Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [5])

Volume 25, Issue 5; May 1, 2005

Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Abstracts
Letters to the Editor

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	Editorials
	P-Selectin and Blood Coagulation: It’s Not Only About Inflammation Any More Bruce Furie Arterioscler Thromb Vasc Biol. 2005;25:877-878, doi:10.1161/01.ATV.0000161049.53535.5d Extract \| Full Text \| PDF
	Soluble Levels of Receptor for Advanced Glycation Endproducts (sRAGE) and Coronary Artery Disease: The Next C-Reactive Protein? Barry I. Hudson, Evis Harja, Bernhard Moser, and Ann Marie Schmidt Arterioscler Thromb Vasc Biol. 2005;25:879-882, doi:10.1161/01.ATV.0000164804.05324.8b Extract \| Full Text \| PDF
	FGFR1 and the Bloodline of the Vasculature Victor W.M. van Hinsbergh and Ton J. Rabelink Arterioscler Thromb Vasc Biol. 2005;25:883-886, doi:10.1161/01.ATV.0000165691.55540.73 Extract \| Full Text \| PDF
	SOD Isoforms and Signaling in Blood Vessels: Evidence for the Importance of ROS Compartmentalization J. Ignacio Mendez, William J. Nicholson, and W. Robert Taylor Arterioscler Thromb Vasc Biol. 2005;25:887-888, doi:10.1161/01.ATV.0000164043.24549.50 Extract \| Full Text \| PDF
	The Union of Vascular and Metabolic Actions of Insulin in Sickness and in Health Jeong-a Kim, Kwang Kon Koh, and Michael J. Quon Arterioscler Thromb Vasc Biol. 2005;25:889-891, doi:10.1161/01.ATV.0000164044.42910.6b Extract \| Full Text \| PDF
	Making Up and Breaking Up: The Tortuous Ways of the Vascular Wall Stéphanie Lehoux and Alain Tedgui Arterioscler Thromb Vasc Biol. 2005;25:892-894, doi:10.1161/01.ATV.0000164622.81752.9a Extract \| Full Text \| PDF
	Brief Reviews
	Role of Caspases in Death and Survival of the Plaque Macrophage Thomas Q. Nhan, W. Conrad Liles, and Stephen M. Schwartz Arterioscler Thromb Vasc Biol. 2005;25:895-903; published online before print February 17 2005, doi:10.1161/01.ATV.0000159519.07181.33 Abstract \| Full Text \| PDF Recent literature shows that physiological and developmental functions of many cell types require active caspases without progressing to cell death. We discuss the role of macrophage cell death in plaque progression, possible mediators of macrophage cell death, and the possible functions of plaque macrophage using the nondeath caspase pathway.
	Nuclear Factor ${kappa}$ B Signaling in Atherogenesis Menno P.J. de Winther, Edwin Kanters, Georg Kraal, and Marten H. Hofker Arterioscler Thromb Vasc Biol. 2005;25:904-914; published online before print February 24 2005, doi:10.1161/01.ATV.0000160340.72641.87 Abstract \| Full Text \| PDF Atherosclerosis is an inflammatory disease, and a major transcription factor in inflammatory and immune responses is NF-{kappa}B. We address recent literature on the function of NF-{kappa}B in inflammatory responses and atherosclerosis and discuss its proatherogenic and antiatherogenic properties.
