Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (29 [11])

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Volume 29, Issue 11; November 1, 2009

Editorials
History of Discovery
Brief Reviews
Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Clinical and Population Studies

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

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	Editorials
	Tyrosine Sulfation of Leukocyte Adhesion Molecules and Chemokine Receptors Promotes Atherosclerosis Ekaterina Koltsova and Klaus Ley Arterioscler Thromb Vasc Biol. 2009;29:1709-1711, doi:10.1161/ATVBAHA.109.195552 Extract \| Full Text \| PDF
	Dimorphisms in the Membrane-Spanning Domain of EPCR Impact Systemic Coagulation Charles T. Esmon Arterioscler Thromb Vasc Biol. 2009;29:1712-1713, doi:10.1161/ATVBAHA.109.195701 Extract \| Full Text \| PDF
	History of Discovery
	The Discovery of Cellular Immunity in the Atherosclerotic Plaque Göran K. Hansson and Lena Jonasson Arterioscler Thromb Vasc Biol. 2009;29:1714-1717, doi:10.1161/ATVBAHA.108.179713 Abstract \| Full Text \| PDF
	The Molecular Mechanisms of HDL and Associated Vesicular Trafficking Mechanisms to Mediate Cellular Lipid Homeostasis Gerd Schmitz and Margot Grandl Arterioscler Thromb Vasc Biol. 2009;29:1718-1722, doi:10.1161/ATVBAHA.108.179507 Abstract \| Full Text \| PDF
	Brief Reviews
	Adipose Tissue-Derived Stem Cells: Characterization and Potential for Cardiovascular Repair Rosalinda Madonna, Yong-Jian Geng, and Raffaele De Caterina Arterioscler Thromb Vasc Biol. 2009;29:1723-1729; published online before print July 23 2009, doi:10.1161/ATVBAHA.109.187179 Abstract \| Full Text \| PDF Stromal cells derived from the adipose tissue (adipose tissue-derived stromal cells) contain a population of adult multipotent mesenchymal stem cells and endothelial progenitor cells that can differentiate into several lineages, including endothelial cells, smooth muscle cells, and cardiomyocytes, and act through paracrine mechanisms for potential myocardial repair.
	Integrative Physiology/Experimental Medicine
	Lack of Tyrosylprotein Sulfotransferase Activity in Hematopoietic Cells Drastically Attenuates Atherosclerosis in Ldlr^–/– Mice Andrew D. Westmuckett and Kevin L. Moore Arterioscler Thromb Vasc Biol. 2009;29:1730-1736; published online before print August 13 2009, doi:10.1161/ATVBAHA.109.192963 Abstract \| Full Text \| PDF Leukocyte recruitment is a major contributor in the development of atherosclerosis. Several key proteins implicated in this process require tyrosine sulfation for optimal function in vitro. In this study we found that transplantation of Ldlr-/- mice with hematopoietic progenitors lacking tyrosylprotein sulfotransferase activity drastically attenuated development of atherosclerosis.
	Level of Macrophage uPA Expression Is an Important Determinant of Atherosclerotic Lesion Growth in Apoe^–/– Mice Ranjini Krishnan, Michal Kremen, Jie Hong Hu, Isaac Emery, Stephen D. Farris, Katherine I. Slezicki, Talyn Chu, Liang Du, Helén L. Dichek, and David A. Dichek Arterioscler Thromb Vasc Biol. 2009;29:1737-1744; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.195529 Abstract \| Full Text \| PDF \| Data Supplement We generated mice with either macrophage-specific overexpression of urokinase (uPA) or macrophage-specific loss of uPA. Macrophage uPA overexpression accelerated atherosclerosis and macrophage uPA deletion retarded atherosclerosis. The level of macrophage uPA expression--over a broad range--is an important determinant of atherosclerotic lesion growth in Apoe-/- mice.
	Moderately Decreased Cholesterol Absorption Rates Are Associated With a Large Atheroprotective Effect Michael E. Greenberg, Jonathan D. Smith, and Ephraim Sehayek Arterioscler Thromb Vasc Biol. 2009;29:1745-1750; published online before print August 6 2009, doi:10.1161/ATVBAHA.109.194605 Abstract \| Full Text \| PDF The atheroprotective effect of moderately decreased cholesterol absorption rates was examined in apolipoprotein E knockout mice. A 41% decrease in cholesterol absorption was associated with a 30% to 37% decrease in plasma cholesterol levels, a 60% increase in RCT, and a 70% decrease in atherosclerosis formation.
	Heat Shock Protein 27 Protects Against Atherogenesis via an Estrogen-Dependent Mechanism: Role of Selective Estrogen Receptor Beta Modulation Katey Rayner, Jiangfeng Sun, Yong-Xiang Chen, Melissa McNulty, Trevor Simard, Xiaoling Zhao, Dominic J. Wells, Jacqueline de Belleroche, and Edward R. O'Brien Arterioscler Thromb Vasc Biol. 2009;29:1751-1756; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.193656 Abstract \| Full Text \| PDF \| Data Supplement Heat shock protein 27 has previously been shown to be atheroprotective in a mouse model of atherosclerosis, but only in females. We now report that both the atheroprotective effects and the release of HSP27 into the serum are dependent on estrogen, and can be stimulated using a specific estrogen-receptor β modulator.
