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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 29, Issue 5; May 1, 2009
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Key:  VB = Vascular Biology  AL = Atherosclerosis/Lipoproteins  TH = Thrombosis
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EditorialsBack

AL gif  Recipients of the 2009 New Investigator Awards

Mark B. Taubman
Arterioscler Thromb Vasc Biol. 2009;29:613-614, doi:10.1161/ATVBAHA.109.187187
Extract | Full Text | PDF Free Article  

AL gif  Weight of Pericardial Fat on Coronaropathy

Karine Clément, Arnaud Basdevant, and Anne Dutour
Arterioscler Thromb Vasc Biol. 2009;29:615-616, doi:10.1161/ATVBAHA.108.182907
Extract | Full Text | PDF Free Article  

TH gif  Kallikrein–Kinin System in Neovascularization

Michael Bader
Arterioscler Thromb Vasc Biol. 2009;29:617-619, doi:10.1161/ATVBAHA.109.184549
Extract | Full Text | PDF Free Article  

TH gif   Statin Islands and PPAR Ligands in Platelets

Richard P. Phipps and Neil Blumberg
Arterioscler Thromb Vasc Biol. 2009;29:620-621, doi:10.1161/ATVBAHA.109.184648
Extract | Full Text | PDF Free Article  

 

Brief ReviewsBack

TH gif  Developmental Biology in the Vasculature—Review Series

Mark W. Majesky
Arterioscler Thromb Vasc Biol. 2009;29:622, doi:10.1161/ATVBAHA.109.187112
Extract | Full Text | PDF  

TH gif  The Opening Act: Vasculogenesis and the Origins of Circulation

Suk-Won Jin and Cam Patterson
Arterioscler Thromb Vasc Biol. 2009;29:623-629; published online before print November 13 2008, doi:10.1161/ATVBAHA.107.161539
Abstract | Full Text | PDF  

TH gif  Endothelial-Mural Cell Signaling in Vascular Development and Angiogenesis

Konstantin Gaengel, Guillem Genové, Annika Armulik, and Christer Betsholtz
Arterioscler Thromb Vasc Biol. 2009;29:630-638; published online before print January 22 2009, doi:10.1161/ATVBAHA.107.161521
Abstract | Full Text | PDF
Mural cells are essential components of blood vessels, and their defective association with the endothelium is associated with several human diseases. Here we summarize the key signaling pathways in mural cell biology with a focus on PDGFB/PDGFRβ, Angiopoietins, and Tie receptors, sphingosine-1-phosphate, TGFβ, and Notch signaling.  

TH gif  Mechanisms of Vessel Branching: Filopodia on Endothelial Tip Cells Lead the Way

Frederik De Smet, Inmaculada Segura, Katrien De Bock, Philipp J. Hohensinner, and Peter Carmeliet
Arterioscler Thromb Vasc Biol. 2009;29:639-649; published online before print March 5 2009, doi:10.1161/ATVBAHA.109.185165
Abstract | Full Text | PDF  

TH gif  G Protein–Coupled Receptors as Potential Drug Targets for Lymphangiogenesis and Lymphatic Vascular Diseases

William P. Dunworth and Kathleen M. Caron
Arterioscler Thromb Vasc Biol. 2009;29:650-656; published online before print March 5 2009, doi:10.1161/ATVBAHA.109.185066
Abstract | Full Text | PDF
Recently, several GPCRs important for lymphatic vascular development and function have been identified. Given our current lack of pharmacological targets for the treatment of lymphatic vascular diseases, the continued identification and study of GPCRs in lymphatics may eventually lead to new pharmacological strategies for the treatment of lymphedema.  

 

Integrative Physiology/Experimental MedicineBack

TH gif  Critical Role of Tissue Kallikrein in Vessel Formation and Maturation: Implications for Therapeutic Revascularization

Oliver A. Stone, Christine Richer, Costanza Emanueli, Vincent van Weel, Paul H.A. Quax, Rajesh Katare, Nicolle Kraenkel, Paola Campagnolo, Luciola S. Barcelos, Mauro Siragusa, Graciela B. Sala-Newby, Danila Baldessari, Marina Mione, Marie P. Vincent, Andrew V. Benest, Ayman Al Haj Zen, Julien Gonzalez, David O. Bates, Francois Alhenc-Gelas, and Paolo Madeddu
Arterioscler Thromb Vasc Biol. 2009;29:657-664; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.182139
Abstract | Full Text | PDF | Data Supplement  