	NO Generation From Nitrite and Its Role in Vascular Control Jon O. Lundberg and Eddie Weitzberg Arterioscler Thromb Vasc Biol. 2005;25:915-922; published online before print March 3 2005, doi:10.1161/01.ATV.0000161048.72004.c2 Abstract \| Full Text \| PDF NO generated from L-arginine by NO synthases in the endothelium and in other cells plays a central role in several aspects of vascular biology. The biological activity of NO is acutely terminated by oxidation to nitrite and nitrate, and these compounds have long been considered only as inert end-products of NO. However, this dogma is now being challenged, as new knowledge suggests that nitrate and nitrite should probably be viewed as storage pools for NO rather than inert waste products. Here we discuss novel aspects of nitrite-dependent NO generation in vivo and its role in vascular control.
	Role of Lipoprotein-Associated Phospholipase A₂ in Atherosclerosis: Biology, Epidemiology, and Possible Therapeutic Target Andrew Zalewski and Colin Macphee Arterioscler Thromb Vasc Biol. 2005;25:923-931; published online before print February 24 2005, doi:10.1161/01.ATV.0000160551.21962.a7 Abstract \| Full Text \| PDF Recent studies suggest lipoprotein-associated phospholipase A2 may play an important role in atherogenesis. This enzyme generates proinflammatory products implicated in every stage of atherosclerosis, from atheroma initiation to destabilization. The potential clinical benefit associated with Lp-PLA2 inhibition is intriguing; however, more studies are needed to better define the biological role of this enzyme.
	Mechanisms, Pathophysiology, and Therapy of Arterial Stiffness Susan J. Zieman, Vojtech Melenovsky, and David A. Kass Arterioscler Thromb Vasc Biol. 2005;25:932-943; published online before print February 24 2005, doi:10.1161/01.ATV.0000160548.78317.29 Abstract \| Full Text \| PDF Arterial stiffness is an epidemic with increased risk. We review the structural, cellular, and genetic components of stiffness and the effect of salt, glucose, and neurohormones. The hemodynamic impact of stiffness and a comprehensive review of therapeutic tools to increase vascular compliance from lifestyle changes to novel drugs are presented.
	Vascular Biology
	Fibroblast Growth Factor Receptor-1 Expression Is Required for Hematopoietic but not Endothelial Cell Development Peetra Ulrica Magnusson, Roberto Ronca, Patrizia Dell’Era, Pia Carlstedt, Lars Jakobsson, Juha Partanen, Anna Dimberg, and Lena Claesson-Welsh Arterioscler Thromb Vasc Biol. 2005;25:944-949; published online before print March 17 2005, doi:10.1161/01.ATV.0000163182.73190.f9 Abstract \| Full Text \| PDF \| Data Supplement Immunostaining using several different antibodies and scoring for FGFR-1 promoter-driven Lac Z activity show that some but not all endothelial cells express FGFR-1. FGFR-1 gene inactivation leads to a block in hematopoietic development; in contrast, endothelial cell development is enhanced.
	Differential Activation of Mitogenic Signaling Pathways in Aortic Smooth Muscle Cells Deficient in Superoxide Dismutase Isoforms Nageswara R. Madamanchi, Sung-Kwon Moon, Zeenat S. Hakim, Shantres Clark, Ali Mehrizi, Cam Patterson, and Marschall S. Runge Arterioscler Thromb Vasc Biol. 2005;25:950-956; published online before print March 3 2005, doi:10.1161/01.ATV.0000161050.77646.68 Abstract \| Full Text \| PDF \| Data Supplement We investigated the effect of subcellular reactive oxygen species (ROS) localization on smooth muscle cell (SMC) phenotype and mitogenic signaling using superoxide dismutase (SOD)-deficient mouse aortic SMCs. ROS location modulates SMC phenotype via divergent signaling pathways, and dysregulation of SOD under pathophysiological conditions may lead to SMC hyperplasia and hypertrophy.
