Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (24 [6])

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Volume 24, Issue 6; June 1, 2004

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

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	Editorials
	Fifty (or More) Ways to Leave Your Platelets (in a Thrombus) Lawrence Brass Arterioscler Thromb Vasc Biol. 2004;24:989-991, doi:10.1161/01.ATV.0000131781.98156.da Extract \| Full Text \| PDF
	Proatherogenic Role for NK Cells Revealed MacRae F. Linton, Amy S. Major, and Sergio Fazio Arterioscler Thromb Vasc Biol. 2004;24:992-994, doi:10.1161/01.ATV.0000128896.45976.f0 Extract \| Full Text \| PDF
	Of Mice, Men, and Hormones Virginia M. Miller, Donald J. Tindall, and Peter Y. Liu Arterioscler Thromb Vasc Biol. 2004;24:995-997, doi:10.1161/01.ATV.0000130660.53541.a4 Extract \| Full Text \| PDF
	Brief Reviews
	Dysfunction of Endothelial Nitric Oxide Synthase and Atherosclerosis Seinosuke Kawashima and Mitsuhiro Yokoyama Arterioscler Thromb Vasc Biol. 2004;24:998-1005; published online before print March 4 2004, doi:10.1161/01.ATV.0000125114.88079.96 Abstract \| Full Text \| PDF In hyperlipidemia and atherosclerosis, eNOS may become dysfunctional because of a lack or deficiency of tissue levels of tetrahydrobiopterin and produces superoxide rather than NO, which leads to the impaired endothelial function. The role of dysfunctional eNOS in atherogenesis is an important issue to be clarified.
	Atherosclerosis in the Apolipoprotein E–Deficient Mouse: A Decade of Progress Karen S. Meir and Eran Leitersdorf Arterioscler Thromb Vasc Biol. 2004;24:1006-1014; published online before print April 15 2004, doi:10.1161/01.ATV.0000128849.12617.f4 Abstract \| Full Text \| PDF The apolipoprotein E-deficient (apoE-/-) mouse is currently the most popular murine model used for atherosclerotic studies. This review outlines the uses and limitations of, and plaque pathology in this mouse, and highlights some of the more recent work on nutritional, pharmacological, and most significantly, genetic factors affecting atherogenesis in this versatile model.
	Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development Nigel Mackman Arterioscler Thromb Vasc Biol. 2004;24:1015-1022; published online before print April 29 2004, doi:10.1161/01.ATV.0000130465.23430.74 Abstract \| Full Text \| PDF Tissue factor (TF) expression by nonvascular cells plays an essential role in hemostasis by activating blood coagulation. In contrast, TF expression by vascular cells induces intravascular thrombosis. Finally, TF-dependent assembly of coagulation proteases on vascular cells activates protease activated receptors, which contributes to inflammation, angiogenesis, and metastasis.
	Cardiovascular Biology of the Asymmetric Dimethylarginine:Dimethylarginine Dimethylaminohydrolase Pathway Patrick Vallance and James Leiper Arterioscler Thromb Vasc Biol. 2004;24:1023-1030; published online before print April 22 2004, doi:10.1161/01.ATV.0000128897.54893.26 Abstract \| Full Text \| PDF An increasing number of reports indicate that endogenously produced inhibitors of nitric oxide synthase, particularly asymmetric dimethylarginine (ADMA), regulate nitric oxide generation in disease states. This article describes the biology of ADMA and the implications for cardiovascular physiology and pathophysiology.
	Vascular Biology
	Stable Compounds of Cigarette Smoke Induce Endothelial Superoxide Anion Production via NADPH Oxidase Activation Edgar A. Jaimes, Eugene G. DeMaster, Run-Xia Tian, and Leopoldo Raij Arterioscler Thromb Vasc Biol. 2004;24:1031-1036; published online before print April 1 2004, doi:10.1161/01.ATV.0000127083.88549.58 Abstract \| Full Text \| PDF Exposure of pulmonary artery endothelial cells and pulmonary arteries to CSEs increased O2 production that was prevented by NADPH oxidase inhibition. Exposure to acrolein, a thiol-reactive agent found in CS, also increased endothelial O2 production. We conclude that stable thiol-reactive compounds in CS activate endothelial NADPH oxidase.