	Laminar Shear Stress Regulates Endothelial Kinin B1 Receptor Expression and Function: Potential Implication in Atherogenesis Johan Duchene, Cécile Cayla, Sandrine Vessillier, Ramona Scotland, Kazuo Yamashiro, Florence Lecomte, Irfan Syed, Phuong Vo, Alessandra Marrelli, Costantino Pitzalis, Francesco Cipollone, Joost Schanstra, Jean-Loup Bascands, Adrian J. Hobbs, Mauro Perretti, and Amrita Ahluwalia Arterioscler Thromb Vasc Biol. 2009;29:1757-1763; published online before print August 6 2009, doi:10.1161/ATVBAHA.109.191775 Abstract \| Full Text \| PDF \| Data Supplement Low laminar shear stress (LSS) underlies the proinflammatory processes in atherogenesis. Herein, we demonstrate that whilst physiological LSS represses inflammatory kinin B1 receptor (B1R) expression/function, low atherogenic LSS is associated with profound upregulation of both in atherosclerosis in both humans and animal models, highlighting B1R as an exciting potential therapeutic target.
	Simvastatin Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-Knockout Mice: Possible Role of ERK Yali Zhang, Jack C. Naggar, C. Michael Welzig, Debbie Beasley, Karen S. Moulton, Ho-Jin Park, and Jonas B. Galper Arterioscler Thromb Vasc Biol. 2009;29:1764-1771; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.192609 Abstract \| Full Text \| PDF \| Data Supplement Infusion of angiotensin (Ang) II in apolipoprotein E-knockout (ApoE-/-) mice is an animal model for abdominal aortic aneurysm (AAA). Our data support the conclusion that simvastatin interferes with AngII-stimulated AAA formation in these mice at least in part via the inhibition of ERK.
	Smooth Muscle LDL Receptor-Related Protein-1 Inactivation Reduces Vascular Reactivity and Promotes Injury-Induced Neointima Formation Joshua E. Basford, Zachary W.Q. Moore, Li Zhou, Joachim Herz, and David Y. Hui Arterioscler Thromb Vasc Biol. 2009;29:1772-1778; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.194357 Abstract \| Full Text \| PDF \| Data Supplement Previous studies have shown the importance of smooth muscle cell low-density lipoprotein-related protein-1 (Lrp1) expression in maintenance of vascular integrity in hypercholesterolemic mice. The current study demonstrated that vascular smooth muscle Lrp1 expression is also important in modulating vascular contractility and limiting injury-induced neointimal hyperplasia in normolipidemic mice.
	Thiol Oxidative Stress Induced by Metabolic Disorders Amplifies Macrophage Chemotactic Responses and Accelerates Atherogenesis and Kidney Injury in LDL Receptor-Deficient Mice Mu Qiao, Qingwei Zhao, Chi Fung Lee, Lisa R. Tannock, Eric J. Smart, Richard G. LeBaron, Clyde F. Phelix, Yolanda Rangel, and Reto Asmis Arterioscler Thromb Vasc Biol. 2009;29:1779-1786; published online before print July 10 2009, doi:10.1161/ATVBAHA.109.191759 Abstract \| Full Text \| PDF \| Data Supplement
	Ccl2 and Ccl3 Mediate Neutrophil Recruitment via Induction of Protein Synthesis and Generation of Lipid Mediators Christoph Andreas Reichel, Markus Rehberg, Max Lerchenberger, Nina Berberich, Peter Bihari, Alexander Georg Khandoga, Stefan Zahler, and Fritz Krombach Arterioscler Thromb Vasc Biol. 2009;29:1787-1793; published online before print July 16 2009, doi:10.1161/ATVBAHA.109.193268 Abstract \| Full Text \| PDF \| Data Supplement The present study demonstrates that CC chemokines Ccl2/JE/MCP-1 and Ccl3/MIP-1{alpha} mediate firm adherence and (subsequent) transmigration of neutrophils via induction of protein synthesis and secondary generation of leukotrienes and PAF, which in turn directly activate neutrophils. Thereby, neutrophils facilitate basement membrane remodeling and promote microvascular leakage.
	Bone Marrow–Derived Cell-Specific Chemokine (C-C Motif) Receptor-2 Expression is Required for Arteriolar Remodeling Meghan M. Nickerson, Ji Song, Joshua K. Meisner, Sameer Bajikar, Caitlin W. Burke, Casey W. Shuptrine, Gary K. Owens, Thomas C. Skalak, and Richard J. Price Arterioscler Thromb Vasc Biol. 2009;29:1794-1801; published online before print September 4 2009, doi:10.1161/ATVBAHA.109.194019 Abstract \| Full Text \| PDF \| Data Supplement Dorsal skinfold window chamber implantation elicits inflammation, arteriolar remodeling, and bone marrow-derived cell recruitment without transdifferentiation into smooth muscle. In this model, both arteriolar remodeling and monocyte/macrophage recruitment are dependent on bone marrow-derived cell-specific CCR2 expression.
