Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (29 [9])

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Volume 29, Issue 9; September 1, 2009

Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Clinical and Population Studies
National Cholesterol Awareness Month

Key: VB = Vascular Biology AL = Atherosclerosis/Lipoproteins TH = Thrombosis

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	Integrative Physiology/Experimental Medicine
	Imaging and Quantitative Analysis of Atherosclerotic Lesions by CARS-Based Multimodal Nonlinear Optical Microscopy Han-Wei Wang, Ingeborg M. Langohr, Michael Sturek, and Ji-Xin Cheng Arterioscler Thromb Vasc Biol. 2009;29:1342-1348; published online before print June 11 2009, doi:10.1161/ATVBAHA.109.189316 Abstract \| Full Text \| PDF \| Data Supplement \| Article Figures in Color A multimodal nonlinear optical (NLO) microscope, which integrated CARS, TPEF, and SFG on the same platform, was applied to interrogate atherosclerotic lesions without labels. Early and advanced lesions were distinguished with subcellular resolution and with compositional specificity such that in situ quantitative analyses of lipid and collagen contents could be performed.
	Lack of Phosphatidylethanolamine N-Methyltransferase Alters Plasma VLDL Phospholipids and Attenuates Atherosclerosis in Mice Yang Zhao, Brian Su, René L. Jacobs, Brian Kennedy, Gordon A. Francis, Emma Waddington, John T. Brosnan, Jean E. Vance, and Dennis E. Vance Arterioscler Thromb Vasc Biol. 2009;29:1349-1355; published online before print June 11 2009, doi:10.1161/ATVBAHA.109.188672 Abstract \| Full Text \| PDF \| Data Supplement Phosphatidylethanolamine N-methyltransferase (PEMT) catalyzes phosphatidylcholine biosynthesis in the liver. PEMT deficiency in LDLR-deficient mice significantly reduced plasma atherogenic lipoprotein levels and atherosclerotic lesion area, altered the phospholipid composition of hepatic apoB-containing lipoproteins, modestly decreased hepatic lipoprotein secretion, and altered the rate of lipoprotein clearance from plasma.
	Syndecan-1: An Inhibitor of Arterial Smooth Muscle Cell Growth and Intimal Hyperplasia Nozomi Fukai, Richard D. Kenagy, Lihua Chen, Lu Gao, Guenter Daum, and Alexander W. Clowes Arterioscler Thromb Vasc Biol. 2009;29:1356-1362; published online before print July 10 2009, doi:10.1161/ATVBAHA.109.190132 Abstract \| Full Text \| PDF \| Data Supplement
	Cell Biology/Signaling
	Interferon-Gamma Induces Prolyl Hydroxylase (PHD)3 Through a STAT1-Dependent Mechanism in Human Endothelial Cells Scott A. Gerber, Bogdan Yatsula, Cheryl L. Maier, Timothy J. Sadler, Laurence W. Whittaker, and Jordan S. Pober Arterioscler Thromb Vasc Biol. 2009;29:1363-1369; published online before print July 2 2009, doi:10.1161/ATVBAHA.109.192542 Abstract \| Full Text \| PDF \| Data Supplement There is growing evidence of linkage between immune and hypoxic responses. We show that IFN{gamma} induces prolyl hydroxylase (PHD)3, a HIF-inducible negative regulator of HIF expression, selectively in human endothelial cells through JAK/STAT1 signaling independent of HIF-1. Pharmacological inhibition of PHDs suppresses the induction of IFN{gamma}-dependent genes after IFN{gamma} treatment.
	Activation of NF- ${kappa}$ B by Palmitate in Endothelial Cells: A Key Role for NADPH Oxidase-Derived Superoxide in Response to TLR4 Activation Ezekiel Maloney, Ian R. Sweet, David M. Hockenbery, Matilda Pham, Norma O. Rizzo, Sanshiro Tateya, Priya Handa, Michael W. Schwartz, and Francis Kim Arterioscler Thromb Vasc Biol. 2009;29:1370-1375; published online before print June 18 2009, doi:10.1161/ATVBAHA.109.188813 Abstract \| Full Text \| PDF \| Data Supplement These studies were undertaken to delineate the pathways linking TLR4 activation to the activation of IKKβ/NF-{kappa}B signaling in vascular tissue. We demonstrate in cultured human endothelial cells that superoxide production is required for palmitate to induce NF-{kappa}B signaling, and further that palmitate increases superoxide production by activating NADPH oxidase through the TLR4 signaling pathway.