	Partial Off-Loading of Longitudinal Tension Induces Arterial Tortuosity Zane S. Jackson, Dorota Dajnowiec, Avrum I. Gotlieb, and B. Lowell Langille Arterioscler Thromb Vasc Biol. 2005;25:957-962; published online before print March 3 2005, doi:10.1161/01.ATV.0000161277.46464.11 Abstract \| Full Text \| PDF \| Data Supplement We used interposition grafts to demonstrate that only partial off-loading of longitudinal arterial strain initiates arterial growth and tortuosity. Wall growth and remodeling comprised cell proliferation and apoptosis and extracellular matrix accumulation and remodeling. Surprisingly, (metalloproteinase-dependent) tortuosity occurred despite the persistence of significant longitudinal strain.
	Shear Stress Inhibits Smooth Muscle Cell–Induced Inflammatory Gene Expression in Endothelial Cells: Role of NF- ${kappa}$ B Jeng-Jiann Chiu, Li-Jing Chen, Shun-Fu Chang, Pei-Ling Lee, Chih-I Lee, Min-Chien Tsai, Ding-Yu Lee, Hsing-Pang Hsieh, Shunichi Usami, and Shu Chien Arterioscler Thromb Vasc Biol. 2005;25:963-969; published online before print February 17 2005, doi:10.1161/01.ATV.0000159703.43374.19 Abstract \| Full Text \| PDF \| Data Supplement ECs are influenced by shear stress and SMCs. DNA microarrays showed increased proinflammatory gene expressions in ECs by static SMC coculture. Shear stress inhibits these coculture-induced expressions. NF-{kappa}B is involved in these coculture and shear stress modulations of gene expressions. Our results suggest shear stress as a protective regulator against inflammation.
	Activator Protein-1 Mediates Shear Stress–Induced Prostaglandin D Synthase Gene Expression in Vascular Endothelial Cells Megumi Miyagi, Yoshikazu Miwa, Fumi Takahashi-Yanaga, Sachio Morimoto, and Toshiyuki Sasaguri Arterioscler Thromb Vasc Biol. 2005;25:970-975; published online before print February 17 2005, doi:10.1161/01.ATV.0000159702.68591.0d Abstract \| Full Text \| PDF \| Data Supplement We attempted to determine the molecular mechanism for fluid shear stress-induced lipocalin-type PG D synthase (L-PGDS) expression in endothelial cells. Examination of the promoter region of the L-PGDS gene revealed that shear stress induces L-PGDS expression by transcriptional activation through the AP-1 binding site.
	Sphingosine-1-Phosphate Prevents Tumor Necrosis Factor- ${alpha}$ –Mediated Monocyte Adhesion to Aortic Endothelium in Mice David T. Bolick, Suseela Srinivasan, Kyu W. Kim, Melissa E. Hatley, Jeremy J. Clemens, Angela Whetzel, Nicole Ferger, Timothy L. Macdonald, Michael D. Davis, Philip S. Tsao, Kevin R. Lynch, and Catherine C. Hedrick Arterioscler Thromb Vasc Biol. 2005;25:976-981; published online before print March 10 2005, doi:10.1161/01.ATV.0000162171.30089.f6 Abstract \| Full Text \| PDF \| Data Supplement We examined the role of sphingosine-1-phosphate (S1P) in modulating monocyte-endothelial cell (EC) interactions. S1P and a specific S1P1 receptor agonist prevented monocyte adhesion to aorta in tumor necrosis factor (TNF)-{alpha}-treated mice in vivo. We provide the first evidence to our knowledge that S1P signaling through the endothelial S1P1 receptor protects the vasculature against TNF-{alpha}-mediated monocyte-EC interactions in vivo.