	CXCR4 Expression Determines Functional Activity of Bone Marrow–Derived Mononuclear Cells for Therapeutic Neovascularization in Acute Ischemia Florian H. Seeger, Tina Rasper, Masamichi Koyanagi, Henrik Fox, Andreas M. Zeiher, and Stefanie Dimmeler Arterioscler Thromb Vasc Biol. 2009;29:1802-1809; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.194688 Abstract \| Full Text \| PDF \| Data Supplement BMCs comprise a heterogeneous mixture of cells, and it is not known which cell types are responsible for neovascularization. Here, we show that CXCR4+ BMCs exhibit an increased potential for blood-flow recovery after ischemia. Mechanistically, their higher migratory capacity and their increased release of paracrine factors may contribute to enhanced tissue repair.
	Monocyte Chemoattractant Proteins Mediate Myocardial Microvascular Dysfunction in Swine Renovascular Hypertension Jing Lin, Xiangyang Zhu, Alejandro R. Chade, Kyra L. Jordan, Ronit Lavi, Elena Daghini, Matthew E. Gibson, Angelo Guglielmotti, Amir Lerman, and Lilach O. Lerman Arterioscler Thromb Vasc Biol. 2009;29:1810-1816; published online before print July 23 2009, doi:10.1161/ATVBAHA.109.190546 Abstract \| Full Text \| PDF \| Data Supplement This study tested the hypothesis that monocyte chemoattractant proteins (MCPs) regulate cardiac microvascular function and structure in experimental hypertension. Pigs with renovascular hypertension were studied after treatment with bindarit (MCPs inhibitor). It was found that MCPs partly mediate myocardial fibrosis, vascular remodeling, and impaired vascular integrity induced by hypertension.
	Stimulation of Coronary Collateral Growth by Granulocyte Stimulating Factor: Role of Reactive Oxygen Species Ana Catarina R. Carrão, William M. Chilian, June Yun, Christopher Kolz, Petra Rocic, Kerstin Lehmann, Jeroen P.H.M. van den Wijngaard, Pepijn van Horssen, Jos A.E. Spaan, Vahagn Ohanyan, Yuh Fen Pung, and Ivo Buschmann Arterioscler Thromb Vasc Biol. 2009;29:1817-1822; published online before print June 18 2009, doi:10.1161/ATVBAHA.109.186445 Abstract \| Full Text \| PDF We hypothesized that G-CSF stimulates coronary collateral growth (CCG) via production of ROS. G-CSF increased CCG with or without myocardial ischemia. G-CSF-induced ROS production occurred in cardiomyocytes but not in granulocytes. We conclude G-CSF stimulates ROS production in cardiomyocytes, which elicits growth of coronary collaterals via stimulation of angiogenic factors.
	Somitovasculin, a Novel Endothelial-Specific Transcript Involved in the Vasculature Development Devi Mariappan, Rabea Niemann, Martin Gajewski, Johannes Winkler, Shuhua Chen, Suma Choorapoikayil, Marco Bitzer, Herbert Schulz, Jürgen Hescheler, and Agapios Sachinidis Arterioscler Thromb Vasc Biol. 2009;29:1823-1829; published online before print June 18 2009, doi:10.1161/ATVBAHA.109.190751 Abstract \| Full Text \| PDF \| Data Supplement
	Therapeutic Potential of Unrestricted Somatic Stem Cells Isolated from Placental Cord Blood for Cardiac Repair Post Myocardial Infarction Hiroto Iwasaki, Atsuhiko Kawamoto, Christina Willwerth, Miki Horii, Akira Oyamada, Hiroshi Akimaru, Toshihiko Shibata, Hidekazu Hirai, Shigefumi Suehiro, Stephan Wnendt, William L. Fodor, and Takayuki Asahara Arterioscler Thromb Vasc Biol. 2009;29:1830-1835; published online before print August 13 2009, doi:10.1161/ATVBAHA.109.192203 Abstract \| Full Text \| PDF \| Data Supplement USSCs can be expanded up to 1015 cells without losing pluripotency in culture. The USSC therapy resulted in dose-dependent enhancement of neovascularization, inhibition of LV remodeling, and improvement of LV function post MI. USSCs could be used as a highly valuable resource for cellular cardiomyoplasty in the future clinical application.
	c-Jun DNAzymes Inhibit Myocardial Inflammation, ROS Generation, Infarct Size, and Improve Cardiac Function After Ischemia-Reperfusion Injury Xiao Luo, Hong Cai, Jun Ni, Ravinay Bhindi, Harry C. Lowe, Colin N. Chesterman, and Levon M. Khachigian Arterioscler Thromb Vasc Biol. 2009;29:1836-1842; published online before print July 10 2009, doi:10.1161/ATVBAHA.109.189753 Abstract \| Full Text \| PDF \| Data Supplement
	Nrf2 Protects Against Maladaptive Cardiac Responses to Hemodynamic Stress Jinqing Li, Tomonaga Ichikawa, Luis Villacorta, Joseph S. Janicki, Gregory L. Brower, Masayuki Yamamoto, and Taixing Cui Arterioscler Thromb Vasc Biol. 2009;29:1843-1850; published online before print July 10 2009, doi:10.1161/ATVBAHA.109.189480 Abstract \| Full Text \| PDF \| Data Supplement Herein we show that a sustained pressure overload to the hearts of Nrf2 knockout mice results in elevated oxidative stress, enhanced cardiac hypertrophy, significant myocardial fibrosis and apoptosis, and overt heat failure.
