Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (27 [5])

About This Cover

Volume 27, Issue 5; May 1, 2007

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

To see an article, click its "Full Text" or "PDF" link. To review many abstracts, check the boxes to the left of the titles you want, and click the "Get All Checked Abstract(s)" button. To see one abstract at a time, click its "Abstract" link.

button_lock_image article is free immediately upon publication

	Announcement
	Recipients of the 2007 New Investigator Awards Arterioscler Thromb Vasc Biol. 2007;27:981, doi:10.1161/ATVBAHA.107.143495 Extract \| Full Text \| PDF
	Editorials
	Summary of the American Heart Association’s Scientific Statement on Drug Therapy of High-Risk Lipid Abnormalities in Children and Adolescents Brian W. McCrindle for the Writing Group Arterioscler Thromb Vasc Biol. 2007;27:982-985, doi:10.1161/ATVBAHA.107.143644 Extract \| Full Text \| PDF
	Is Pathologic Intimal Thickening the Key to Understanding Early Plaque Progression in Human Atherosclerotic Disease? Frank D. Kolodgie, Allen P. Burke, Gaku Nakazawa, and Renu Virmani Arterioscler Thromb Vasc Biol. 2007;27:986-989, doi:10.1161/ATVBAHA.0000258865.44774.41 Extract \| Full Text \| PDF
	Inflammatory Blues Turns Velvet Skin Into Rawhide: Monocyte Rolling on Modified Endothelial PSGL-1 Rory R. Koenen, Philipp von Hundelshausen, and Christian Weber Arterioscler Thromb Vasc Biol. 2007;27:990-992, doi:10.1161/ATVBAHA.107.141689 Extract \| Full Text \| PDF
	Choking off Plaque Neovascularity: A Promising Atheroprotective Strategy or A Double-Edged Sword? Kuang-Yuh Chyu and Prediman K. Shah Arterioscler Thromb Vasc Biol. 2007;27:993-995, doi:10.1161/ATVBAHA.0000265524.41376.e7 Extract \| Full Text \| PDF
	Brief Reviews
	Adipose Tissue and Atherosclerosis: Exploring the Connection Giamila Fantuzzi and Theodore Mazzone Arterioscler Thromb Vasc Biol. 2007;27:996-1003; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.131755 Abstract \| Full Text \| PDF The increasing prevalence of obesity in the United States will have a direct impact on atherosclerosis and subsequent rates of cardiovascular disease. This article considers potential mechanisms for the adverse effect of excess adipose tissue on the vessel wall, the importance of different adipose tissue depots, and the evidence that reduction of adipose tissue can reverse atherosclerosis risk.
	Physiological Roles of Vascular Nucleoside Transporters Michaela Löffler, Julio C. Morote-Garcia, Shelley A. Eltzschig, Imogen R. Coe, and Holger K. Eltzschig Arterioscler Thromb Vasc Biol. 2007;27:1004-1013; published online before print March 1 2007, doi:10.1161/ATVBAHA.106.126714 Abstract \| Full Text \| PDF Changes in vascular NT expression or function result in changes of extracellular nucleoside levels, thereby directly modulating vascular adenosine signaling. Therefore, vascular NT functions are involved in multiple innate adaptive pathways of the vasculature including modulation of barrier function, acute inflammation, vascular tone, ischemic preconditioning, or platelet aggregation.
	cAMP Signaling in Leukocyte Transendothelial Migration Magdalena J. Lorenowicz, Mar Fernandez-Borja, and Peter L. Hordijk Arterioscler Thromb Vasc Biol. 2007;27:1014-1022; published online before print March 8 2007, doi:10.1161/ATVBAHA.106.132282 Abstract \| Full Text \| PDF In this review we discuss the role of cAMP in the control of leukocyte transendothelial migration. Focusing on two major targets of cAMP, protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac), we provide an overview of the current knowledge on the regulation of leukocyte transendothelial migration by cAMP-driven signaling in both leukocytes and endothelium.
	Vascular Biology