	N-Cadherin–Dependent Cell–Cell Contacts Promote Human Saphenous Vein Smooth Muscle Cell Survival Evgenia Koutsouki, Cressida A. Beeching, Sadie C. Slater, Orest W. Blaschuk, Graciela B. Sala-Newby, and Sarah J. George Arterioscler Thromb Vasc Biol. 2005;25:982-988; published online before print March 17 2005, doi:10.1161/01.ATV.0000163183.27658.4b Abstract \| Full Text \| PDF \| Data Supplement We investigated the role of N-cadherin, a transmembrane protein that mediates cell-cell contacts, in VSMC survival. Inhibition of N-cadherin significantly decreased cell-cell contact and survival. Conversely, overexpression of N-cadherin significantly decreased VSMC apoptosis. We suggest that N-cadherin promotes VSMC survival by initiating survival signals via phosphorylation of Akt and Bad.
	Free Fatty Acid Impairment of Nitric Oxide Production in Endothelial Cells Is Mediated by IKKß Francis Kim, Kelly A. Tysseling, Julie Rice, Matilda Pham, Lutfiyah Haji, Byron M. Gallis, Arnold S. Baas, Pathmaja Paramsothy, Cecilia M. Giachelli, Marshall A. Corson, and Elaine W. Raines Arterioscler Thromb Vasc Biol. 2005;25:989-994; published online before print February 24 2005, doi:10.1161/01.ATV.0000160549.60980.a8 Abstract \| Full Text \| PDF Free fatty acids (FFA) are commonly elevated in diabetes and obesity and have been shown to impair nitric oxide (NO) production by endothelial cells. Overexpression of a kinase inactive form of IKKß blocks the ability of FFA to inhibit insulin-dependent NO production, whereas overexpression of wild-type IKKß recapitulates the effect of FFA on insulin-dependent NO production. Elevated levels of common FFA found in human serum activate IKKß in endothelial cells leading to reduced NO production, and thus may serve to link pathways involved in inflammation and endothelial dysfunction.
	C-Reactive Protein Inhibits Endothelium-Dependent NO-Mediated Dilation in Coronary Arterioles by Activating p38 Kinase and NAD(P)H Oxidase Erion Qamirani, Yi Ren, Lih Kuo, and Travis W. Hein Arterioscler Thromb Vasc Biol. 2005;25:995-1001; published online before print February 17 2005, doi:10.1161/01.ATV.0000159890.10526.1e Abstract \| Full Text \| PDF C-reactive protein (CRP) is not only a marker but also a mediator of inflammation and atherogenesis. Treatment of isolated coronary arterioles with CRP attenuated endothelium-dependent NO-mediated dilation by producing superoxide from NAD(P)H oxidase via p38 kinase activation. By impairing NO-mediated vasoreactivity, CRP could facilitate the initiation of numerous cardiovascular diseases.
	Atherosclerosis and Lipoproteins
	Role of Gas-6 in Adipogenesis and Nutritionally Induced Adipose Tissue Development in Mice Erik Maquoi, Gabor Vörös, Peter Carmeliet, Désiré Collen, and H. Roger Lijnen Arterioscler Thromb Vasc Biol. 2005;25:1002-1007; published online before print February 24 2005, doi:10.1161/01.ATV.0000160611.68791.c6 Abstract \| Full Text \| PDF \| Data Supplement A role of Gas-6 in adipose tissue homeostasis was investigated in murine models of obesity. Gas-6 expression was transiently downregulated during nutritionally induced expansion of adipose tissues. On exposure to a high-fat-diet, Gas-6 mice were leaner than their wild-type counterparts, suggesting that Gas-6 enhances the accumulation of adipose tissue in diet-induced obesity.