	Activation of Nrf2 in Endothelial Cells Protects Arteries From Exhibiting a Proinflammatory State Mustafa Zakkar, Kim Van der Heiden, Le Anh Luong, Hera Chaudhury, Simon Cuhlmann, Shahir S. Hamdulay, Rob Krams, Indika Edirisinghe, Irfan Rahman, Harald Carlsen, Dorian O. Haskard, Justin C. Mason, and Paul C. Evans Arterioscler Thromb Vasc Biol. 2009;29:1851-1857; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.193375 Abstract \| Full Text \| PDF \| Data Supplement \| Color Figures Atherosclerosis is a focal disease. Here we demonstrate that the transcription factor Nrf2 suppresses endothelial activation at atheroprotected sites by inhibiting p38 phosphorylation. Moreover, pharmacological activation of Nrf2 reduced endothelial activation at an atherosusceptible site and may provide a novel therapeutic strategy to prevent or reduce atherosclerosis.
	Dynamic Observation of Mechanically-Injured Mouse Femoral Artery Reveals an Antiinflammatory Effect of Renin Inhibitor Jun Ino, Chiari Kojima, Mizuko Osaka, Kosaku Nitta, and Masayuki Yoshida Arterioscler Thromb Vasc Biol. 2009;29:1858-1863; published online before print September 24 2009, doi:10.1161/ATVBAHA.108.182519 Abstract \| Full Text \| PDF \| Data Supplement This study indicates a pivotal role for renin inhibition in vascular inflammation independent of blood pressure in vivo and in vitro. Our findings also suggest a novel antiinflammatory role for aliskiren.
	The ${alpha}$ 11β1 Integrin Has a Mechanistic Role in Control of Interstitial Fluid Pressure and Edema Formation in Inflammation Ø.S. Svendsen, M.M. Barczyk, S.N. Popova, Å Lidén, D. Gullberg, and H. Wiig Arterioscler Thromb Vasc Biol. 2009;29:1864-1870; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.194308 Abstract \| Full Text \| PDF \| Data Supplement {alpha}11β1 integrins on fibroblasts are capable of increasing the contraction of collagen gels in vitro. {alpha}11-/- mice, in contrast to wild-type mice, did not show a reduction in skin interstitial fluid pressure during acute inflammation, suggesting that the {alpha}11β1 integrin has a mechanistic role in edema formation during inflammation.
	Cell Biology/Signaling
	PPARβ/ ${delta}$ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKC ${alpha}$ –Brief Report Ferhana Y. Ali, Matthew G. Hall, Béatrice Desvergne, Timothy D. Warner, and Jane A. Mitchell Arterioscler Thromb Vasc Biol. 2009;29:1871-1873; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.193367 Abstract \| Full Text \| PDF \| Data Supplement We show activation of platelet PPARβ/{delta} results in binding to and repression of PKC{alpha}, thus providing a signaling pathway for PPARβ/{delta} in platelets. Deletion of PPARβ/{delta} in murine platelets resulted in a loss of the inhibitory effects on adhesion and cAMP release, indicating PPARβ/{delta} is involved in platelet activation pathways.
	Foxp3 Regulates Megakaryopoiesis and Platelet Function Jamie J. Bernard, Kathryn E. Seweryniak, Anne D. Koniski, Sherry L. Spinelli, Neil Blumberg, Charles W. Francis, Mark B. Taubman, James Palis, and Richard P. Phipps Arterioscler Thromb Vasc Biol. 2009;29:1874-1882; published online before print August 6 2009, doi:10.1161/ATVBAHA.109.193805 Abstract \| Full Text \| PDF We discovered that human and mouse megakaryocytes express Foxp3 mRNA and protein. Humans with IPEX and the scurfy (Foxp3sf) mouse have mutations in the Foxp3 gene that lead to autoimmunity, skin diseases, hemorrhage, and thrombocytopenia. Our studies suggest that Foxp3 is needed for proper megakaryopoiesis and platelet function.
	Rapid Procoagulant Phosphatidylserine Exposure Relies on High Cytosolic Calcium Rather Than on Mitochondrial Depolarization Amal Arachiche, Danièle Kerbiriou-Nabias, Isabelle Garcin, Thierry Letellier, and Jeanne Dachary-Prigent Arterioscler Thromb Vasc Biol. 2009;29:1883-1889; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.190926 Abstract \| Full Text \| PDF \| Data Supplement The data showed that rapid procoagulant phosphatidylserine exposure in platelets and Jurkat cells is not controlled by mitochondrial depolarization. Furthermore, results demonstrate that CsA prevents membrane scrambling by inhibiting the high cytosolic calcium increase essential to trigger the process, independently of its blocking effect on mitochondrial permeability transition pores.