	P-Selectin Glycoprotein Ligand-1 Is Expressed on Endothelial Cells and Mediates Monocyte Adhesion to Activated Endothelium Paula da Costa Martins, Juan-Jesús García-Vallejo, Johannes V. van Thienen, Mar Fernandez-Borja, Janine M. van Gils, Cora Beckers, Anton J. Horrevoets, Peter L. Hordijk, and Jaap-Jan Zwaginga Arterioscler Thromb Vasc Biol. 2007;27:1023-1029; published online before print February 22 2007, doi:10.1161/ATVBAHA.107.140442 Abstract \| Full Text \| PDF \| Data Supplement We describe here the presence of PSGL-1 on human endothelial cells, both in vitro and in vivo (arteriosclerotic coronary lesions). Only activated endothelial cells showed functional PSGL-1, suggesting a role for this molecule in the arrest of monocytes during inflammation.
	Characterization of Phosphate Transport in Rat Vascular Smooth Muscle Cells: Implications for Vascular Calcification Ricardo Villa-Bellosta, Yolanda E. Bogaert, Moshe Levi, and Víctor Sorribas Arterioscler Thromb Vasc Biol. 2007;27:1030-1036; published online before print February 22 2007, doi:10.1161/ATVBAHA.106.132266 Abstract \| Full Text \| PDF \| Data Supplement
	Smooth Muscle–Targeted Knockout of Connexin43 Enhances Neointimal Formation in Response to Vascular Injury Yongbo Liao, Christopher P. Regan, Ichiro Manabe, Gary K. Owens, Kathy H. Day, Dave N. Damon, and Brian R. Duling Arterioscler Thromb Vasc Biol. 2007;27:1037-1042; published online before print March 1 2007, doi:10.1161/ATVBAHA.106.137182 Abstract \| Full Text \| PDF \| Data Supplement Injury to carotid arteries in which Cx43 had been deleted from the vascular smooth muscle produced markedly greater neointimal and adventitial growth than seen in control animals. Thus, smooth muscle Cx43 gap junctions may play a key role in modulating the growth response of vascular smooth muscle cells to vascular injury.
	Simvastatin Reduces MMP1 Expression in Human Smooth Muscle Cells Cultured on Polymerized Collagen by Inhibiting Rac1 Activation Nicola Ferri, Giulia Colombo, Corrado Ferrandi, Elaine W. Raines, Bodo Levkau, and Alberto Corsini Arterioscler Thromb Vasc Biol. 2007;27:1043-1049; published online before print February 15 2007, doi:10.1161/ATVBAHA.107.139881 Abstract \| Full Text \| PDF \| Data Supplement Interaction of smooth muscle cells with polymerized collagen induces MMP1 expression. Here, we show that simvastatin inhibits MMP1 promoter activity, reduces MMP1 mRNA and protein levels and, finally, collagen degradation. These effects were also observed after the expression of either Rac1 dominant-negative or knockdown Rac1, a molecular target of simvastatin.
	A Secreted Soluble Form of LR11, Specifically Expressed in Intimal Smooth Muscle Cells, Accelerates Formation of Lipid-Laden Macrophages Kenji Ohwaki, Hideaki Bujo, Meizi Jiang, Hiroyuki Yamazaki, Wolfgang J. Schneider, and Yasushi Saito Arterioscler Thromb Vasc Biol. 2007;27:1050-1056; published online before print March 1 2007, doi:10.1161/ATVBAHA.106.137091 Abstract \| Full Text \| PDF \| Data Supplement LR11 is secreted from intimal SMCs in a soluble form. Here we report that solLR11 modulates multiple functions of macrophages toward increased adhesion, migration, scavenger receptor expression, and uptake of modified lipid. This functional characterization of solLR11 provides novel insights into the pathophysiological significance of intimal SMCs in the regulation of macrophage function.
	Hydrogen Peroxide Derived From Beating Heart Mediates Coronary Microvascular Dilation During Tachycardia Yasunori Kokusho, Tatsuya Komaru, Satoru Takeda, Katsuaki Takahashi, Ryoji Koshida, Kunio Shirato, and Hiroaki Shimokawa Arterioscler Thromb Vasc Biol. 2007;27:1057-1063; published online before print March 1 2007, doi:10.1161/01.ATV.0000261570.85983.4f Abstract \| Full Text \| PDF \| Data Supplement To determine the mediator of metabolic coronary flow increase, we observed isolated coronary microvessels placed on the beating heart. We conclude that H2O2 derived from the beating heart mediates tachypacing-induced metabolic coronary vasodilation. The present studies may provide a new insight for the understanding of the coronary flow regulation.
