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Volume 28, Issue 9; September 1, 2008
In Memoriam
Editorials
Brief Reviews
Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Letters to the Editor
Clinical and Population Studies
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In Memoriam
Ross Gerrity, 1945–2008
J.A. Berliner and C.C. Hedrick
Arterioscler Thromb Vasc Biol. 2008;28:e155, doi:10.1161/ATVBAHA.108.174268
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Basil Rifkind
David J. Gordon
Arterioscler Thromb Vasc Biol. 2008;28:e156, doi:10.1161/ATVBAHA.108.174078
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Editorials
VEGF-B Taken to Our Hearts: Specific Effect of VEGF-B in Myocardial Ischemia
Lena Claesson-Welsh
Arterioscler Thromb Vasc Biol. 2008;28:1575-1576, doi:10.1161/ATVBAHA.108.170878
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NO Targets SIRT1: A Novel Signaling Network in Endothelial Senescence
Michael Potente and Stefanie Dimmeler
Arterioscler Thromb Vasc Biol. 2008;28:1577-1579, doi:10.1161/ATVBAHA.108.173682
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Targeted Increases in Endothelial Cell Superoxide Anion Production Stimulate eNOS-Dependent Nitric Oxide Production, Not Uncoupled eNOS Activity
Hao Xu and Kirkwood A. Pritchard, Jr
Arterioscler Thromb Vasc Biol. 2008;28:1580-1581, doi:10.1161/ATVBAHA.108.171801
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Is LDL-C Passed Its Prime?: The Emerging Role of Non-HDL, LDL-P, and ApoB in CHD Risk Assessment
Michael H. Davidson
Arterioscler Thromb Vasc Biol. 2008;28:1582-1583, doi:10.1161/ATVBAHA.108.172718
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Brief Reviews
Assessing Identity, Phenotype, and Fate of Endothelial Progenitor Cells
Karen K. Hirschi, David A. Ingram, and Mervin C. Yoder
Arterioscler Thromb Vasc Biol. 2008;28:1584-1595; published online before print July 31 2008, doi:10.1161/ATVBAHA.107.155960
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Murine Models of Hyperhomocysteinemia and Their Vascular Phenotypes
Sanjana Dayal and Steven R. Lentz
Arterioscler Thromb Vasc Biol. 2008;28:1596-1605; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.166421
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Integrative Physiology/Experimental Medicine
Disruption of Ang-1/Tie-2 Signaling Contributes to the Impaired Myocardial Vascular Maturation and Angiogenesis in Type II Diabetic Mice
Jian-Xiong Chen and Amanda Stinnett
Arterioscler Thromb Vasc Biol. 2008;28:1606-1613; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.169235
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Data Supplement
Reevaluation of the Role of VEGF-B Suggests a Restricted Role in the Revascularization of the Ischemic Myocardium
Xuri Li, Marc Tjwa, Inge Van Hove, Berndt Enholm, Elke Neven, Karri Paavonen, Michael Jeltsch, Toni Diez Juan, Richard E. Sievers, Emmanuel Chorianopoulos, Hiromichi Wada, Maarten Vanwildemeersch, Agnes Noel, Jean-Michel Foidart, Matthew L. Springer, Georges von Degenfeld, Mieke Dewerchin, Helen M. Blau, Kari Alitalo, Ulf Eriksson, Peter Carmeliet, and Lieve Moons
Arterioscler Thromb Vasc Biol. 2008;28:1614-1620; published online before print May 29 2008, doi:10.1161/ATVBAHA.107.158725
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Using loss- and gain-of-function approaches, we studied the role of VEGF-B in various models of pathological angiogenesis. VEGF-B appears to have a relatively restricted role in pathological blood vessel formation in the ischemic heart.