	Disinhibition of SOD-2 Expression to Compensate for a Genetically Determined NO Deficit in Endothelial Cells–Brief Report Abdul R. Asif, Markus Hecker, and Marco Cattaruzza Arterioscler Thromb Vasc Biol. 2009;29:1890-1893; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.190678 Abstract \| Full Text \| PDF \| Data Supplement Fluid shear stress-induced SOD-2 expression, mediated by the NO-sensitive activation of the transcription factor Egr-1, protects endothelial cells from oxidative stress, and may constitute a mechanism through which individuals homozygous for the -786C-variant of the nos-3 gene, despite an increased genetic risk, do not develop coronary artery disease early in life.
	Upregulation of Glutathione Peroxidase Offsets Stretch-Induced Proatherogenic Gene Expression in Human Endothelial Cells Andreas H. Wagner, Ocko Kautz, Kathrin Fricke, Murielle Zerr-Fouineau, Elena Demicheva, Björn Güldenzoph, Justo Lorenzo Bermejo, Thomas Korff, and Markus Hecker Arterioscler Thromb Vasc Biol. 2009;29:1894-1901; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.194738 Abstract \| Full Text \| PDF \| Data Supplement Upregulation of glutathione peroxidase-1 in human endothelial cells prevents hydrogen peroxide-mediated proatherosclerotic gene expression in response to cyclic stretch. In comparison with the dismutation of superoxide anions, accelerating the degradation of hydrogen peroxide may constitute an at least equally important adaptive mechanism to maintain the antiatherosclerotic properties of these cells.
	Flow Activation of AMP-Activated Protein Kinase in Vascular Endothelium Leads to Krüppel-Like Factor 2 Expression Angela Young, Wei Wu, Wei Sun, Harry B. Larman, Nanping Wang, Yi-Shuan Li, John Y. Shyy, Shu Chien, and Guillermo García-Cardeña Arterioscler Thromb Vasc Biol. 2009;29:1902-1908; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.193540 Abstract \| Full Text \| PDF \| Data Supplement AMPK mediated the shear-induced phosphorylation of ERK5 and MEF2, which leads to the augmentation of KLF2 and the subsequent regulation of its downstream targets eNOS and ET-1 in cultured endothelial cells and the aortic wall.
	Alzheimer Disease–Associated Peptide, Amyloid β40, Inhibits Vascular Regeneration With Induction of Endothelial Autophagy Shin-ichiro Hayashi, Naoyuki Sato, Akitsugu Yamamoto, Yuka Ikegame, Shigeru Nakashima, Toshio Ogihara, and Ryuichi Morishita Arterioscler Thromb Vasc Biol. 2009;29:1909-1915; published online before print October 8 2009, doi:10.1161/ATVBAHA.109.188516 Abstract \| Full Text \| PDF \| Data Supplement The cause and progression of AD still remains unclear. Our present findings indicate that the initial progression of AD might be in part driven by Aβ40-induced phenotypic alterations in neurovascular endothelium with induction of endothelial autophagy and impairment of neurovascular regeneration, suggesting important implications for therapeutic approaches to AD.
	The Phosphorylation Motif at Serine 225 Governs the Localization and Function of Sphingosine Kinase 1 in Resistance Arteries Darcy Lidington, Bernhard Friedrich Peter, Anja Meissner, Jeffrey T. Kroetsch, Stuart M. Pitson, Ulrich Pohl, and Steffen-Sebastian Bolz Arterioscler Thromb Vasc Biol. 2009;29:1916-1922; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.194803 Abstract \| Full Text \| PDF \| Data Supplement We demonstrate in hamster resistance arteries that the serine 225 phosphorylation site on sphingosine kinase 1 (Sk1) is a molecular switch for its regulatory function in smooth muscle cells. It is critical for pressure-dependent Sk1 activation/translocation and cannot be bypassed by an artificial membrane anchor.
	Liver X Receptor–Mediated Induction of Cholesteryl Ester Transfer Protein Expression Is Selectively Impaired in Inflammatory Macrophages Daniela Lakomy, Cédric Rébé, Anne-Laure Sberna, David Masson, Thomas Gautier, Angélique Chevriaux, Magalie Raveneau, Nicolas Ogier, Anh Thoai Nguyen, Philippe Gambert, Jacques Grober, Bernard Bonnotte, Eric Solary, and Laurent Lagrost Arterioscler Thromb Vasc Biol. 2009;29:1923-1929; published online before print August 13 2009, doi:10.1161/ATVBAHA.109.193201 Abstract \| Full Text \| PDF \| Data Supplement In the monocyte-macrophage lineage, both in mice and humans, LXR-mediated induction of CETP gene expression is switched on during monocyte-to-macrophage differentiation, magnified by lipid loading, and selectively lost when macrophages become inflammatory.
	Stimulation of Cholesterol Efflux by LXR Agonists in Cholesterol-Loaded Human Macrophages Is ABCA1-Dependent but ABCG1-Independent Sandra Larrede, Carmel M. Quinn, Wendy Jessup, Eric Frisdal, Maryline Olivier, Victar Hsieh, Mi-Jurng Kim, Miranda Van Eck, Philippe Couvert, Alain Carrie, Philippe Giral, M. John Chapman, Maryse Guerin, and Wilfried Le Goff Arterioscler Thromb Vasc Biol. 2009;29:1930-1936; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.194548 Abstract \| Full Text \| PDF \| Data Supplement