	Toll-Like Receptors 2-Deficient Mice Are Protected Against Postischemic Coronary Endothelial Dysfunction Julie Favre, Philippe Musette, Victorine Douin-Echinard, Karine Laude, Jean-Paul Henry, Jean-François Arnal, Christian Thuillez, and Vincent Richard Arterioscler Thromb Vasc Biol. 2007;27:1064-1071; published online before print March 1 2007, doi:10.1161/ATVBAHA.107.140723 Abstract \| Full Text \| PDF Toll-like receptor 2 deficient mice (TLR2-/-) displayed a complete protection against endothelial dysfunction induced by ischemia/reperfusion (unaltered relaxing response to acetylcholine ex vivo). TLR2-/- mice also had reduced infarct size, production of reactive oxygen species and leukocyte infiltration. TLR2 thus contribute to coronary endothelial dysfunction after reperfusion.
	Dysregulated Bone Morphogenetic Protein Signaling in Monocrotaline-Induced Pulmonary Arterial Hypertension Rory E. Morty, Bozena Nejman, Grazyna Kwapiszewska, Matthias Hecker, Anka Zakrzewicz, Fotini M. Kouri, Dorothea M. Peters, Rio Dumitrascu, Werner Seeger, Petra Knaus, Ralph T. Schermuly, and Oliver Eickelberg Arterioscler Thromb Vasc Biol. 2007;27:1072-1078; published online before print March 8 2007, doi:10.1161/ATVBAHA.107.141200 Abstract \| Full Text \| PDF \| Data Supplement The expression and function of the BMP/Smad signaling axis is perturbed in monocrotaline-induced pulmonary arterial hypertension in rats, whereas MAP kinase signaling appears unaffected. These data support a role for dysregulated BMP/Smad signaling in the pathogenesis of pulmonary arterial hypertension.
	Atherosclerosis and Lipoproteins
	Circulating Apoptotic Progenitor Cells: A Novel Biomarker in Patients With Acute Coronary Syndromes Shmuel Schwartzenberg, Varda Deutsch, Sofia Maysel-Auslender, Sarina Kissil, Gad Keren, and Jacob George Arterioscler Thromb Vasc Biol. 2007;27:e27-e31; published online before print March 1 2007, doi:10.1161/ATVBAHA.107.139626 Abstract \| Full Text \| PDF We established for the first time to our knowledge an assay to detect circulating apoptotic progenitor cells using fluorescein isothiocyanate-anti-CD34 MAb, annexin V-PE, and 7-AAD and found that apoptotic CD34+ cells are increased in ACS patients and in patients with more extensive coronary artery disease. This novel assay may shed new light on the factors governing the hemeostasis of progenitor CD34+ cells.
	Circulating Apoptotic Progenitor Cells: A Novel Biomarker in Patients With Acute Coronary Syndromes Shmuel Schwartzenberg, Varda Deutsch, Sofia Maysel-Auslender, Sarina Kissil, Gad Keren, and Jacob George Arterioscler Thromb Vasc Biol. 2007;27:1079 Abstract \| Full Text \| PDF
	Inhibition of the Renin-Angiotensin System Abolishes the Proatherogenic Effect of Uremia in Apolipoprotein E-Deficient Mice Susanne Bro, Christoph J. Binder, Joseph L. Witztum, Klaus Olgaard, and Lars B. Nielsen Arterioscler Thromb Vasc Biol. 2007;27:1080-1086; published online before print March 8 2007, doi:10.1161/ATVBAHA.107.139634 Abstract \| Full Text \| PDF \| Data Supplement Uremia markedly accelerates atherosclerosis in apolipoprotein E-deficient (apoE-/-) mice. RAS inhibition, but not blood pressure reduction with a non-RAS-dependent vasodilator, abolished the proatherogenic effect of uremia in apoE-/- mice, possibly because of antiinflammatory or antioxidative mechanisms.
