin V. Horvath, Hanna E. Bloomfield, Sander J. Robins, and Ernst J. Schaefer Arterioscler Thromb Vasc Biol. 2005;25:2185-2191; published online before print August 25 2005, doi:10.1161/01.ATV.0000183727.90611.4f Abstract \| Full Text \| PDF VA-HIT subjects with new CVD events had low HDL-C and apoA-I, large cholesterol-rich HDL particle levels, high TG, and small poorly lipidated HDL particle levels. Low {alpha}-1 and {alpha}-2 levels and high {alpha}-3 levels were independent positive risk factors for recurrent CVD events, {alpha}-1 and {alpha}-2 being superior to HDL-C in risk-assessment.
	Associations Between Soluble CD40 Ligand, Atherosclerosis Risk Factors, and Subclinical Atherosclerosis: Results from the Dallas Heart Study James A. de Lemos, Andreas Zirlik, Uwe Schönbeck, Nerea Varo, Sabina A. Murphy, Amit Khera, Darren K. McGuire, Greg Stanek, Hao S. Lo, Rebecca Nuzzo, David A. Morrow, Ronald Peshock, and Peter Libby Arterioscler Thromb Vasc Biol. 2005;25:2192-2196; published online before print August 18 2005, doi:10.1161/01.ATV.0000182904.08513.60 Abstract \| Full Text \| PDF Plasma levels of soluble CD40 ligand were not associated with most atherosclerotic risk factors or with subclinical atherosclerosis, suggesting limited utility in screening for subclinical atherosclerosis. Further evaluation of this biomarker should focus on settings where platelet activation is common, such as following acute coronary syndromes or coronary revascularization procedures.
	Lifecourse Socioeconomic Position, C-Reactive Protein, and Carotid Intima-Media Thickness in Young Adults: The Cardiovascular Risk in Young Finns Study Mika Kivimäki, Debbie A. Lawlor, Markus Juonala, George Davey Smith, Marko Elovainio, Liisa Keltikangas-Järvinen, Jussi Vahtera, Jorma S.A. Viikari, and Olli T. Raitakari Arterioscler Thromb Vasc Biol. 2005;25:2197-2202; published online before print August 25 2005, doi:10.1161/01.ATV.0000183729.91449.6e Abstract \| Full Text \| PDF \| Data Supplement It has been suggested that confounding by lifecourse socioeconomic position largely explains the association between C-reactive protein (CRP) and coronary heart disease risk, but the evidence is limited to elderly subjects. In this study of 2290 young adults, the association between CRP and carotid atherosclerosis was largely explained by adiposity.
	The Use of Achilles Tendon Sonography to Distinguish Familial Hypercholesterolemia from Other Genetic Dyslipidemias Mireia Junyent, Rosa Gilabert, Daniel Zambón, Isabel Núñez, María Vela, Fernando Civeira, Miguel Pocoví, and Emilio Ros Arterioscler Thromb Vasc Biol. 2005;25:2203-2208; published online before print August 25 2005, doi:10.1161/01.ATV.0000183888.48105.d1 Abstract \| Full Text \| PDF \| Data Supplement Achilles tendon sonography was performed in 290 subjects with various genetic dyslipidemias and 88 controls. Familial hypercholesterolemia mutation carriers had thicker tendons than all other groups. Sonography was more sensitive than physical examination to detect xanthomas. Achilles tendon sonography is useful to distinguish familial hypercholesterolemia from other genetic dyslipidemias