Restoration of Plasma von Willebrand Factor Deficiency Is Sufficient to Correct Thrombus Formation After Gene Therapy for Severe von Willebrand Disease
Simon F. De Meyer, Nele Vandeputte, Inge Pareyn, Inge Petrus, Peter J. Lenting, Marinee K.L. Chuah, Thierry VandenDriessche, Hans Deckmyn, and Karen Vanhoorelbeke
Arterioscler Thromb Vasc Biol. 2008;28:1621-1626; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.168369
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To investigate the feasibility of ectopic vWF expression by targeting the liver, vWF liver gene transfer was established in vWD mice. Multimerized vWF was expressed that could restore proper platelet plug formation in severe vWD, suggesting that the liver is an attractive target for gene therapy for severe vWD.
Paradoxical Activation of Endothelial Nitric Oxide Synthase by NADPH Oxidase
Qian Zhang, Pulkit Malik, Deepesh Pandey, Sonali Gupta, Davin Jagnandan, Eric Belin de Chantemele, Botond Banfi, Mario B. Marrero, R. Daniel Rudic, David W. Stepp, and David J.R. Fulton
Arterioscler Thromb Vasc Biol. 2008;28:1627-1633; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.168278
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Cell Biology/Signaling
Cilostazol Inhibits Oxidative Stress–Induced Premature Senescence Via Upregulation of Sirt1 in Human Endothelial Cells
Hidetaka Ota, Masato Eto, Mitsunobu R. Kano, Sumito Ogawa, Katsuya Iijima, Masahiro Akishita, and Yasuyoshi Ouchi
Arterioscler Thromb Vasc Biol. 2008;28:1634-1639; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.164368
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ECSM2, An Endothelial Specific Filamin A Binding Protein That Mediates Chemotaxis
Laura-Jane Armstrong, Victoria L. Heath, Sharon Sanderson, Sukhbir Kaur, James F.J. Beesley, John M.J. Herbert, John A. Legg, Richard Poulsom, and Roy Bicknell
Arterioscler Thromb Vasc Biol. 2008;28:1640-1646; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.162511
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Expression of a novel endothelial specific gene called ECSM2 has been characterized in vitro and in vivo. ECSM2 is a transmembrane protein with no homology to known proteins that regulates endothelial tube formation and chemotaxis in vitro, and couples to filamin-A.
Low Tissue Inhibitor of Metalloproteinases 3 and High Matrix Metalloproteinase 14 Levels Defines a Subpopulation of Highly Invasive Foam-Cell Macrophages
Jason L. Johnson, Graciela B. Sala-Newby, Yasmin Ismail, Concepción M. Aguilera, and Andrew C. Newby
Arterioscler Thromb Vasc Biol. 2008;28:1647-1653; published online before print June 19 2008, doi:10.1161/ATVBAHA.108.170548
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We report here that a subset of rabbit foam-cell macrophages exhibits reduced TIMP-3/MT1-MMP balance and is highly invasive, proliferative, and prone to undergo apoptosis, characteristics associated with plaque instability. Foam-cell macrophages lacking TIMP-3 and overexpressing MMP-14 were also identified in advanced human plaques, underlying their potential proatherogenic role.
Letters to the Editor
Patterns of USPIO Deposition in Murine Atherosclerosis
G. Klug, L. Bauer, and W.R. Bauer
Arterioscler Thromb Vasc Biol. 2008;28:e157, doi:10.1161/ATVBAHA.108.170506
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Patterns of USPIO Deposition in Murine Atherosclerosis
Joanne B. Morris, Alan R. Olzinski, and Beat M. Jucker
Arterioscler Thromb Vasc Biol. 2008;28:e158-e159, doi:10.1161/ATVBAHA.108.170704
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Clinical and Population Studies
Adipose Macrophage Infiltration Is Associated With Insulin Resistance and Vascular Endothelial Dysfunction in Obese Subjects
Caroline M. Apovian, Sherman Bigornia, Melanie Mott, Melissa R. Meyers, Jagadish Ulloor, Manana Gagua, Marie McDonnell, Donald Hess, Lija Joseph, and Noyan Gokce
Arterioscler Thromb Vasc Biol. 2008;28:1654-1659; published online before print June 19 2008, doi:10.1161/ATVBAHA.108.170316
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Triglyceride-Rich Lipoprotein-Associated Apolipoprotein C-III Production Is Stimulated by Plasma Free Fatty Acids in Humans
Mirjana Pavlic, René Valéro, Hélène Duez, Changting Xiao, Linda Szeto, Bruce W. Patterson, and Gary F. Lewis
Arterioscler Thromb Vasc Biol. 2008;28:1660-1665; published online before print June 12 2008, doi:10.1161/ATVBAHA.108.169383
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The mechanism of the increase in triglyceride-rich lipoprotein (TRL) apoC-III concentration and production in insulin resistant states is not known. We investigated this phenomenon in healthy men using stable isotope enrichment methodology, and demonstrated that TRL apoC-III production is stimulated by an acute elevation of plasma FFAs.