	Expression of Tumor Necrosis Factor Receptor-1 in Arterial Wall Cells Promotes Atherosclerosis Lisheng Zhang, Karsten Peppel, Perumal Sivashanmugam, Eric S. Orman, Leigh Brian, Sabrina T. Exum, and Neil J. Freedman Arterioscler Thromb Vasc Biol. 2007;27:1087-1094; published online before print March 1 2007, doi:10.1161/01.ATV.0000261548.49790.63 Abstract \| Full Text \| PDF \| Data Supplement In carotid arterial grafts implanted into apolipoprotein E-deficient mice, TNF receptor-1 deficiency reduced atherosclerotic lesion size by 2-fold. This reduction in atherosclerosis correlated with reduced arterial wall expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and MCP-1, and reduced medial SMC proliferation. TNFR1 deficiency also reduced SMC migration toward activated macrophages.
	DNA Vaccination Against VEGF Receptor 2 Reduces Atherosclerosis in LDL Receptor–Deficient Mice Ramona J. Petrovan, Charles D. Kaplan, Ralph A. Reisfeld, and Linda K. Curtiss Arterioscler Thromb Vasc Biol. 2007;27:1095-1100; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.139246 Abstract \| Full Text \| PDF \| Data Supplement Experimental data indicate that intimal neovascularization plays an important role in development of atherosclerotic lesions. An oral Flk-1-based anti-angiogenic DNA vaccine led to a marked reduction in atherosclerosis in hyperlipidemic LDLr-/- mice suggesting that genetic immunization may provide an additional treatment choice with long lasting protective effects for this chronic disease.
	TRAF-1, -2, -3, -5, and -6 Are Induced in Atherosclerotic Plaques and Differentially Mediate Proinflammatory Functions of CD40L in Endothelial Cells Andreas Zirlik, Udo Bavendiek, Peter Libby, Lindsey MacFarlane, Norbert Gerdes, Joanna Jagielska, Sandra Ernst, Masanori Aikawa, Hiroyasu Nakano, Erdyni Tsitsikov, and Uwe Schönbeck Arterioscler Thromb Vasc Biol. 2007;27:1101-1107; published online before print March 1 2007, doi:10.1161/ATVBAHA.107.140566 Abstract \| Full Text \| PDF \| Data Supplement This study tested the hypothesis that TRAF-1, -2, -3, -5, and -6 participate in CD40 signaling in ECs. TRAFs differentially mediated CD40L-induced IL-6, IL-8, and MCP-1 expression and atherosclerotic arteries overexpressed TRAFs, identifying these signaling molecules as potential therapeutic targets.
	Oxysterol Binding Protein Induces Upregulation of SREBP-1c and Enhances Hepatic Lipogenesis Daoguang Yan, Markku Lehto, Laura Rasilainen, Jari Metso, Christian Ehnholm, Seppo Ylä-Herttuala, Matti Jauhiainen, and Vesa M. Olkkonen Arterioscler Thromb Vasc Biol. 2007;27:1108-1114; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.138545 Abstract \| Full Text \| PDF \| Data Supplement Overexpression of OSBP in mouse liver induced an increase of VLDL and liver triglycerides, upregulation of hepatic SREBP-1c, and reduction of ERK phosphorylation. Silencing of OSBP suppressed SREBP-1c induction by insulin and resulted in reduction of triglyceride synthesis, demonstrating a new role of OSBP in regulation of hepatic lipogenesis.
	Predominance of a Proinflammatory Phenotype in Monocyte-Derived Macrophages From Subjects With Low Plasma HDL-Cholesterol Lea Sarov-Blat, Robert S. Kiss, Bassam Haidar, Nihan Kavaslar, Michael Jaye, Melissa Bertiaux, Klaudia Steplewski, Mark R. Hurle, Dennis Sprecher, Ruth McPherson, and Yves L. Marcel Arterioscler Thromb Vasc Biol. 2007;27:1115-1122; published online before print February 22 2007, doi:10.1161/ATVBAHA.106.138990 Abstract \| Full Text \| PDF \| Data Supplement We demonstrate that cholesterol loaded monocyte-derived macrophages from low HDL-C subjects exhibit a complex inflammatory gene response, related to altered expression of PPAR{gamma}, PPAR{delta}, and a cluster of metallothionein genes. Our results suggest that a heightened macrophage inflammatory response may contribute to the pathophysiological consequences of HDL deficiency.