	Lysophosphatidylcholine Activates a Novel PKD2-Mediated Signaling Pathway That Controls Monocyte Migration Mingqi Tan, Feng Hao, Xuemin Xu, Guy M. Chisolm, and Mei-Zhen Cui Arterioscler Thromb Vasc Biol. 2009;29:1376-1382; published online before print June 11 2009, doi:10.1161/ATVBAHA.109.191585 Abstract \| Full Text \| PDF \| Data Supplement Lysophosphatidylcholine activates protein kinase D (PKD), and the PKD2-activated p38 pathway is responsible for lysophosphatidylcholine-induced monocyte migration. Thus, PKD is a novel and functional intracellular regulator in lysophosphatidylcholine signaling, and PKD mediates monocyte migration. These results suggest a new role for PKD2 in the development of atherosclerosis.
	Clinical and Population Studies
	Targeted Metabolomic Evaluation of Arginine Methylation and Cardiovascular Risks: Potential Mechanisms Beyond Nitric Oxide Synthase Inhibition Zeneng Wang, W. H. Wilson Tang, Leslie Cho, Danielle M. Brennan, and Stanley L. Hazen Arterioscler Thromb Vasc Biol. 2009;29:1383-1391; published online before print June 18 2009, doi:10.1161/ATVBAHA.109.185645 Abstract \| Full Text \| PDF We analyzed posttranslational modification products of arginine in stable patients undergoing cardiac evaluation, and found that the ratio of dimethyl- versus monomethylarginine metabolites provided the strongest independent risk prediction for significant coronary artery disease and incident adverse clinical events. This "arginine methylation index" maintains its prognostic value independent of measures of arginine bioavailability. These findings imply that pathophysiologic contributions of arginine methylation may be beyond direct nitric oxide synthases inhibition.
	Cadmium Is a Novel and Independent Risk Factor for Early Atherosclerosis Mechanisms and In Vivo Relevance Barbara Messner, Michael Knoflach, Andreas Seubert, Andreas Ritsch, Kristian Pfaller, Blair Henderson, Ying H. Shen, Iris Zeller, Johann Willeit, Günther Laufer, Georg Wick, Stefan Kiechl, and David Bernhard Arterioscler Thromb Vasc Biol. 2009;29:1392-1398; published online before print June 25 2009, doi:10.1161/ATVBAHA.109.190082 Abstract \| Full Text \| PDF \| Data Supplement Here we demonstrate that high cadmium (Cd) level is associated with increased intima-media thickness in 195 healthy young women, and that Cd causes endothelial damage and increases atherosclerotic plaque formation in mice. In vitro, physiological doses of Cd increase endothelial permeability by DNA damage-induced inhibition of endothelial proliferation and cell death induction, which is inhibited by zinc.
	Is Diabetes Mellitus an Independent Risk Factor for Venous Thromboembolism?: A Population-Based Case-Control Study John A. Heit, Cynthia L. Leibson, Aneel A. Ashrani, Tanya M. Petterson, Kent R. Bailey, and L. Joseph Melton, III Arterioscler Thromb Vasc Biol. 2009;29:1399-1405; published online before print June 18 2009, doi:10.1161/ATVBAHA.109.189290 Abstract \| Full Text \| PDF In a large population-based case-control study, diabetes mellitus and diabetes complications (retinopathy, nephropathy or neuropathy, ketoacidosis) were not risk factors for incident venous thromboembolism after controlling for hospitalization for medical illness or for surgery, or nursing home confinement.
	National Cholesterol Awareness Month