	Connective Tissue Growth Factor Is Overexpressed in Complicated Atherosclerotic Plaques and Induces Mononuclear Cell Chemotaxis In Vitro Iwona Cicha, Atilla Yilmaz, Michael Klein, Dieter Raithel, David R. Brigstock, Werner G. Daniel, Margarete Goppelt-Struebe, and Christoph D. Garlichs Arterioscler Thromb Vasc Biol. 2005;25:1008-1013; published online before print March 10 2005, doi:10.1161/01.ATV.0000162173.27682.7b Abstract \| Full Text \| PDF \| Data Supplement CTGF protein expression in carotid plaque development was investigated. CTGF levels were significantly increased in vulnerable complicated lesions compared with stable fibrous plaques. CTGF was also shown to act as chemoattractant for human mononuclear cells in vitro, suggesting its importance in atherosclerosis.
	Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development Jian Guo, Vivian de Waard, Miranda Van Eck, Reeni B. Hildebrand, Eva J.A. van Wanrooij, Johan Kuiper, Nobuyo Maeda, G. Martin Benson, Pieter H.E. Groot, and Theo J.C. Van Berkel Arterioscler Thromb Vasc Biol. 2005;25:1014-1019; published online before print March 17 2005, doi:10.1161/01.ATV.0000163181.40896.42 Abstract \| Full Text \| PDF \| Data Supplement Repopulation of apoE knockout mice with CCR2-deficient bone marrow progenitor cells demonstrates that hematopoietic CCR2 does not have a great effect on the progression of established atherosclerotic lesions and lesion composition, ie, macrophage and collagen content, and certainly does not result in lesion regression.
	Matrix Metalloproteinase-9 Modulation by Resident Arterial Cells Is Responsible for Injury-Induced Accelerated Atherosclerotic Plaque Development in Apolipoprotein E–Deficient Mice Eric T. Choi, Emily T. Collins, Leopoldo A. Marine, Maria G. Uberti, Hisashi Uchida, Jeremy E. Leidenfrost, M. Faisal Khan, Kenneth P. Boc, Dana R. Abendschein, and William C. Parks Arterioscler Thromb Vasc Biol. 2005;25:1020-1025; published online before print March 3 2005, doi:10.1161/01.ATV.0000161275.82687.f6 Abstract \| Full Text \| PDF We studied the role of MMP-9 in rapid atherosclerotic plaque development in a mouse model. Compared with apoE-/- MMP-9+/+ mice, plaque volume and cellular accumulation were significantly reduced in apoE-/- MMP-9-/- mice. Furthermore, plaque burden is intimately linked to MMP-9 generated by resident arterial cells and not the bone marrow-derived cells.
	Role of Insulin Resistance in Familial Combined Hyperlipidemia M.J. Veerkamp, J. de Graaf, and A.F.H. Stalenhoef Arterioscler Thromb Vasc Biol. 2005;25:1026-1031; published online before print February 24 2005, doi:10.1161/01.ATV.0000160612.18065.29 Abstract \| Full Text \| PDF FCH subjects are insulin resistant even after correction for obesity, which is dependent on lipid phenotype expression. A change in insulin resistance is associated with a change in lipid phenotype expression in time. Finally, insulin resistance or obesity does not fully account for the increased plasma levels of apoB or high occurrence of small dense LDL in FCH.
	Plasma Levels of Soluble Receptor for Advanced Glycation End Products and Coronary Artery Disease in Nondiabetic Men Colomba Falcone, Enzo Emanuele, Angela D’Angelo, Maria P. Buzzi, Chiara Belvito, Mariaclara Cuccia, and Diego Geroldi Arterioscler Thromb Vasc Biol. 2005;25:1032-1037; published online before print February 24 2005, doi:10.1161/01.ATV.0000160342.20342.00 Abstract \| Full Text \| PDF Soluble RAGE could prevent the adverse effects of RAGE signaling by acting as a decoy. We found that low levels of sRAGE in plasma are independently associated with the presence of CAD in nondiabetic men. These findings suggest that sRAGE is one of the clinically important molecules associated with atherosclerosis.