	Thrombosis
	In Vivo Clearance of Human Protein S in a Mouse Model: Influence of C4b-Binding Protein and the Heerlen Polymorphism Cécile V. Denis, Sarah J. Roberts, Tilman M. Hackeng, and Peter J. Lenting Arterioscler Thromb Vasc Biol. 2005;25:2209-2215; published online before print August 11 2005, doi:10.1161/01.ATV.0000181760.55269.6b Abstract \| Full Text \| PDF \| Data Supplement We established that binding and degradation of protein S by macrophages was partially inhibited by C4BP. C4BP mimicked this effect in vivo by prolonging the half-life of protein S from 2 to 4 hours in a mouse model. The presence of the Heerlen polymorphism reduced survival of protein S 3-fold to 0.6 hours.
	C-Reactive Protein Decreases Tissue Plasminogen Activator Activity in Human Aortic Endothelial Cells: Evidence that C-Reactive Protein Is a Procoagulant Uma Singh, Sridevi Devaraj, and Ishwarlal Jialal Arterioscler Thromb Vasc Biol. 2005;25:2216-2221; published online before print August 25 2005, doi:10.1161/01.ATV.0000183718.62409.ea Abstract \| Full Text \| PDF C-reactive protein (CRP) treatment of human aortic endothelial cells significantly decreased secreted tissue plasminogen activator (tPA) antigen and activity. CRP treatment increased IL-1ß and TNF{alpha}, and neutralization of these reversed CRP-mediated inhibition of tPA. CRP inhibits tPA activity via generation of proinflammatory cytokines, providing further evidence that CRP is a procoagulant.
	Endothelial Cell Activation by IL-1ß in the Presence of Fibrinogen Requires ${alpha}$ _Vß₃ Abha Sahni, Sanjeev K. Sahni, and Charles W. Francis Arterioscler Thromb Vasc Biol. 2005;25:2222-2227; published online before print August 25 2005, doi:10.1161/01.ATV.0000183605.27125.6f Abstract \| Full Text \| PDF The ability of fibrinogen-bound IL-1ß to stimulate NO secretion by ECs is blocked by anti-{alpha}vß3. Also, fibrinogen-bound IL-1ß promotes the specific association of {alpha}vß3 with IL-1R, as shown by coimmunoprecipitation or immunofluorescence staining. Fibrinogen binding enhances IL-1ß-induced secretion of NO through the coordinated effects of colocalized {alpha}vß3 and IL-1R.
	Does Elevated Plasma Fibrinogen Increase the Risk of Coronary Heart Disease?: Evidence from a Meta-Analysis of Genetic Association Studies George Davey Smith, Roger Harbord, Julie Milton, Shah Ebrahim, and Jonathan A.C. Sterne Arterioscler Thromb Vasc Biol. 2005;25:2228-2233; published online before print August 25 2005, doi:10.1161/01.ATV.0000183937.65887.9c Abstract \| Full Text \| PDF Observational studies demonstrate that circulating fibrinogen levels are associated with increased coronary heart disease risk. However, in a meta-analysis of studies that relate genetic variants associated with differences in fibrinogen level to coronary heart disease risk, we find no association. These data suggest that fibrinogen is not a cause of increased coronary heart disease risk.
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2005;25:e139 Extract \| Full Text \| PDF
	Correction Arterioscler Thromb Vasc Biol. 2005;25:e140 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 10; October 1, 2005