	Lipoprotein-Associated Phosphatidylethanol Increases the Plasma Concentration of Vascular Endothelial Growth Factor Marja K. Liisanantti, Minna L. Hannuksela, Maria E. Rämet, and Markku J. Savolainen Arterioscler Thromb Vasc Biol. 2004;24:1037-1042; published online before print April 15 2004, doi:10.1161/01.ATV.0000128409.62292.d6 Abstract \| Full Text \| PDF \| Data Supplement The present study shows that phosphatidylethanol in HDL particles can regulate vascular endothelial growth factor in endothelial cells by increasing the phosphorylation of mitogen-activated protein kinase and protein kinase C. This may contribute to the beneficial effects of alcohol on atherosclerosis.
	Bradykinin Contributes to the Systemic Hemodynamic Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure Nicholas L.M. Cruden, Fraser N. Witherow, David J. Webb, Keith A.A. Fox, and David E. Newby Arterioscler Thromb Vasc Biol. 2004;24:1043-1048; published online before print April 22 2004, doi:10.1161/01.ATV.0000129331.21092.1d Abstract \| Full Text \| PDF In an invasive hemodynamic study of patients with heart failure, bradykinin antagonism caused changes in systemic hemodynamic variables when treated with enalapril. These findings suggest that bradykinin contributes to the systemic hemodynamic effects of ACE inhibition and may explain the apparent clinical differences between ACE inhibitors and angiotensin receptor blockers.
	Atherosclerosis and Lipoproteins
	Depletion of Natural Killer Cell Function Decreases Atherosclerosis in Low-Density Lipoprotein Receptor Null Mice Stewart C. Whitman, Debra L. Rateri, Stephen J. Szilvassy, Wayne Yokoyama, and Alan Daugherty Arterioscler Thromb Vasc Biol. 2004;24:1049-1054; published online before print February 26 2004, doi:10.1161/01.ATV.0000124923.95545.2c Abstract \| Full Text \| PDF Natural killer (NK) cells are found in atherosclerotic lesions, yet their role in the disease process is unknown. Using bone marrow transplantation, we created atherosclerosis-susceptible mice that were deficient in functional NK cells. NK cell deficiency did not affect serum cholesterol values but did significantly reduce (70%) atherosclerotic lesion formation.
	Susceptibility to Early Atherosclerosis in Male Mice Is Mediated by Estrogen Receptor ${alpha}$ Amparo Villablanca, Dennis Lubahn, Lauren Shelby, Kent Lloyd, and Stephen Barthold Arterioscler Thromb Vasc Biol. 2004;24:1055-1061; published online before print April 29 2004, doi:10.1161/01.ATV.0000130467.65290.d4 Abstract \| Full Text \| PDF \| Data Supplement The role of ERs ER{alpha} and ERß in early atherosclerosis remains poorly understood in males. We developed and characterized an atherosclerosis model in ER{alpha} knockout male mice to investigate directly its role in atheroma. In males, the ER{alpha} mediates susceptibility to early atherosclerosis by a testosterone-dependent pathway.
	Lack of Complement Factor C3, but Not Factor B, Increases Hyperlipidemia and Atherosclerosis in Apolipoprotein E–/– Low-Density Lipoprotein Receptor–/– Mice Linda Persson, Jan Borén, Anna-Karin L. Robertson, Ville Wallenius, Göran K. Hansson, and Marcela Pekna Arterioscler Thromb Vasc Biol. 2004;24:1062-1067; published online before print April 1 2004, doi:10.1161/01.ATV.0000127302.24266.40 Abstract \| Full Text \| PDF \| Data Supplement Deficiency in C3, but not in factor B, leads to more extensive atherosclerotic lesions, increased hyperlipidemia, and reduced body fat in Apoe-/- LDLR-/- mice. Complement activation by the classical or lectin pathway exerts atheroprotective effects, possibly through the regulation of lipid metabolism.
	Lack of Interleukin-1 Receptor Antagonist Modulates Plaque Composition in Apolipoprotein E–Deficient Mice Kikuo Isoda, Shojiro Sawada, Norio Ishigami, Taizo Matsuki, Koji Miyazaki, Masatoshi Kusuhara, Yoichiro Iwakura, and Fumitaka Ohsuzu Arterioscler Thromb Vasc Biol. 2004;24:1068-1073; published online before print April 1 2004, doi:10.1161/01.ATV.0000127025.48140.a3 Abstract \| Full Text \| PDF \| Data Supplement We investigated the contribution of interleukin-1 receptor antagonist (IL-1Ra) to atherosclerosis by comparing apolipoprotein E single knockout (IL-1Ra+/+/apoE-/-) with IL-1Ra+/-/apoE-/- mice. Immunostaining at age 32 weeks old showed an 86% increase in the MOMA-2-stained lesion area of IL-1Ra+/-/apoE-/-, whereas {alpha}-actin staining was significantly diminished compared with IL-1Ra+/+/apoE-/- mice.