	Association Between Serum Uric Acid, Metabolic Syndrome, and Carotid Atherosclerosis in Japanese Individuals Nobukazu Ishizaka, Yuko Ishizaka, Ei-Ichi Toda, Ryozo Nagai, and Minoru Yamakado Arterioscler Thromb Vasc Biol. 2005;25:1038-1044; published online before print March 3 2005, doi:10.1161/01.ATV.0000161274.87407.26 Abstract \| Full Text \| PDF Whether there is an independent association of uric acid with prevalence of carotid atherosclerosis was analyzed. Serum uric acid values are associated with carotid plaque independently of other atherogenic risk factors in men without but not with metabolic syndrome or in women at all.
	Nonalcoholic Fatty Liver Disease Is Associated With Carotid Atherosclerosis: A Case–Control Study Angel Brea, Daniel Mosquera, Eva Martín, Ana Arizti, José L. Cordero, and Emilio Ros Arterioscler Thromb Vasc Biol. 2005;25:1045-1050; published online before print February 24 2005, doi:10.1161/01.ATV.0000160613.57985.18 Abstract \| Full Text \| PDF In a case-control study, we examined whether nonalcoholic patients with an ultrasound diagnosis of fatty liver had carotid atherosclerosis. Compared with controls, cases showed increased intima-media thickness and plaque prevalence. The casual detection of a fatty liver by abdominal ultrasound should alert to the existence of a high cardiovascular risk.
	Association of C-Reactive Protein With Blood Pressure and Hypertension: Life Course Confounding and Mendelian Randomization Tests of Causality George Davey Smith, Debbie A. Lawlor, Roger Harbord, Nic Timpson, Ann Rumley, Gordon D.O. Lowe, Ian N.M. Day, and Shah Ebrahim Arterioscler Thromb Vasc Biol. 2005;25:1051-1056; published online before print February 24 2005, doi:10.1161/01.ATV.0000160351.95181.d0 Abstract \| Full Text \| PDF In a large study, we demonstrate that CRP levels but not a genetic variant associated with CRP levels were related to hypertension. Furthermore, the CRP association with hypertension was essentially abolished by statistical adjustment for confounding factors. We conclude that elevated CRP levels do not lead to elevated blood pressure.
	Effects of Cholesteryl Ester Transfer Protein Inhibition on High-Density Lipoprotein Subspecies, Apolipoprotein A-I Metabolism, and Fecal Sterol Excretion Margaret E. Brousseau, Margaret R. Diffenderfer, John S. Millar, Chorthip Nartsupha, Bela F. Asztalos, Francine K. Welty, Megan L. Wolfe, Mats Rudling, Ingemar Björkhem, Bo Angelin, James P. Mancuso, Andres G. Digenio, Daniel J. Rader, and Ernst J. Schaefer Arterioscler Thromb Vasc Biol. 2005;25:1057-1064; published online before print March 10 2005, doi:10.1161/01.ATV.0000161928.16334.dd Abstract \| Full Text \| PDF \| Data Supplement The effects of cholesteryl ester transfer protein (CETP) inhibition on HDL apoA-I kinetics and surrogate markers of cholesterol synthesis and fecal sterol excretion were assessed in 19 subjects with low HDL. Our data indicate that CETP inhibition with with torcetrapib significantly increased HDL apoA-I pool size because of delayed catabolism, but did not alter fecal sterol excretion.