	National Cholesterol Month Edward A. Fisher Arterioscler Thromb Vasc Biol. 2009;29:1243; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.194449 Extract \| Full Text \| PDF
	Interrelationships Among HDL Metabolism, Aging, and Atherosclerosis Michael Walter Arterioscler Thromb Vasc Biol. 2009;29:1244-1250; published online before print August 10 2009, doi:10.1161/ATVBAHA.108.181438 Abstract \| Full Text \| PDF
	TGF-β1 Limits Plaque Growth, Stabilizes Plaque Structure, and Prevents Aortic Dilation in Apolipoprotein E-Null Mice Andrew D. Frutkin, Goro Otsuka, April Stempien-Otero, Casilde Sesti, Liang Du, Mia Jaffe, Helén L. Dichek, Caroline J. Pennington, Dylan R. Edwards, Madeline Nieves-Cintrón, Daniel Minter, Michael Preusch, Jie Hong Hu, Julien C. Marie, and David A. Dichek Arterioscler Thromb Vasc Biol. 2009;29:1251-1257; published online before print March 26 2009, doi:10.1161/ATVBAHA.109.186593 Abstract \| Full Text \| PDF \| Data Supplement Overexpression of active transforming growth-β1 (TGF-β1) in the heart and plasma of apolipoprotein E-deficient mice retarded aortic root atherosclerosis and slowed the development of aortic aneurysmal disease. Plasma TGF-β1 is an antiatherogenic and vasculoprotective cytokine that alters cellularity, lipid accumulation, inflammation, and gene expression in the artery wall.
	Inactivation of the LRP1 Intracellular NPxYxxL Motif in LDLR-Deficient Mice Enhances Postprandial Dyslipidemia and Atherosclerosis Philip L.S.M. Gordts, Sara Reekmans, Annick Lauwers, Amber Van Dongen, Leen Verbeek, and Anton J.M. Roebroek Arterioscler Thromb Vasc Biol. 2009;29:1258-1264; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.192211 Abstract \| Full Text \| PDF \| Data Supplement LRP1 knock-in mice carrying an inactivated NPxYxxL motif were crossed with LDLR-deficient mice. On this background knock-in mice had increased levels of postprandial lipids and atherogenic and inflammatory LRP1 ligands. These findings were associated with an aggravated atherosclerosis phenotype. No pronounced effect, however, was seen on LRP1-mediated PDGFR-β properties.
	Inhibition of Soluble Epoxide Hydrolase Attenuated Atherosclerosis, Abdominal Aortic Aneurysm Formation, and Dyslipidemia Le-Ning Zhang, Jon Vincelette, Ying Cheng, Upasana Mehra, Dawn Chen, Sampath-Kumar Anandan, Richard Gless, Heather K. Webb, and Yi-Xin (Jim) Wang Arterioscler Thromb Vasc Biol. 2009;29:1265-1270; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.186064 Abstract \| Full Text \| PDF \| Data Supplement In Ang II-infused apoE KO mice, the s-EH inhibitor AR9276 attenuated aneurysm formation and atherosclerosis development. These effects are associated with reduction of inflammatory cell infiltration in the vascular wall and downregulation of the expression of proinflammatory mediators in the vasculature and blood, as well as correction of dyslipidemia.
	Inhibition of Platelet-Rich Arterial Thrombus In Vivo: Acute Antithrombotic Effect of Intravenous HMG-CoA Reductase Therapy Chike Obi, Waldemar Wysokinski, Krzystof Karnicki, Whyte G. Owen, and Robert D. McBane, II Arterioscler Thromb Vasc Biol. 2009;29:1271-1276; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.190884 Abstract \| Full Text \| PDF Sequential carotid crush injury augments the thrombus size by 50% when comparing the second to the first carotid injury in control pigs. This augmentation is acutely attenuated by intravenous lovastatin which appears at least in part attributable to platelet inhibition as evidenced by in vitro measures of platelet function.