AL gif  HIF-1{alpha} Overexpression and Experimental Murine Atherosclerosis

Jeremy Ben-Shoshan, Arnon Afek, Sofia Maysel-Auslender, Aya Barzelay, Ardon Rubinstein, Gad Keren, and Jacob George
Arterioscler Thromb Vasc Biol. 2009;29:665-670; published online before print February 26 2009, doi:10.1161/ATVBAHA.108.183319
Abstract | Full Text | PDF
We used a HIF-1{alpha} plasmid delivered by hydrodynamic injection to assess the effects on cellular immunity and atherosclerotic plaque size in ApoE-/- mice. HIF-1{alpha} plasmid was expressed predominantly in CD4 cells and shifted their phenotype to the TH2 lineage concomitantly with a significant reduction in atherosclerotic plaque size.  

AL gif  NKT Cell Subsets Mediate Differential Proatherogenic Effects in ApoE–/– Mice

Kelly To, Alex Agrotis, Gurdyal Besra, Alex Bobik, and Ban-Hock Toh
Arterioscler Thromb Vasc Biol. 2009;29:671-677; published online before print February 26 2009, doi:10.1161/ATVBAHA.108.182592
Abstract | Full Text | PDF | Data Supplement
We examined the role of NKT cell subtypes in atherosclerosis. Adoptive transfer of CD4+ but not DN NKT cells into thymectomized NKT cell-deficient ApoE-/- mice augmented development of atherosclerosis. Activation of inhibitory Ly49 receptors, which are less abundant on CD4+ NKT cells, appears responsible for the differential proatherogenic effects.  

AL gif  Novel Strategy Using F1-Congenic Mice for Validation of QTLs: Studies at the Proximal Chromosome 10 Atherosclerosis Susceptibility Locus

Daniel Teupser, Susanne Wolfrum, Marietta Tan, Adam D. Persky, Hayes M. Dansky, and Jan L. Breslow
Arterioscler Thromb Vasc Biol. 2009;29:678-683; published online before print February 26 2009, doi:10.1161/ATVBAHA.108.179408
Abstract | Full Text | PDF | Data Supplement | Data Supplement
A novel method of testing genetic effects with interval-specific congenic strains heterozygous (F1) across the genome that allows for possible major genetic interactions not present on a pure background was used to validate an atherosclerosis susceptibility QTL on proximal Chr10.  

AL gif  Proprotein Convertase Subtilisin Kexin Type 9 Null Mice Are Protected From Postprandial Triglyceridemia

Cédric Le May, Sanae Kourimate, Cédric Langhi, Maud Chétiveaux, Anne Jarry, Christine Comera, Xavier Collet, Folkert Kuipers, Michel Krempf, Bertrand Cariou, and Philippe Costet
Arterioscler Thromb Vasc Biol. 2009;29:684-690; published online before print March 5 2009, doi:10.1161/ATVBAHA.108.181586
Abstract | Full Text | PDF | Data Supplement
This study shows that PCSK9 is expressed throughout the entire small intestine and in human enterocytes. In mice, PCSK9 deficiency dramatically reduces postprandial triglyceridemia. This phenotype can be explained by qualitative modifications of intestinal chylomicron production and an enhanced hepatic catabolism.  

TH gif  PDGF-A, -C, and -D but not PDGF-B Increase TGF-β1 and Chronic Rejection in Rat Cardiac Allografts

Raimo Tuuminen, Antti I. Nykänen, Rainer Krebs, Jarkko Soronen, Katri Pajusola, Mikko A.I. Keränen, Petri K. Koskinen, Kari Alitalo, and Karl B. Lemström
Arterioscler Thromb Vasc Biol. 2009;29:691-698; published online before print February 12 2009, doi:10.1161/ATVBAHA.108.178558
Abstract | Full Text | PDF | Data Supplement
Alloimmune response induces PDGF-A, PDGF-C, and PDGF-D in the graft vasculature, and overexpression of these ligands upregulates TGF-β1 mRNA and enhances cardiac fibrosis and arteriosclerotic changes in cardiac allografts. Our results suggest that inhibition of signaling of all PDGF ligands except that of PDGF-B may be needed to inhibit chronic rejection in cardiac allografts.  