	Vascular Endothelial Growth Factor Gene Transfer Inhibits Neointimal Macrophage Accumulation in Hypercholesterolemic Rabbits Rohit Khurana, Shahida Shafi, John Martin, and Ian Zachary Arterioscler Thromb Vasc Biol. 2004;24:1074-1080; published online before print April 8 2004, doi:10.1161/01.ATV.0000128127.57688.e0 Abstract \| Full Text \| PDF Periadventitial VEGF gene delivery inhibits intimal thickening, macrophage accumulation, and endothelial VCAM-1 expression induced by collar placement around the carotid artery in hypercholesterolemic rabbits. These findings indicate that VEGF can exert a local arterioprotective effect in the presence of high blood cholesterol.
	Inhibition of Accelerated Graft Arteriosclerosis by Gene Transfer of Soluble Fibroblast Growth Factor Receptor-1 in Rat Aortic Transplants Wensheng Luo, Ailian Liu, Yong Chen, Hyung M. Lim, Jennifer Marshall-Neff, James H. Black, William Baldwin, III, Ralph H. Hruban, Susan C. Stevenson, Peter Mouton, Alan Dardik, and Barbara J. Ballermann Arterioscler Thromb Vasc Biol. 2004;24:1081-1086; published online before print April 8 2004, doi:10.1161/01.ATV.0000128201.65443.ea Abstract \| Full Text \| PDF \| Data Supplement We explored whether local gene transfer of soluble FGF receptor 1 can blunt the development of accelerated graft arteriosclerosis in rat aortic transplants. After adenoviral gene transfer, sFGFR-1 protein was expressed in endothelium and adventitia. Neointima formation was inhibited in aortic allografts transduced with sFGFR-1, but not Null virus.
	Physical Fitness and Reverse Cholesterol Transport Beata Olchawa, Bronwyn A. Kingwell, Anh Hoang, Laurence Schneider, Osamu Miyazaki, Paul Nestel, and Dmitri Sviridov Arterioscler Thromb Vasc Biol. 2004;24:1087-1091; published online before print April 8 2004, doi:10.1161/01.ATV.0000128124.72935.0f Abstract \| Full Text \| PDF Parameters of reverse cholesterol transport in athletes were compared with controls. Plasma concentrations of high-density lipoprotein (HDL), apolipoprotein A-I, preß1-HDL, lecithin:cholesterol acyltransferase and capacity of plasma to promote cholesterol efflux were higher in athletes. We conclude that the likely reason for higher HDL concentration in physically fit people is increased formation of HDL.
	Dietary Hydrogenated Fat Increases High-Density Lipoprotein apoA-I Catabolism and Decreases Low-Density Lipoprotein apoB-100 Catabolism in Hypercholesterolemic Women Nirupa R. Matthan, Francine K. Welty, P. Hugh R. Barrett, Carrie Harausz, Gregory G. Dolnikowski, John S. Parks, Robert H. Eckel, Ernst J. Schaefer, and Alice H. Lichtenstein Arterioscler Thromb Vasc Biol. 2004;24:1092-1097; published online before print April 15 2004, doi:10.1161/01.ATV.0000128410.23161.be Abstract \| Full Text \| PDF \| Data Supplement Hydrogenated fat intake decreases HDL-C and increases LDL-C concentrations. To determine mechanism, apoprotein kinetic studies were conducted in 8 women after consumption of an unsaturated, hydrogenated, or saturated diet. Hydrogenated fat intake resulted in higher HDL-apoA-I and lower LDL-apoB-100 catabolism, which were negatively correlated with HDL-C and LDL-C concentrations, respectively.
	Bronchial Hyperresponsiveness to Methacholine Is Associated With Increased Common Carotid Intima-Media Thickness in Men Mahmoud Zureik, Sabine Kony, Catherine Neukirch, Dominique Courbon, Bénédicte Leynaert, Daniel Vervloet, Pierre Ducimetière, and Françoise Neukirch Arterioscler Thromb Vasc Biol. 2004;24:1098-1103; published online before print April 8 2004, doi:10.1161/01.ATV.0000128128.65312.05 Abstract \| Full Text \| PDF Respiratory alterations have been associated with subsequent coronary heart diseases in numerous population-based studies. The results of the present study suggest that bronchial hyperresponsiveness (which reflects local inflammation in the bronchus) is independently associated with common carotid intima-media thickness in men free of cardiovascular diseases. The interrelationships between cardiovascular and respiratory alterations should be further investigated.