	Renal Dysfunction Potentiates Foam Cell Formation by Repressing ABCA1 Yiqin Zuo, Patricia Yancey, Iris Castro, Wasif Khan, Masaru Motojima, Iekuni Ichikawa, Agnes B. Fogo, MacRae F. Linton, Sergio Fazio, and Valentina Kon Arterioscler Thromb Vasc Biol. 2009;29:1277-1282; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.188995 Abstract \| Full Text \| PDF \| Data Supplement Chronic kidney disease imparts tremendous risk for cardiovascular disease. We found that mild renal dysfunction induced by uninephrectomy dramatically increases macrophage cholesterol, blunts cholesterol efflux, downregulates cholesterol transporter ABCA1, and activates nuclear factor-kappa B. These effects are ameliorated by treatment with an angiotensin receptor blocker.
	Glucose Metabolism Is Required for Oxidized LDL–Induced Macrophage Survival: Role of PI3K and Bcl-2 Family Proteins Caryn L. Elsegood, Margaret Chang, Wendy Jessup, Glen M. Scholz, and John A. Hamilton Arterioscler Thromb Vasc Biol. 2009;29:1283-1289; published online before print August 10 2009, doi:10.1161/ATVBAHA.108.180778 Abstract \| Full Text \| PDF \| Data Supplement Atherosclerotic lesion-associated macrophages take up large amounts of glucose. Oxidized LDL, which is found in atherosclerotic lesions, enhances in vitro macrophage survival by inducing PI3K-dependent glucose uptake. Metabolism of the glucose is required to maintain Bcl-2 and Bcl-xL protein levels, and hence for macrophage survival.
	Membrane Cholesterol Is a Biomechanical Regulator of Neutrophil Adhesion Hana Oh, Emile R. Mohler, III, Aiwei Tian, Tobias Baumgart, and Scott L. Diamond Arterioscler Thromb Vasc Biol. 2009;29:1290-1297; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.189571 Abstract \| Full Text \| PDF \| Data Supplement Neutrophils and HL-60 cells were perfused into flow chambers at 100 s-1 after cholesterol enrichment or depletion. Cholesterol enrichment increased P-selectin-mediated adhesion, membrane tethering fraction, membrane tether length and growth rate. Cells with higher cholesterol content were more deformable and rolled more slowly and uniformly on P-selectin or activated endothelium.
	SR-BI Selective Lipid Uptake: Subsequent Metabolism of Acute Phase HDL Maria C. de Beer, Nancy R. Webb, Nathan L. Whitaker, Joanne M. Wroblewski, Anisa Jahangiri, Deneys R. van der Westhuyzen, and Frederick C. de Beer Arterioscler Thromb Vasc Biol. 2009;29:1298-1303; published online before print March 19 2009, doi:10.1161/ATVBAHA.109.186502 Abstract \| Full Text \| PDF SR-BI processing of AP HDL segregates apolipoprotein metabolism. A small apoA-I only remnant is generated. It fails to associate with preformed HDL. SAA displaces apoA-I from SR-BI remnants.
	Decision Analysis Supports the Paradigm That Indiscriminate Supplementation of Vitamin E Does More Harm than Good Yedidya Dotan, Ilya Pinchuk, Dov Lichtenberg, and Moshe Leshno Arterioscler Thromb Vasc Biol. 2009;29:1304-1309; published online before print March 12 2009, doi:10.1161/ATVBAHA.108.178699 Abstract \| Full Text \| PDF \| Data Supplement \| Data Supplement Our objective was to reassess the outcome of nondiscriminatory supplementation of vitamin E with respect to its effects on cardiovascular-related events and mortality. Our analysis, applying a Markov model, revealed that supplementing the general public with vitamin E results in loss of quality-adjusted life years.
	Identification of Genetic Variants Associated With Response to Statin Therapy Jessica L. Mega, David A. Morrow, Alison Brown, Christopher P. Cannon, and Marc S. Sabatine Arterioscler Thromb Vasc Biol. 2009;29:1310-1315; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.188474 Abstract \| Full Text \| PDF \| Data Supplement In this study involving statin-treated subjects and polymorphisms in 9 genes, carriers of the APOE {epsilon}2 haplotype versus {epsilon}4 haplotype had significantly lower baseline LDL-C, greater LDL-C reduction with atorvastatin and pravastatin, and more frequently achieved a guideline-recommended LDL-C <=70 mg/dL. A variant in ABCB1 was associated with the degree of LDL lowering with pravastatin.