	A Pathway-Dependent on ApoE, ApoAI, and ABCA1 Determines Formation of Buoyant High-Density Lipoprotein by Macrophage Foam Cells Patricia G. Yancey, Hong Yu, MacRae F. Linton, and Sergio Fazio Arterioscler Thromb Vasc Biol. 2007;27:1123-1131; published online before print February 15 2007, doi:10.1161/ATVBAHA.107.139592 Abstract \| Full Text \| PDF \| Data Supplement ABCA1-independent and ABCA1-dependent pathways may operate in lipidation of macrophage apoE. We demonstrate that ABCA1 is required for lipidation of macrophage foam cell apoE, and that apoE promotes formation of buoyant HDL in the presence of apoAI. Thus, apoE, apoAI, and ABCA1 work in concert to maximize cholesterol mobilization.
	Inhibition of Cholesteryl Ester Transfer Protein by Torcetrapib Modestly Increases Macrophage Cholesterol Efflux to HDL Laurent Yvan-Charvet, Fumihiko Matsuura, Nan Wang, Mark J. Bamberger, Tu Nguyen, Franz Rinninger, Xian-Cheng Jiang, Charles L. Shear, and Alan R. Tall Arterioscler Thromb Vasc Biol. 2007;27:1132-1138; published online before print February 22 2007, doi:10.1161/ATVBAHA.106.138347 Abstract \| Full Text \| PDF \| Data Supplement This study shows that CETP inhibition via torcetrapib has a dose-related effect on the ability of HDL to promote cholesterol efflux from macrophage foam cells in an ABCG1-dependent fashion.
	Genetic Etiology of Isolated Low HDL Syndrome: Incidence and Heterogeneity of Efflux Defects Robert S. Kiss, Nihan Kavaslar, Kei-ichiro Okuhira, Mason W. Freeman, Stephanie Walter, Ross W. Milne, Ruth McPherson, and Yves L. Marcel Arterioscler Thromb Vasc Biol. 2007;27:1139-1145; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.137646 Abstract \| Full Text \| PDF Cholesterol efflux defects are a common feature in subjects with low HDL, in the absence of coding sequence variants in ABCA1, suggesting that the majority of low HDL syndromes have novel genetic causes. Furthermore, we provide preliminary evidence that this is a heritable cellular phenotype, which cosegregates with low HDL.
	HDL Oxidation Compromises its Influence on Paraoxonase-1 Secretion and its Capacity to Modulate Enzyme Activity Sara Deakin, Xenia Moren, and Richard W. James Arterioscler Thromb Vasc Biol. 2007;27:1146-1152; published online before print March 8 2007, doi:10.1161/ATVBAHA.107.141747 Abstract \| Full Text \| PDF \| Data Supplement Oxidation of HDL reduced its ability to promote paraoxonase-1 secretion and to improve the activity of the secreted enzyme. It was not related to modified affinity of HDL for the cell, or lipoperoxide-mediated enzyme inactivation. The degree of HDL oxidation was inversely correlated with the concentration of associated paraoxonase-1.
	High-Density Lipoprotein Attenuates Inflammation and Coagulation Response on Endotoxin Challenge in Humans Rakesh S. Birjmohun, Sander I. van Leuven, Johannes H.M. Levels, Cornelis van ‘t Veer, Jan Albert Kuivenhoven, Joost C.M. Meijers, Marcel Levi, John J.P. Kastelein, Tom van der Poll, and Erik S.G. Stroes Arterioscler Thromb Vasc Biol. 2007;27:1153-1158; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.136325 Abstract \| Full Text \| PDF Low high-density lipoprotein (HDL) cholesterol is a strong independent cardiovascular risk factor, which has been attributed to its role in reverse cholesterol transport. Whereas HDL also has potent antiinflammatory effects, the relevance of this property remains to be established in humans. In the present study, we evaluated whether there is a relation between HDL and sensitivity toward a low-dose endotoxin challenge.
	Early Human Atherosclerosis: Accumulation of Lipid and Proteoglycans in Intimal Thickenings Followed by Macrophage Infiltration Yutaka Nakashima, Hiroshi Fujii, Shinji Sumiyoshi, Thomas N. Wight, and Katsuo Sueishi Arterioscler Thromb Vasc Biol. 2007;27:1159-1165; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.134080 Abstract \| Full Text \| PDF \| Data Supplement Little is known how early human atherosclerosis evolves. Our results showed that fatty streaks develop via extracellular lipid deposition in the proteoglycan-enriched outer layer of preexisting diffuse intimal thickening. As the amount of lipid increases, macrophages infiltrate toward the deposited lipid to form pathologic intimal thickening with foam cells.