Editorials

Fat, Fit, and Leading the Charge: The Evolution of Measuring High-Density Lipoprotein Subpopulations

A Role for the Pregnane X Receptor in High-Density Lipoprotein Metabolism

Gain-of-Function Mutations and Therapeutic Implications: Lipoprotein Lipase S447X to the Rescue

Brief Reviews

The Farnesoid X Receptor: A Molecular Link Between Bile Acid and Lipid and Glucose Metabolism

An Unsuspected Metabolic Role for Atrial Natriuretic Peptides: The Control of Lipolysis, Lipid Mobilization, and Systemic Nonesterified Fatty Acids Levels in Humans

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage

Vascular Biology

A Paracrine Loop Between Adipocytes and Macrophages Aggravates Inflammatory Changes: Role of Free Fatty Acids and Tumor Necrosis Factor

The Effects of Leukocyte-Type 12/15-Lipoxygenase on Id3-Mediated Vascular Smooth Muscle Cell Growth

Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors

Regulation of Vein Graft Hyperplasia by Survivin, an Inhibitor of Apoptosis Protein

Rho/Rho-Kinase Pathway Contributes to C-Reactive Protein–Induced Plasminogen Activator Inhibitor-1 Expression in Endothelial Cells

Estrogen Treatment Abrogates Neointima Formation in Human C-Reactive Protein Transgenic Mice

-Lipoic Acid–Induced Heme Oxygenase-1 Expression Is Mediated by Nuclear Factor Erythroid 2-Related Factor 2 and p38 Mitogen-Activated Protein Kinase in Human Monocytic Cells

Reduced Vascular Remodeling, Endothelial Dysfunction, and Oxidative Stress in Resistance Arteries of Angiotensin II–Infused Macrophage Colony-Stimulating Factor–Deficient Mice: Evidence for a Role in Inflammation in Angiotensin-Induced Vascular Injury

Oxidative Stress Promotes Endothelial Cell Apoptosis and Loss of Microvessels in the Spontaneously Hypertensive Rats

Bradycardia Stimulates Vascular Growth During Gradual Coronary Occlusion

Targeted Delivery of Bone Marrow Mononuclear Cells by Ultrasound Destruction of Microbubbles Induces Both Angiogenesis and Arteriogenesis Response

Atherosclerosis and Lipoproteins

Proteomic and Metabolomic Analyses of Atherosclerotic Vessels From Apolipoprotein E-Deficient Mice Reveal Alterations in Inflammation, Oxidative Stress, and Energy Metabolism

Complete Rescue of Lipoprotein Lipase–Deficient Mice by Somatic Gene Transfer of the Naturally Occurring LPLS447X Beneficial Mutation

Lack of the Cysteine Protease Inhibitor Cystatin C Promotes Atherosclerosis in Apolipoprotein E–Deficient Mice

Advanced Glycosylation End Products Might Promote Atherosclerosis Through Inducing the Immune Maturation of Dendritic Cells

Expression of the Pregnane X Receptor in Mice Antagonizes the Cholic Acid–Mediated Changes in Plasma Lipoprotein Profile

Extracellular Signal-Regulated Kinase–Dependent Stabilization of Hepatic Low-Density Lipoprotein Receptor mRNA by Herbal Medicine Berberine

Cholesteryl Ester Transfer Protein Directly Mediates Selective Uptake of High Density Lipoprotein Cholesteryl Esters by the Liver

Value of High-Density Lipoprotein (HDL) Subpopulations in Predicting Recurrent Cardiovascular Events in the Veterans Affairs HDL Intervention Trial

Associations Between Soluble CD40 Ligand, Atherosclerosis Risk Factors, and Subclinical Atherosclerosis: Results from the Dallas Heart Study

Lifecourse Socioeconomic Position, C-Reactive Protein, and Carotid Intima-Media Thickness in Young Adults: The Cardiovascular Risk in Young Finns Study

The Use of Achilles Tendon Sonography to Distinguish Familial Hypercholesterolemia from Other Genetic Dyslipidemias

Thrombosis

In Vivo Clearance of Human Protein S in a Mouse Model: Influence of C4b-Binding Protein and the Heerlen Polymorphism

C-Reactive Protein Decreases Tissue Plasminogen Activator Activity in Human Aortic Endothelial Cells: Evidence that C-Reactive Protein Is a Procoagulant

Endothelial Cell Activation by IL-1ß in the Presence of Fibrinogen Requires Vß3

Does Elevated Plasma Fibrinogen Increase the Risk of Coronary Heart Disease?: Evidence from a Meta-Analysis of Genetic Association Studies

Corrections

Correction

Correction

Spotlight

A Paracrine Loop Between Adipocytes and Macrophages Aggravates Inflammatory Changes: Role of Free Fatty Acids and Tumor Necrosis Factor ${alpha}$

${alpha}$ -Lipoic Acid–Induced Heme Oxygenase-1 Expression Is Mediated by Nuclear Factor Erythroid 2-Related Factor 2 and p38 Mitogen-Activated Protein Kinase in Human Monocytic Cells

Complete Rescue of Lipoprotein Lipase–Deficient Mice by Somatic Gene Transfer of the Naturally Occurring LPL^S447X Beneficial Mutation

Endothelial Cell Activation by IL-1ß in the Presence of Fibrinogen Requires ${alpha}$ _Vß₃