Lipoprotein Particle Concentrations May Explain the Absence of Coronary Protection in the Womens Health Initiative Hormone Trials
Judith Hsia, James D. Otvos, Jacques E. Rossouw, LieLing Wu, Sylvia Wassertheil-Smoller, Susan L. Hendrix, Jennifer G. Robinson, Bernedine Lund, Lewis H. Kuller for the Womens Health Initiative Research Group
Arterioscler Thromb Vasc Biol. 2008;28:1666-1671; published online before print July 3 2008, doi:10.1161/ATVBAHA.108.170431
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In the Women's Health Initiative randomized trials, postmenopausal hormone therapy raised high density lipoprotein-cholesterol and particle concentration and reduced low density lipoprotein-cholesterol (P<0.001 versus placebo). Neither unopposed estrogen nor estrogen with progestin lowered low density lipoprotein particle concentration.
Extended-Release Niacin Alters the Metabolism of Plasma Apolipoprotein (Apo) A-I and ApoB-Containing Lipoproteins
Stefania Lamon-Fava, Margaret R. Diffenderfer, P. Hugh R. Barrett, Aaron Buchsbaum, Mawuli Nyaku, Katalin V. Horvath, Bela F. Asztalos, Seiko Otokozawa, Masumi Ai, Nirupa R. Matthan, Alice H. Lichtenstein, Gregory G. Dolnikowski, and Ernst J. Schaefer
Arterioscler Thromb Vasc Biol. 2008;28:1672-1678; published online before print June 19 2008, doi:10.1161/ATVBAHA.108.164541
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We investigated the effects of niacin (2 g/d), without or with lovastatin (40 mg/d) on apolipoprotein kinetics in 5 subjects. Niacin treatment significantly increased HDL apoA-I concentrations and production, as well as enhanced clearance of TG-rich lipoprotein apoB-100 and apoB-48. The addition of lovastatin to niacin further promoted an enhanced clearance of LDL apoB-100.
Coronary Artery Disease–Associated Locus on Chromosome 9p21 and Early Markers of Atherosclerosis
Nilesh J. Samani, Olli T. Raitakari, Kalle Sipilä, Martin D. Tobin, Heribert Schunkert, Markus Juonala, Peter S. Braund, Jeanette Erdmann, Jorma Viikari, Leena Moilanen, Leena Taittonen, Antti Jula, Eero Jokinen, Tomi Laitinen, Nina Hutri-Kähönen, Markku S. Nieminen, Y. Antero Kesäniemi, Alistair S. Hall, Janne Hulkkonen, Mika Kähönen, and Terho Lehtimäki
Arterioscler Thromb Vasc Biol. 2008;28:1679-1683; published online before print July 3 2008, doi:10.1161/ATVBAHA.108.170332
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We examined the association with carotid intima-media thickness and brachial flow mediated dilatation of the recently identified susceptibility locus for coronary artery disease on chromosome 9p21. We found no evidence that the risk variant affects either of these early markers of atherosclerosis, suggesting an alternate mechanism for its effect on risk of CAD.
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