	Alpha Defensins 1, 2, and 3: Potential Roles in Dyslipidemia and Vascular Dysfunction in Humans Abel López-Bermejo, Berta Chico-Julià, Antoni Castro, Mònica Recasens, Eduardo Esteve, Josefina Biarnés, Roser Casamitjana, Wifredo Ricart, and José-Manuel Fernández-Real Arterioscler Thromb Vasc Biol. 2007;27:1166-1171; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.138594 Abstract \| Full Text \| PDF \| Data Supplement {alpha}-Defensins (natural antibiotics made by neutrophils) can modulate cholesterol metabolism and vascular function. In apparently-healthy White men, plasma {alpha}-defensins 1 to 3 (DEFA1-3) were decreased with increasing body weight and smoking, and reduced circulating DEFA1-3 was associated with higher total and LDL-cholesterol concentrations. Decreased DEFA1-3 was also associated with poorer endothelial-independent vasomotor responses in these subjects. {alpha}-Defensins may have clinical implications in patients with either hypercholesterolemia or vascular dysfunction.
	What Is the Most Appropriate Methodology for Detection of Conduit Artery Endothelial Dysfunction? Sasidhar Guthikonda, Christine A. Sinkey, and William G. Haynes Arterioscler Thromb Vasc Biol. 2007;27:1172-1176; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.131011 Abstract \| Full Text \| PDF Reactive hyperemia after lower arm arterial occlusion (LAO) is used to study conduit vessel endothelial function. Upper arm brachial artery occlusion (UAO) has been suggested as an alternative and better method to assess endothelial function. We tested upper arm occlusion to evaluate endothelial dysfunction in smokers before and after xanthine oxidase inhibition with allopurinol. LAO demonstrated significant impairment in endothelial function in smokers and improved with allopurinol, whereas UAO did not. Responses to nitroglycerin and in controls were not significantly different. In conclusion, LAO is better means of studying endothelial dysfunction than UAO.
	Circulating Secretory Phospholipase A2 Activity and Risk of Incident Coronary Events in Healthy Men and Women: The EPIC-NORFOLK Study Ziad Mallat, Joelle Benessiano, Tabassome Simon, Stéphane Ederhy, Carla Sebella-Arguelles, Ariel Cohen, Virginie Huart, Nicholas J. Wareham, Robert Luben, Kay-Tee Khaw, Alain Tedgui, and S. Matthijs Boekholdt Arterioscler Thromb Vasc Biol. 2007;27:1177-1183; published online before print February 15 2007, doi:10.1161/ATVBAHA.107.139352 Abstract \| Full Text \| PDF In a nested case-control study among 25 663 healthy participants of EPIC-Norfolk cohort, the risk of incident coronary artery disease was associated with increasing quartiles of serum sPLA2 activity. sPLA2 activity and CRP levels provided better prediction of risk than either biomarker alone. The odds ratio of risk was 2.89 (95% CI, 1.78 to 4.68; P<0.001) in the highest quartiles of sPLA2 activity and CRP, compared with those in the lowest quartiles of both markers.
	Thrombosis
	EXP3179 Inhibits Collagen-Dependent Platelet Activation via Glycoprotein Receptor-VI Independent of AT₁-Receptor Antagonism: Potential Impact on Atherothrombosis Christina Grothusen, Sumaira Umbreen, Ildiko Konrad, Konstantinos Stellos, Christian Schulz, Boris Schmidt, Elisabeth Kremmer, Omke Teebken, Steffen Massberg, Maren Luchtefeld, Bernhard Schieffer, and Meinrad Gawaz Arterioscler Thromb Vasc Biol. 2007;27:1184-1190; published online before print March 8 2007, doi:10.1161/ATVBAHA.106.138693 Abstract \| Full Text \| PDF \| Data Supplement This study investigated the impact of EXP3179, an active metabolite of Losartan on collagen-induced platelet activation via the GPVI-receptor. EXP3179 inhibits collagen-dependent platelet activation by GPVI-receptor blockade independent of AT1-receptor antagonism, suggesting a novel role for EXP3179 as a platelet-inhibitory agent.