	A Common Variant in Low-Density Lipoprotein Receptor–Related Protein 6 Gene (LRP6) Is Associated With LDL-Cholesterol Maciej Tomaszewski, Fadi J. Charchar, Timothy Barnes, Magdalena Gawron-Kiszka, Agnieszka Sedkowska, Ewa Podolecka, Jacek Kowalczyk, Wendy Rathbone, Zbigniew Kalarus, Wladyslaw Grzeszczak, Alison H. Goodall, Nilesh J. Samani, and Ewa Zukowska-Szczechowska Arterioscler Thromb Vasc Biol. 2009;29:1316-1321; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.185355 Abstract \| Full Text \| PDF \| Data Supplement We have hypothesized that common alleles in the locus underlying monogenic form of coronary artery disease (low-density lipoprotein receptor-related protein 6 gene [LRP6]) are associated with LDL-cholesterol. Through genetic association analyses we identified a common variant (rs10845493) in LRP6 as a significant determinant of LDL-cholesterol.
	The ATF6-Met[67]Val Substitution Is Associated With Increased Plasma Cholesterol Levels Steven J.R. Meex, Daphna Weissglas-Volkov, Carla J.H. van der Kallen, Donna J. Thuerauf, Marleen M.J. van Greevenbroek, Casper G. Schalkwijk, Coen D.A. Stehouwer, Edith J.M. Feskens, Lonneke Heldens, Torik A. Ayoubi, Marten H. Hofker, Bradly G. Wouters, Robert Vlietinck, Janet S. Sinsheimer, Marja-Riitta Taskinen, Johanna Kuusisto, Markku Laakso, Tjerk W.A. de Bruin, Päivi Pajukanta, and Christopher C. Glembotski Arterioscler Thromb Vasc Biol. 2009;29:1322-1327; published online before print August 10 2009, doi:10.1161/ATVBAHA.108.180240 Abstract \| Full Text \| PDF \| Data Supplement We report the association of the ATF6-methionine [67]valine amino-acid substitution with plasma cholesterol levels. Association analyses in 2674 subjects and functional data suggest that the ATF6 gene may influence cholesterol levels in subjects at increased risk to develop cardiovascular disease.
	Association of Scavenger Receptors in Adipose Tissue With Insulin Resistance in Nondiabetic Humans Neda Rasouli, Aiwei Yao-Borengasser, Vijayalakshmi Varma, Horace J. Spencer, Robert E. McGehee, Jr, Charlotte A. Peterson, Jawahar L. Mehta, and Philip A. Kern Arterioscler Thromb Vasc Biol. 2009;29:1328-1335; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.186957 Abstract \| Full Text \| PDF \| Data Supplement The relationship between scavenger receptors and insulin resistance is not well understood. We demonstrated that adipose tissue scavenger receptors are strongly associated with insulin resistance in nondiabetic subjects. Pioglitazone and adiponectin regulated the expression of scavenger receptor A and lectin-like oxidized LDL, and this may have important clinical implications.
	Nevirapine Increases High-Density Lipoprotein Cholesterol Concentration by Stimulation of Apolipoprotein A-I Production Remco Franssen, Raaj R. Sankatsing, Elly Hassink, Barbara Hutten, Mariette T. Ackermans, Kees Brinkman, René Oesterholt, Alejandro Arenas-Pinto, Stephen P. Storfer, John J. Kastelein, Hans P. Sauerwein, Peter Reiss, and Erik S. Stroes Arterioscler Thromb Vasc Biol. 2009;29:1336-1341; published online before print August 10 2009, doi:10.1161/ATVBAHA.109.192088 Abstract \| Full Text \| PDF \| Data Supplement In this study the nonnucleoside reverse transcriptase inhibitor (NNRTI) nevirapine (NVP) was shown to increase HDLc in treatment-experienced human immunodeficiency virus-1 infected patients by means of increasing the absolute production rate of apoA-I. This observed increase may contribute to the favorable cardiovascular profile associated with NVP.