	Inhibition of Long-Chain Acyl Coenzyme A Synthetases During Fatty Acid Loading Induces Lipotoxicity in Macrophages Viswanathan Saraswathi and Alyssa H. Hasty Arterioscler Thromb Vasc Biol. 2009;29:1937-1943; published online before print August 13 2009, doi:10.1161/ATVBAHA.109.195362 Abstract \| Full Text \| PDF \| Data Supplement Inhibition of macrophage ACSLs during fatty acid loading increased intracellular FFAs and induced apoptosis. Adipose tissue from obese mice had increased FFA levels, and SVCs displayed foam cell morphology and exhibited increased expression of macrophage markers and ACSL1. ACSLs play an important role in regulating fatty acid homeostasis in macrophages.
	Saturated Fatty Acids Do Not Directly Stimulate Toll-Like Receptor Signaling Clett Erridge and Nilesh J. Samani Arterioscler Thromb Vasc Biol. 2009;29:1944-1949; published online before print August 6 2009, doi:10.1161/ATVBAHA.109.194050 Abstract \| Full Text \| PDF \| Data Supplement The effects of saturated fatty acids (SFAs) on Toll-like receptor (TLR) signaling were examined using diverse cell types and readouts. Although SFAs alone did not promote TLR-signaling in endothelial, adipocyte, smooth muscle, macrophage, or transfected HEK-293 cells, contaminants in fatty-acid-free bovine serum albumin promoted both TLR2 and TLR4 dependent signaling.
	Statins Block Calcific Nodule Formation of Valvular Interstitial Cells by Inhibiting ${alpha}$ -Smooth Muscle Actin Expression Julie A. Benton, Hanna B. Kern, Leslie A. Leinwand, Peter D. Mariner, and Kristi S. Anseth Arterioscler Thromb Vasc Biol. 2009;29:1950-1957; published online before print August 13 2009, doi:10.1161/ATVBAHA.109.195271 Abstract \| Full Text \| PDF \| Data Supplement We observed that VIC monolayers spontaneously contract into nodules, suggesting myofibroblastic contractility is critical. Overexpression of {alpha}SMA increased nodule formation, whereas knockdown of {alpha}SMA with siRNAs reduced these phenotypes. Statin treatment reduced {alpha}SMA expression and decreased nodules. When statins were used to treat preformed nodules, no decrease in nodules was observed.
	Clinical and Population Studies
	Genome-Wide Association Identifies the ABO Blood Group as a Major Locus Associated With Serum Levels of Soluble E-Selectin Andrew D. Paterson, Maria F. Lopes-Virella, Daryl Waggott, Andrew P. Boright, S. Mohsen Hosseini, Rickey E. Carter, Enqing Shen, Lucia Mirea, Bhupinder Bharaj, Lei Sun, Shelley B. Bull, and the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group Arterioscler Thromb Vasc Biol. 2009;29:1958-1967; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.192971 Abstract \| Full Text \| PDF \| Data Supplement Previous studies have identified various biomarkers and diseases that are associated with ABO, but the physiological mechanisms are mostly unclear. Here, we show the ABO gene locus accounts for 19% of the variance in serum soluble E-selectin levels, which is produced by damage to endothelial cells, and an inflammatory marker.
	FVII, FVIIa, and Downstream Markers of Extrinsic Pathway Activation Differ by EPCR Ser219Gly Variant in Healthy Men Helen A. Ireland, Jackie A. Cooper, Fotios Drenos, Jayshree Acharya, Jacqueline P. Mitchell, Ken A. Bauer, James H. Morrissey, M. Peter Esnouf, and Stephen E. Humphries Arterioscler Thromb Vasc Biol. 2009;29:1968-1974; published online before print August 20 2009, doi:10.1161/ATVBAHA.109.191551 Abstract \| Full Text \| PDF In {approx}2000 healthy middle aged men (NPHSII), FVII, FVIIa, FIX activation peptide, FX activation peptide, and prothrombin F1+2 levels were significantly higher in those with the rare allele for a variant (EPCR Ser219Gly) previously shown to have functional consequences for EPCR shedding. These findings extend previous in vitro analysis for FVII and FVIIa binding to membrane associated EPCR.
	Ion Mobility Analysis of Lipoprotein Subfractions Identifies Three Independent Axes of Cardiovascular Risk Kiran Musunuru, Marju Orho-Melander, Michael P. Caulfield, Shuguang Li, Wael A. Salameh, Richard E. Reitz, Göran Berglund, Bo Hedblad, Gunnar Engström, Paul T. Williams, Sekar Kathiresan, Olle Melander, and Ronald M. Krauss Arterioscler Thromb Vasc Biol. 2009;29:1975-1980; published online before print September 3 2009, doi:10.1161/ATVBAHA.109.190405 Abstract \| Full Text \| PDF \| Data Supplement We tested whether combinations of lipoprotein subfractions independently predict cardiovascular disease in a prospective cohort of 4594 initially healthy men and women (Malmo Diet and Cancer Study). Principal component analysis on lipoprotein subfractions yielded 3 independent components of risk, the strongest of which is consistent with the atherogenic lipoprotein phenotype.