	Circulating Tissue Kallikrein Levels Correlate With Severity of Carotid Atherosclerosis Paolo Porcu, Costanza Emanueli, Elisa Desortes, Giovanni M. Marongiu, Franco Piredda, Lee Chao, Julie Chao, and Paolo Madeddu Arterioscler Thromb Vasc Biol. 2004;24:1104-1110; published online before print April 8 2004, doi:10.1161/01.ATV.0000128126.57688.a9 Abstract \| Full Text \| PDF \| Data Supplement A case-control study was conducted to determine possible association between biomarkers of angiogenesis or inflammation and characteristics of carotid stenosis. No association was found between circulating VEGF, bFGF, or hs-CRP and obstruction grading. Circulating tissue kallikrein increasingly augmented across categories of stenosis severity and upregulation was reversed by revascularization.
	Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis Chiang-Ting Chien, Wei-Tien Chang, Heui-Wen Chen, Tzung-Dau Wang, Shaw-Yih Liou, Tzay-Jinn Chen, Yen-Lin Chang, Yuan-Teh Lee, and Su-Ming Hsu Arterioscler Thromb Vasc Biol. 2004;24:1111-1117; published online before print April 8 2004, doi:10.1161/01.ATV.0000127620.12310.89 Abstract \| Full Text \| PDF Apheresis with ascorbate treatment provides a therapeutic potential in reducing atherosclerotic risk via inhibition of H2O2-induced oxidative stress in dyslipidemic patients with uremia or hyperlipidemia.
	Thrombosis
	Mer Receptor Tyrosine Kinase Signaling Participates in Platelet Function Cailin Chen, Quan Li, Andrew L. Darrow, Yuanping Wang, Claudia K. Derian, Jing Yang, Lawrence de Garavilla, Patricia Andrade-Gordon, and Bruce P. Damiano Arterioscler Thromb Vasc Biol. 2004;24:1118-1123; published online before print May 6 2004, doi:10.1161/01.ATV.0000130662.30537.08 Abstract \| Full Text \| PDF Mer is a receptor tyrosine kinase expressed in platelets. Mice made deficient in mer had decreased platelet aggregation in vitro and less platelet-dependent thrombosis in vivo. Our data provide the first evidence that mer, presumably through activation by its ligand Gas6, participates in regulation of platelet function.
	Critical Role of Platelet P-Selectin in the Response to Arterial Injury in Apolipoprotein-E–Deficient Mice David Manka, S. Bradley Forlow, John M. Sanders, Debra Hurwitz, Daniel K. Bennett, Samuel A. Green, Klaus Ley, and Ian J. Sarembock Arterioscler Thromb Vasc Biol. 2004;24:1124-1129; published online before print April 8 2004, doi:10.1161/01.ATV.0000127619.04687.f4 Abstract \| Full Text \| PDF \| Data Supplement Lack of platelet P-selectin reduced neointima formation and macrophage infiltration by 62% and 30%, respectively, versus control, and protected against the development of plaque neovascularization in wire-injured carotid arteries of apoE-deficient mice. This indicates that platelet P-selectin plays a critical role in inflammation after vascular injury.
	Deep Vein Thrombosis Resolution Is Modulated by Monocyte CXCR2-Mediated Activity in a Mouse Model Peter K. Henke, Andrea Varga, Sumit De, C. Barry Deatrick, Jonathon Eliason, Douglas A. Arenberg, Pasu Sukheepod, Porama Thanaporn, Steven L. Kunkel, Gilbert R. Upchurch, Jr, and Thomas W. Wakefield Arterioscler Thromb Vasc Biol. 2004;24:1130-1137; published online before print April 22 2004, doi:10.1161/01.ATV.0000129537.72553.73 Abstract \| Full Text \| PDF The role of CXCR2 activity on DVT resolution was determined. Thrombi in CXCR2-/- or anti-CXCR2-treated mice had fewer PMN and monocytes and impaired early DVT resolution. PMN depletion did not affect DVT resolution to the same degree, suggesting monocytic CXCR2-mediated activity is more important for DVT resolution.
	Factor XI–Dependent Reciprocal Thrombin Generation Consolidates Blood Coagulation when Tissue Factor Is Not Available Simone J.H. Wielders, Suzette Béguin, H. Coenraad Hemker, and Theo Lindhout Arterioscler Thromb Vasc Biol. 2004;24:1138-1142; published online before print April 8 2004, doi:10.1161/01.ATV.0000128125.80559.9c Abstract \| Full Text \| PDF Our study demonstrates that thrombin initiates thrombin generation in platelet-rich plasma. Factor XI is fundamental in supporting this process that is restricted to the surface of activated platelets, implying that feedback activation of factor XI by thrombin or indirectly by factor VIIa is important in maintaining normal hemostasis as well as in mediating thrombus formation.
	Letters to the Editor
	TGF-ß in Atherosclerosis Göran K. Hansson, Anna-Karin L. Robertson, and David J. Grainger Arterioscler Thromb Vasc Biol. 2004;24:e137-e138, doi:10.1161/01.ATV.0000130728.38755.09 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 24, Issue 6; June 1, 2004