TH gif   Protein Kinase C{delta} Differentially Regulates Platelet Functional Responses

Ramya Chari, Todd Getz, Bela Nagy, Jr, Kamala Bhavaraju, Yingying Mao, Yamini Saraswathy Bynagari, Swaminathan Murugappan, Keiko Nakayama, and Satya P. Kunapuli
Arterioscler Thromb Vasc Biol. 2009;29:699-705; published online before print February 12 2009, doi:10.1161/ATVBAHA.109.184010
Abstract | Full Text | PDF
These studies using pharmacological inhibitors as well as knockout mice show that PKC{delta} differentially regulates PAR- and GPVI-mediated dense granule secretion and TXA2 generation. However, in a murine model of FeCl3-induced carotid artery injury model, lack of PKC{delta} did not affect thrombus formation in vivo  

 

Cell Biology/SignalingBack

TH gif   Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs

Ferhana Y. Ali, Paul C.J. Armstrong, Al-Rehan A. Dhanji, Arthur T. Tucker, Mark J. Paul-Clark, Jane A. Mitchell, and Timothy D. Warner
Arterioscler Thromb Vasc Biol. 2009;29:706-711; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.183160
Abstract | Full Text | PDF
We show statins and fibrates inhibit platelet activation while activating PPAR{alpha} and PPAR{gamma} in vitro and in vivo. Addition of antagonists for these receptors tohuman platelets or deletion of PPAR{alpha} in murine platelets resulted in a reduction of the inhibitory effects of these drugs.  

TH gif   Effects of Aspirin on Clot Structure and Fibrinolysis Using a Novel In Vitro Cellular System

R.A. Ajjan, K.F. Standeven, M. Khanbhai, F. Phoenix, K.C. Gersh, J.W. Weisel, M.T. Kearney, R.A.S. Ariëns, and P.J. Grant
Arterioscler Thromb Vasc Biol. 2009;29:712-717; published online before print March 12 2009, doi:10.1161/ATVBAHA.109.183707
Abstract | Full Text | PDF | Data Supplement
We investigated the direct effects of aspirin on fibrin clot structure and fibrinolysis both in vitro and ex vivo. We showed that aspirin mainly acetylates the alpha chain of fibrinogen, resulting in the formation of clots with thicker fibers, larger pores, and reduced rigidity, which are easier to lyse.  

TH gif  Signaling Hierarchy Regulating Human Endothelial Cell Development

Melissa A. Kelly and Karen K. Hirschi
Arterioscler Thromb Vasc Biol. 2009;29:718-724; published online before print February 12 2009, doi:10.1161/ATVBAHA.109.184200
Abstract | Full Text | PDF | Data Supplement
The signaling hierarchy that regulates human endothelial cell differentiation is currently unknown. Our studies revealed that Ihh promoted endothelial cell differentiation from pluripotent human embryonic stem cells via BMP signaling, providing novel insights applicable to modulating human endothelial cell formation and vascular regeneration for human clinical therapies.  

AL gif  Human IL-8 Regulates Smooth Muscle Cell VCAM-1 Expression in Response to Endothelial Cells Exposed to Atheroprone Flow

Nicole E. Hastings, Ryan E. Feaver, Monica Y. Lee, Brian R. Wamhoff, and Brett R. Blackman
Arterioscler Thromb Vasc Biol. 2009;29:725-731; published online before print February 19 2009, doi:10.1161/ATVBAHA.109.184382
Abstract | Full Text | PDF | Data Supplement
The human chemokine interleukin-8 (IL-8) is implicated in atherosclerosis development. Contrary to our hypothesis that IL-8 has proinflammatory effects on the vasculature, we show herein that IL-8 limits SMC VCAM-1 expression in response to inflammatory stimuli by reducing activation of p38 and NF-{kappa}B, and thereby decreasing VCAM-1 expression and suppressing monocyte adhesion.  

TH gif  Prolonged Exposure to LPS Increases Iron, Heme, and p22phox Levels and NADPH Oxidase Activity in Human Aortic Endothelial Cells: Inhibition by Desferrioxamine

Lixin Li and Balz Frei
Arterioscler Thromb Vasc Biol. 2009;29:732-738; published online before print February 26 2009, doi:10.1161/ATVBAHA.108.183210
Abstract | Full Text | PDF
This study indicates that LPS increases NADPH oxidase activity in endothelial cells by increasing cellular levels of iron, heme, and p22phox, a heme-containing, catalytic subunit of the enzyme. All of these effects of LPS were inhibited by the iron chelator, desferrioxamine. Removing excess iron may help attenuate vascular oxidative stress and inflammation in atherosclerosis.  

TH gif  Bradykinin-Induced Dilation of Human Coronary Arterioles Requires NADPH Oxidase–Derived Reactive Oxygen Species

Brandon T. Larsen, Aaron H. Bubolz, Suelhem A. Mendoza, Kirkwood A. Pritchard, Jr, and David D. Gutterman
Arterioscler Thromb Vasc Biol. 2009;29:739-745; published online before print February 12 2009, doi:10.1161/ATVBAHA.108.169367
Abstract | Full Text | PDF | Data Supplement
H2O2 mediates bradykinin-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids in human coronary arterioles, but the source of H2O2 was previously unknown. We identified NADPH oxidase as a functionally relevant source of H2O2 in this vascular bed. This enzyme complex may therefore modulate human coronary vascular resistance and myocardial perfusion.  