Spotlight

TOC Spotlight File

Volume 29, Issue 11; November 1, 2009

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

Editorials

Tyrosine Sulfation of Leukocyte Adhesion Molecules and Chemokine Receptors Promotes Atherosclerosis

Dimorphisms in the Membrane-Spanning Domain of EPCR Impact Systemic Coagulation

History of Discovery

The Discovery of Cellular Immunity in the Atherosclerotic Plaque

The Molecular Mechanisms of HDL and Associated Vesicular Trafficking Mechanisms to Mediate Cellular Lipid Homeostasis

Brief Reviews

Adipose Tissue-Derived Stem Cells: Characterization and Potential for Cardiovascular Repair

Integrative Physiology/Experimental Medicine

Lack of Tyrosylprotein Sulfotransferase Activity in Hematopoietic Cells Drastically Attenuates Atherosclerosis in Ldlr–/– Mice

Level of Macrophage uPA Expression Is an Important Determinant of Atherosclerotic Lesion Growth in Apoe–/– Mice

Moderately Decreased Cholesterol Absorption Rates Are Associated With a Large Atheroprotective Effect

Heat Shock Protein 27 Protects Against Atherogenesis via an Estrogen-Dependent Mechanism: Role of Selective Estrogen Receptor Beta Modulation

Laminar Shear Stress Regulates Endothelial Kinin B1 Receptor Expression and Function: Potential Implication in Atherogenesis

Simvastatin Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-Knockout Mice: Possible Role of ERK