Editorials

Fifty (or More) Ways to Leave Your Platelets (in a Thrombus)

Proatherogenic Role for NK Cells Revealed

Of Mice, Men, and Hormones

Brief Reviews

Dysfunction of Endothelial Nitric Oxide Synthase and Atherosclerosis

Atherosclerosis in the Apolipoprotein E–Deficient Mouse: A Decade of Progress

Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development

Cardiovascular Biology of the Asymmetric Dimethylarginine:Dimethylarginine Dimethylaminohydrolase Pathway

Vascular Biology

Stable Compounds of Cigarette Smoke Induce Endothelial Superoxide Anion Production via NADPH Oxidase Activation

Lipoprotein-Associated Phosphatidylethanol Increases the Plasma Concentration of Vascular Endothelial Growth Factor

Bradykinin Contributes to the Systemic Hemodynamic Effects of Chronic Angiotensin-Converting Enzyme Inhibition in Patients With Heart Failure

Atherosclerosis and Lipoproteins

Depletion of Natural Killer Cell Function Decreases Atherosclerosis in Low-Density Lipoprotein Receptor Null Mice

Susceptibility to Early Atherosclerosis in Male Mice Is Mediated by Estrogen Receptor

Lack of Complement Factor C3, but Not Factor B, Increases Hyperlipidemia and Atherosclerosis in Apolipoprotein E–/– Low-Density Lipoprotein Receptor–/– Mice

Lack of Interleukin-1 Receptor Antagonist Modulates Plaque Composition in Apolipoprotein E–Deficient Mice

Vascular Endothelial Growth Factor Gene Transfer Inhibits Neointimal Macrophage Accumulation in Hypercholesterolemic Rabbits

Inhibition of Accelerated Graft Arteriosclerosis by Gene Transfer of Soluble Fibroblast Growth Factor Receptor-1 in Rat Aortic Transplants

Physical Fitness and Reverse Cholesterol Transport

Dietary Hydrogenated Fat Increases High-Density Lipoprotein apoA-I Catabolism and Decreases Low-Density Lipoprotein apoB-100 Catabolism in Hypercholesterolemic Women

Bronchial Hyperresponsiveness to Methacholine Is Associated With Increased Common Carotid Intima-Media Thickness in Men

Circulating Tissue Kallikrein Levels Correlate With Severity of Carotid Atherosclerosis

Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

Thrombosis

Mer Receptor Tyrosine Kinase Signaling Participates in Platelet Function

Critical Role of Platelet P-Selectin in the Response to Arterial Injury in Apolipoprotein-E–Deficient Mice

Deep Vein Thrombosis Resolution Is Modulated by Monocyte CXCR2-Mediated Activity in a Mouse Model

Factor XI–Dependent Reciprocal Thrombin Generation Consolidates Blood Coagulation when Tissue Factor Is Not Available

Letters to the Editor

TGF-ß in Atherosclerosis

Spotlight

Susceptibility to Early Atherosclerosis in Male Mice Is Mediated by Estrogen Receptor ${alpha}$