Spotlight

TOC Spotlight File

Volume 29, Issue 9; September 1, 2009

Key: VB = Vascular Biology AL = Atherosclerosis/Lipoproteins TH = Thrombosis

Integrative Physiology/Experimental Medicine

Imaging and Quantitative Analysis of Atherosclerotic Lesions by CARS-Based Multimodal Nonlinear Optical Microscopy

Lack of Phosphatidylethanolamine N-Methyltransferase Alters Plasma VLDL Phospholipids and Attenuates Atherosclerosis in Mice

Syndecan-1: An Inhibitor of Arterial Smooth Muscle Cell Growth and Intimal Hyperplasia

Cell Biology/Signaling

Interferon-Gamma Induces Prolyl Hydroxylase (PHD)3 Through a STAT1-Dependent Mechanism in Human Endothelial Cells

Activation of NF-B by Palmitate in Endothelial Cells: A Key Role for NADPH Oxidase-Derived Superoxide in Response to TLR4 Activation

Lysophosphatidylcholine Activates a Novel PKD2-Mediated Signaling Pathway That Controls Monocyte Migration

Clinical and Population Studies

Targeted Metabolomic Evaluation of Arginine Methylation and Cardiovascular Risks: Potential Mechanisms Beyond Nitric Oxide Synthase Inhibition

Cadmium Is a Novel and Independent Risk Factor for Early Atherosclerosis Mechanisms and In Vivo Relevance

Is Diabetes Mellitus an Independent Risk Factor for Venous Thromboembolism?: A Population-Based Case-Control Study

National Cholesterol Awareness Month

National Cholesterol Month

Interrelationships Among HDL Metabolism, Aging, and Atherosclerosis

TGF-β1 Limits Plaque Growth, Stabilizes Plaque Structure, and Prevents Aortic Dilation in Apolipoprotein E-Null Mice

Inactivation of the LRP1 Intracellular NPxYxxL Motif in LDLR-Deficient Mice Enhances Postprandial Dyslipidemia and Atherosclerosis

Inhibition of Soluble Epoxide Hydrolase Attenuated Atherosclerosis, Abdominal Aortic Aneurysm Formation, and Dyslipidemia

Inhibition of Platelet-Rich Arterial Thrombus In Vivo: Acute Antithrombotic Effect of Intravenous HMG-CoA Reductase Therapy

Renal Dysfunction Potentiates Foam Cell Formation by Repressing ABCA1

Glucose Metabolism Is Required for Oxidized LDL–Induced Macrophage Survival: Role of PI3K and Bcl-2 Family Proteins

Membrane Cholesterol Is a Biomechanical Regulator of Neutrophil Adhesion

SR-BI Selective Lipid Uptake: Subsequent Metabolism of Acute Phase HDL

Decision Analysis Supports the Paradigm That Indiscriminate Supplementation of Vitamin E Does More Harm than Good

Identification of Genetic Variants Associated With Response to Statin Therapy

A Common Variant in Low-Density Lipoprotein Receptor–Related Protein 6 Gene (LRP6) Is Associated With LDL-Cholesterol

The ATF6-Met[67]Val Substitution Is Associated With Increased Plasma Cholesterol Levels

Association of Scavenger Receptors in Adipose Tissue With Insulin Resistance in Nondiabetic Humans

Nevirapine Increases High-Density Lipoprotein Cholesterol Concentration by Stimulation of Apolipoprotein A-I Production

Spotlight

Activation of NF- ${kappa}$ B by Palmitate in Endothelial Cells: A Key Role for NADPH Oxidase-Derived Superoxide in Response to TLR4 Activation