	Darbepoetin-Alpha Does Not Promote Microvascular Thrombus Formation in Mice: Role of eNOS-Dependent Protection Through Platelet and Endothelial Cell Deactivation Nicole Lindenblatt, Michael D. Menger, Ernst Klar, and Brigitte Vollmar Arterioscler Thromb Vasc Biol. 2007;27:1191-1198; published online before print March 8 2007, doi:10.1161/ATVBAHA.107.141580 Abstract \| Full Text \| PDF EPO treatment is generally assumed to increase the risk for thrombosis. Darbepoetin-alpha (DPO) raised eNOS expression and reduced platelet and endothelial activation without having prothrombogenic effects in vivo. DPO-related erythropoiesis is not associated with an increased risk for thrombosis as long as endothelial NO production serves as compensatory mechanism.
	The Fab Fragment of a Novel Anti-GPVI Monoclonal Antibody, OM4, Reduces In Vivo Thrombosis Without Bleeding Risk in Rats Haiquan Li, Simon Lockyer, Alice Concepcion, Xiaoqi Gong, Hisao Takizawa, Moe Guertin, Yutaka Matsumoto, Junichi Kambayashi, Narendra N. Tandon, and Yongge Liu Arterioscler Thromb Vasc Biol. 2007;27:1199-1205; published online before print February 22 2007, doi:10.1161/ATVBAHA.107.140590 Abstract \| Full Text \| PDF \| Data Supplement The Fab fragment of a novel anti-human GPVI monoclonal antibody, OM4, inhibited ex vivo collagen-induced aggregation of rat platelets and thrombosis in vivo without the prolongation of bleeding time or GPVI-depletion. The inhibition was short-lived (30 to 45 minutes) with full recovery in 90 minutes. Inhibition of GPVI may be a viable antithrombotic strategy.
	Targeting Ligand-Induced Binding Sites on GPIIb/IIIa via Single-Chain Antibody Allows Effective Anticoagulation Without Bleeding Time Prolongation Patrick Stoll, Nicole Bassler, Christoph E. Hagemeyer, Steffen U. Eisenhardt, Yung Chih Chen, Rene Schmidt, Meike Schwarz, Ingo Ahrens, Yasuhiro Katagiri, Benedikt Pannen, Christoph Bode, and Karlheinz Peter Arterioscler Thromb Vasc Biol. 2007;27:1206-1212; published online before print February 22 2007, doi:10.1161/ATVBAHA.106.138875 Abstract \| Full Text \| PDF \| Data Supplement A new strategy of targeting anticoagulants to activated platelets is evaluated. A newly cloned single-chain antibody directed against a LIBS-epitope on GPIIb/IIIa and the potent, direct factor-Xa inhibitor TAP were genetically fused. Anticoagulative efficiency and safety was proven in a mouse model with carotid artery thrombosis and bleeding time measurements.
	Retrospective Analysis of Coagulation Factor II Receptor (F2R) Sequence Variation and Coronary Heart Disease in Hypertensive Patients Bruna Gigante, Alessandro Bellis, Roberta Visconti, Marina Marino, Carmine Morisco, Valentina Trimarco, Gennaro Galasso, Federico Piscione, Nicola De Luca, Jonathan A. Prince, Ulf de Faire, and Bruno Trimarco Arterioscler Thromb Vasc Biol. 2007;27:1213-1219; published online before print March 8 2007, doi:10.1161/ATVBAHA.107.140541 Abstract \| Full Text \| PDF \| Data Supplement The purpose of this study was to evaluate the role of genetic variants within the coagulation factor II receptor (F2R) in the occurrence of coronary heart disease (CHD). F2R genetic variants may influence the natural history of CHD in patients at high risk of cardiovascular events.
	Letters to the Editor
	Letter to the Editor: Gender Differences in Coronary Arteries and Thoracic Aorta Calcification Khurram Nasir, Ariel Roguin, Ammar Sarwar, John A. Rumberger, and Roger S. Blumenthal Arterioscler Thromb Vasc Biol. 2007;27:1220-1222, doi:10.1161/ATVBAHA.107.140079 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 27, Issue 5; May 1, 2007