	Thrombosis
	Effect of P-Selectin on Phosphatidylserine Exposure and Surface-Dependent Thrombin Generation on Monocytes Ian del Conde, Faisal Nabi, Raúl Tonda, Perumal Thiagarajan, José A. López, and Neal S. Kleiman Arterioscler Thromb Vasc Biol. 2005;25:1065-1070; published online before print February 10 2005, doi:10.1161/01.ATV.0000159094.17235.9b Abstract \| Full Text \| PDF Phosphatidylserine expression on monocytes is an important cofactor in the enzymatic reactions of coagulation. Stimulation of monocytes with P-selectin leads to cell activation and the expression of tissue factor, the main initiator of coagulation. Here we show that P-selectin induces phosphatidylserine expression on monocytes through a mechanism dependent on PSGL-1 on the monocyte.
	Rosuvastatin Reduces Platelet Activation in Heart Failure: Role of NO Bioavailability Andreas Schäfer, Daniela Fraccarollo, Martin Eigenthaler, Piet Tas, Andreas Firnschild, Stefan Frantz, Georg Ertl, and Johann Bauersachs Arterioscler Thromb Vasc Biol. 2005;25:1071-1077; published online before print March 10 2005, doi:10.1161/01.ATV.0000161926.43967.df Abstract \| Full Text \| PDF Congestive heart failure is associated with progressive vascular endothelial dysfunction, reduced systemic NO bioavailability, and platelet activation in vivo. Chronic treatment with the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor rosuvastatin in rats with heart failure after myocardial infarction improved NO bioavailability and reduced platelet activation.
	Interleukin-6 and Mevastatin Regulate Plasminogen Activator Inhibitor-1 Through CCAAT/Enhancer-Binding Protein- ${delta}$ Jie Dong, Satoshi Fujii, Hongmei Li, Hidekazu Nakabayashi, Masaharu Sakai, Shinzo Nishi, Daisuke Goto, Tomoo Furumoto, Shogo Imagawa, Tarikuz A.K.M. Zaman, and Akira Kitabatake Arterioscler Thromb Vasc Biol. 2005;25:1078-1084; published online before print February 17 2005, doi:10.1161/01.ATV.0000159701.24372.49 Abstract \| Full Text \| PDF IL-6 increases hepatic PAI-1 expression mediated by the -232- to -210-bp region of the promoter containing a C/EBP{delta} binding site. Mevastatin attenuated IL-6-mediated increase of C/EBP{delta} protein in the nuclear extracts. C/EBP{delta} may be responsible for hepatic PAI-1 expression induced by IL-6 and its attenuation by statins.
	Abstracts
	Abstracts of the 6th Annual Conference on Arteriosclerosis, Thrombosis, and Vascular Biology Arterioscler Thromb Vasc Biol. 2005;25:e43-e109 PDF
	Letters to the Editor
	Lipopolysaccharide, Toll-Like Receptors, and the Immune Contribution to Atherosclerosis Terence M. Doherty, Prediman K. Shah, Moshe Arditi, Lynn L. Stoll, Gerene M. Denning, and Neal L. Weintraub Arterioscler Thromb Vasc Biol. 2005;25:e38-e39, doi:10.1161/01.ATV.0000161318.83751.08 Extract \| Full Text \| PDF
	Natural Killer T Cells in Atherosclerosis Yuri V. Bobryshev, Israel F. Charo, and Ara M. Aslanian Arterioscler Thromb Vasc Biol. 2005;25:e40, doi:10.1161/01.ATV.0000161317.01678.75 Extract \| Full Text \| PDF
	Vitamin D Nutrition Does Not Cause Peripheral Artery Disease Reinhold Vieth, Robert Scragg, P.E. Norman, and J.T. Powell Arterioscler Thromb Vasc Biol. 2005;25:e41-e42, doi:10.1161/01.ATV.0000164308.43228.92 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 5; May 1, 2005