TH gif  CD146 and its Soluble Form Regulate Monocyte Transendothelial Migration

Nathalie Bardin, Marcel Blot-Chabaud, Nicolas Despoix, Abdeldjalil Kebir, Karim Harhouri, Jean-Pierre Arsanto, Leon Espinosa, Pierre Perrin, Stéphane Robert, Frédéric Vely, Florence Sabatier, André Le Bivic, Gilles Kaplanski, José Sampol, and Françoise Dignat-George
Arterioscler Thromb Vasc Biol. 2009;29:746-753; published online before print February 19 2009, doi:10.1161/ATVBAHA.108.183251
Abstract | Full Text | PDF | Data Supplement  

TH gif  Signals Through Glycoprotein 130 Regulate the Endothelial Differentiation of Cardiac Stem Cells

Tomomi Mohri, Yasushi Fujio, Masanori Obana, Tomohiko Iwakura, Koichi Matsuda, Makiko Maeda, and Junichi Azuma
Arterioscler Thromb Vasc Biol. 2009;29:754-760; published online before print February 12 2009, doi:10.1161/ATVBAHA.108.174870
Abstract | Full Text | PDF | Data Supplement
We investigated the molecular mechanisms of cardiac stem cell differentiation. The activation of gp130 by IL-6 family cytokines results in the commitment of Sca-1+ cells to endothelial cell lineage, proposing a novel mechanism for neovascularization. These findings may provide insights into development of regeneration therapies targeting cardiac Sca-1+ cells.  

TH gif  Phosphonoformic Acid Prevents Vascular Smooth Muscle Cell Calcification by Inhibiting Calcium-Phosphate Deposition

Ricardo Villa-Bellosta and Víctor Sorribas
Arterioscler Thromb Vasc Biol. 2009;29:761-766; published online before print February 12 2009, doi:10.1161/ATVBAHA.108.183384
Abstract | Full Text | PDF | Data Supplement
Phosphonoformate prevents calcification in vascular smooth muscle cells but does not inhibit Pi transport. Cytotoxicity and phosphodiesterase inhibition by phosphonoformate have also been discarded. Phosphonoformate prevents calcification in fixed cells, which suggests that the mechanism is independent of any cellular activity. We conclude that phosphonoformate acts as a pyrophosphate analogue.  

AL gif  TIP47, a Lipid Cargo Protein Involved in Macrophage Triglyceride Metabolism

Insa Buers, Horst Robenek, Stefan Lorkowski, Yvonne Nitschke, Nicholas J. Severs, and Oliver Hofnagel
Arterioscler Thromb Vasc Biol. 2009;29:767-773; published online before print March 12 2009, doi:10.1161/ATVBAHA.108.182675
Abstract | Full Text | PDF | Data Supplement
The function of TIP47 on M{Phi} lipid metabolism was investigated. TIP47 protein levels were found to directly correlate with triglyceride levels. From this and other experimental evidence, we propose that TIP47 acts as a carrier protein for free fatty acids and thereby participates in conversion of M{Phi} into foam cells.  

 

Clinical and Population StudiesBack

AL gif  Large Scale Association Analysis of Novel Genetic Loci for Coronary Artery Disease

Coronary Artery Disease Consortium
Arterioscler Thromb Vasc Biol. 2009;29:774-780; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.181388
Abstract | Full Text | PDF | Data Supplement  

AL gif  Pericardial Adipose Tissue Determined by Dual Source CT Is a Risk Factor for Coronary Atherosclerosis

Martin Greif, Alexander Becker, Franz von Ziegler, Corinna Lebherz, Michael Lehrke, Uli C. Broedl, Janine Tittus, Klaus Parhofer, Christoph Becker, Maximilian Reiser, Andreas Knez, and Alexander W. Leber
Arterioscler Thromb Vasc Biol. 2009;29:781-786; published online before print February 19 2009, doi:10.1161/ATVBAHA.108.180653
Abstract | Full Text | PDF | Data Supplement
The amount of PAT volume is significantly elevated in patients with coronary atherosclerosis compared to those without. We could demonstrate that PAT volumes >300 cm3 represent the strongest risk factor for the presence of coronary atherosclerosis in comparison with traditional risk factors.  

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