Announcement

Recipients of the 2007 New Investigator Awards

Editorials

Summary of the American Heart Association’s Scientific Statement on Drug Therapy of High-Risk Lipid Abnormalities in Children and Adolescents

Is Pathologic Intimal Thickening the Key to Understanding Early Plaque Progression in Human Atherosclerotic Disease?

Inflammatory Blues Turns Velvet Skin Into Rawhide: Monocyte Rolling on Modified Endothelial PSGL-1

Choking off Plaque Neovascularity: A Promising Atheroprotective Strategy or A Double-Edged Sword?

Brief Reviews

Adipose Tissue and Atherosclerosis: Exploring the Connection

Physiological Roles of Vascular Nucleoside Transporters

cAMP Signaling in Leukocyte Transendothelial Migration

Vascular Biology

P-Selectin Glycoprotein Ligand-1 Is Expressed on Endothelial Cells and Mediates Monocyte Adhesion to Activated Endothelium

Characterization of Phosphate Transport in Rat Vascular Smooth Muscle Cells: Implications for Vascular Calcification

Smooth Muscle–Targeted Knockout of Connexin43 Enhances Neointimal Formation in Response to Vascular Injury

Simvastatin Reduces MMP1 Expression in Human Smooth Muscle Cells Cultured on Polymerized Collagen by Inhibiting Rac1 Activation

A Secreted Soluble Form of LR11, Specifically Expressed in Intimal Smooth Muscle Cells, Accelerates Formation of Lipid-Laden Macrophages

Hydrogen Peroxide Derived From Beating Heart Mediates Coronary Microvascular Dilation During Tachycardia

Toll-Like Receptors 2-Deficient Mice Are Protected Against Postischemic Coronary Endothelial Dysfunction

Dysregulated Bone Morphogenetic Protein Signaling in Monocrotaline-Induced Pulmonary Arterial Hypertension

Atherosclerosis and Lipoproteins

Circulating Apoptotic Progenitor Cells: A Novel Biomarker in Patients With Acute Coronary Syndromes

Circulating Apoptotic Progenitor Cells: A Novel Biomarker in Patients With Acute Coronary Syndromes

Inhibition of the Renin-Angiotensin System Abolishes the Proatherogenic Effect of Uremia in Apolipoprotein E-Deficient Mice

Expression of Tumor Necrosis Factor Receptor-1 in Arterial Wall Cells Promotes Atherosclerosis

DNA Vaccination Against VEGF Receptor 2 Reduces Atherosclerosis in LDL Receptor–Deficient Mice

TRAF-1, -2, -3, -5, and -6 Are Induced in Atherosclerotic Plaques and Differentially Mediate Proinflammatory Functions of CD40L in Endothelial Cells

Oxysterol Binding Protein Induces Upregulation of SREBP-1c and Enhances Hepatic Lipogenesis

Predominance of a Proinflammatory Phenotype in Monocyte-Derived Macrophages From Subjects With Low Plasma HDL-Cholesterol

A Pathway-Dependent on ApoE, ApoAI, and ABCA1 Determines Formation of Buoyant High-Density Lipoprotein by Macrophage Foam Cells

Inhibition of Cholesteryl Ester Transfer Protein by Torcetrapib Modestly Increases Macrophage Cholesterol Efflux to HDL

Genetic Etiology of Isolated Low HDL Syndrome: Incidence and Heterogeneity of Efflux Defects

HDL Oxidation Compromises its Influence on Paraoxonase-1 Secretion and its Capacity to Modulate Enzyme Activity

High-Density Lipoprotein Attenuates Inflammation and Coagulation Response on Endotoxin Challenge in Humans

Early Human Atherosclerosis: Accumulation of Lipid and Proteoglycans in Intimal Thickenings Followed by Macrophage Infiltration

Alpha Defensins 1, 2, and 3: Potential Roles in Dyslipidemia and Vascular Dysfunction in Humans

What Is the Most Appropriate Methodology for Detection of Conduit Artery Endothelial Dysfunction?

Circulating Secretory Phospholipase A2 Activity and Risk of Incident Coronary Events in Healthy Men and Women: The EPIC-NORFOLK Study

Thrombosis

EXP3179 Inhibits Collagen-Dependent Platelet Activation via Glycoprotein Receptor-VI Independent of AT1-Receptor Antagonism: Potential Impact on Atherothrombosis

Darbepoetin-Alpha Does Not Promote Microvascular Thrombus Formation in Mice: Role of eNOS-Dependent Protection Through Platelet and Endothelial Cell Deactivation

The Fab Fragment of a Novel Anti-GPVI Monoclonal Antibody, OM4, Reduces In Vivo Thrombosis Without Bleeding Risk in Rats

Targeting Ligand-Induced Binding Sites on GPIIb/IIIa via Single-Chain Antibody Allows Effective Anticoagulation Without Bleeding Time Prolongation

Retrospective Analysis of Coagulation Factor II Receptor (F2R) Sequence Variation and Coronary Heart Disease in Hypertensive Patients

Letters to the Editor

Letter to the Editor: Gender Differences in Coronary Arteries and Thoracic Aorta Calcification

Spotlight

EXP3179 Inhibits Collagen-Dependent Platelet Activation via Glycoprotein Receptor-VI Independent of AT₁-Receptor Antagonism: Potential Impact on Atherothrombosis