Editorials

P-Selectin and Blood Coagulation: It’s Not Only About Inflammation Any More

Soluble Levels of Receptor for Advanced Glycation Endproducts (sRAGE) and Coronary Artery Disease: The Next C-Reactive Protein?

FGFR1 and the Bloodline of the Vasculature

SOD Isoforms and Signaling in Blood Vessels: Evidence for the Importance of ROS Compartmentalization

The Union of Vascular and Metabolic Actions of Insulin in Sickness and in Health

Making Up and Breaking Up: The Tortuous Ways of the Vascular Wall

Brief Reviews

Role of Caspases in Death and Survival of the Plaque Macrophage

Nuclear Factor B Signaling in Atherogenesis

NO Generation From Nitrite and Its Role in Vascular Control

Role of Lipoprotein-Associated Phospholipase A2 in Atherosclerosis: Biology, Epidemiology, and Possible Therapeutic Target

Mechanisms, Pathophysiology, and Therapy of Arterial Stiffness

Vascular Biology

Fibroblast Growth Factor Receptor-1 Expression Is Required for Hematopoietic but not Endothelial Cell Development

Differential Activation of Mitogenic Signaling Pathways in Aortic Smooth Muscle Cells Deficient in Superoxide Dismutase Isoforms

Partial Off-Loading of Longitudinal Tension Induces Arterial Tortuosity

Shear Stress Inhibits Smooth Muscle Cell–Induced Inflammatory Gene Expression in Endothelial Cells: Role of NF-B

Activator Protein-1 Mediates Shear Stress–Induced Prostaglandin D Synthase Gene Expression in Vascular Endothelial Cells

Sphingosine-1-Phosphate Prevents Tumor Necrosis Factor-–Mediated Monocyte Adhesion to Aortic Endothelium in Mice

N-Cadherin–Dependent Cell–Cell Contacts Promote Human Saphenous Vein Smooth Muscle Cell Survival

Free Fatty Acid Impairment of Nitric Oxide Production in Endothelial Cells Is Mediated by IKKß

C-Reactive Protein Inhibits Endothelium-Dependent NO-Mediated Dilation in Coronary Arterioles by Activating p38 Kinase and NAD(P)H Oxidase

Atherosclerosis and Lipoproteins

Role of Gas-6 in Adipogenesis and Nutritionally Induced Adipose Tissue Development in Mice

Connective Tissue Growth Factor Is Overexpressed in Complicated Atherosclerotic Plaques and Induces Mononuclear Cell Chemotaxis In Vitro

Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development

Matrix Metalloproteinase-9 Modulation by Resident Arterial Cells Is Responsible for Injury-Induced Accelerated Atherosclerotic Plaque Development in Apolipoprotein E–Deficient Mice

Role of Insulin Resistance in Familial Combined Hyperlipidemia

Plasma Levels of Soluble Receptor for Advanced Glycation End Products and Coronary Artery Disease in Nondiabetic Men

Association Between Serum Uric Acid, Metabolic Syndrome, and Carotid Atherosclerosis in Japanese Individuals

Nonalcoholic Fatty Liver Disease Is Associated With Carotid Atherosclerosis: A Case–Control Study

Association of C-Reactive Protein With Blood Pressure and Hypertension: Life Course Confounding and Mendelian Randomization Tests of Causality

Effects of Cholesteryl Ester Transfer Protein Inhibition on High-Density Lipoprotein Subspecies, Apolipoprotein A-I Metabolism, and Fecal Sterol Excretion

Thrombosis

Effect of P-Selectin on Phosphatidylserine Exposure and Surface-Dependent Thrombin Generation on Monocytes

Rosuvastatin Reduces Platelet Activation in Heart Failure: Role of NO Bioavailability

Interleukin-6 and Mevastatin Regulate Plasminogen Activator Inhibitor-1 Through CCAAT/Enhancer-Binding Protein-

Abstracts

Abstracts of the 6th Annual Conference on Arteriosclerosis, Thrombosis, and Vascular Biology

Letters to the Editor

Lipopolysaccharide, Toll-Like Receptors, and the Immune Contribution to Atherosclerosis

Natural Killer T Cells in Atherosclerosis

Vitamin D Nutrition Does Not Cause Peripheral Artery Disease

Spotlight

Nuclear Factor ${kappa}$ B Signaling in Atherogenesis

Role of Lipoprotein-Associated Phospholipase A₂ in Atherosclerosis: Biology, Epidemiology, and Possible Therapeutic Target

Shear Stress Inhibits Smooth Muscle Cell–Induced Inflammatory Gene Expression in Endothelial Cells: Role of NF- ${kappa}$ B

Sphingosine-1-Phosphate Prevents Tumor Necrosis Factor- ${alpha}$ –Mediated Monocyte Adhesion to Aortic Endothelium in Mice

Interleukin-6 and Mevastatin Regulate Plasminogen Activator Inhibitor-1 Through CCAAT/Enhancer-Binding Protein- ${delta}$