Smooth Muscle LDL Receptor-Related Protein-1 Inactivation Reduces Vascular Reactivity and Promotes Injury-Induced Neointima Formation

Thiol Oxidative Stress Induced by Metabolic Disorders Amplifies Macrophage Chemotactic Responses and Accelerates Atherogenesis and Kidney Injury in LDL Receptor-Deficient Mice

Ccl2 and Ccl3 Mediate Neutrophil Recruitment via Induction of Protein Synthesis and Generation of Lipid Mediators

Bone Marrow–Derived Cell-Specific Chemokine (C-C Motif) Receptor-2 Expression is Required for Arteriolar Remodeling

CXCR4 Expression Determines Functional Activity of Bone Marrow–Derived Mononuclear Cells for Therapeutic Neovascularization in Acute Ischemia

Monocyte Chemoattractant Proteins Mediate Myocardial Microvascular Dysfunction in Swine Renovascular Hypertension

Stimulation of Coronary Collateral Growth by Granulocyte Stimulating Factor: Role of Reactive Oxygen Species

Somitovasculin, a Novel Endothelial-Specific Transcript Involved in the Vasculature Development

Therapeutic Potential of Unrestricted Somatic Stem Cells Isolated from Placental Cord Blood for Cardiac Repair Post Myocardial Infarction

c-Jun DNAzymes Inhibit Myocardial Inflammation, ROS Generation, Infarct Size, and Improve Cardiac Function After Ischemia-Reperfusion Injury

Nrf2 Protects Against Maladaptive Cardiac Responses to Hemodynamic Stress

Activation of Nrf2 in Endothelial Cells Protects Arteries From Exhibiting a Proinflammatory State

Dynamic Observation of Mechanically-Injured Mouse Femoral Artery Reveals an Antiinflammatory Effect of Renin Inhibitor

The 11β1 Integrin Has a Mechanistic Role in Control of Interstitial Fluid Pressure and Edema Formation in Inflammation

Cell Biology/Signaling

PPARβ/ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKC–Brief Report

Foxp3 Regulates Megakaryopoiesis and Platelet Function

Rapid Procoagulant Phosphatidylserine Exposure Relies on High Cytosolic Calcium Rather Than on Mitochondrial Depolarization

Disinhibition of SOD-2 Expression to Compensate for a Genetically Determined NO Deficit in Endothelial Cells–Brief Report

Upregulation of Glutathione Peroxidase Offsets Stretch-Induced Proatherogenic Gene Expression in Human Endothelial Cells

Flow Activation of AMP-Activated Protein Kinase in Vascular Endothelium Leads to Krüppel-Like Factor 2 Expression

Alzheimer Disease–Associated Peptide, Amyloid β40, Inhibits Vascular Regeneration With Induction of Endothelial Autophagy

The Phosphorylation Motif at Serine 225 Governs the Localization and Function of Sphingosine Kinase 1 in Resistance Arteries

Liver X Receptor–Mediated Induction of Cholesteryl Ester Transfer Protein Expression Is Selectively Impaired in Inflammatory Macrophages

Stimulation of Cholesterol Efflux by LXR Agonists in Cholesterol-Loaded Human Macrophages Is ABCA1-Dependent but ABCG1-Independent

Inhibition of Long-Chain Acyl Coenzyme A Synthetases During Fatty Acid Loading Induces Lipotoxicity in Macrophages

Saturated Fatty Acids Do Not Directly Stimulate Toll-Like Receptor Signaling

Statins Block Calcific Nodule Formation of Valvular Interstitial Cells by Inhibiting -Smooth Muscle Actin Expression

Clinical and Population Studies

Genome-Wide Association Identifies the ABO Blood Group as a Major Locus Associated With Serum Levels of Soluble E-Selectin

FVII, FVIIa, and Downstream Markers of Extrinsic Pathway Activation Differ by EPCR Ser219Gly Variant in Healthy Men

Ion Mobility Analysis of Lipoprotein Subfractions Identifies Three Independent Axes of Cardiovascular Risk

Spotlight

Lack of Tyrosylprotein Sulfotransferase Activity in Hematopoietic Cells Drastically Attenuates Atherosclerosis in Ldlr^–/– Mice

Level of Macrophage uPA Expression Is an Important Determinant of Atherosclerotic Lesion Growth in Apoe^–/– Mice

The ${alpha}$ 11β1 Integrin Has a Mechanistic Role in Control of Interstitial Fluid Pressure and Edema Formation in Inflammation

PPARβ/ ${delta}$ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKC ${alpha}$ –Brief Report

Statins Block Calcific Nodule Formation of Valvular Interstitial Cells by Inhibiting ${alpha}$ -Smooth Muscle Actin Expression