Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (29 [12])

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Volume 29, Issue 12; December 1, 2009

Editorials
Brief Reviews
Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Clinical and Population Studies
Corrections
Editorials Board

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

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	Editorials
	Atherosclerosis: Should We Stop TWEAKing It? Victoria L. King Arterioscler Thromb Vasc Biol. 2009;29:1982-1983, doi:10.1161/ATVBAHA.109.197228 Extract \| Full Text \| PDF
	ApoAII Controversy Still in Rabbit? Hitoshi Shimano Arterioscler Thromb Vasc Biol. 2009;29:1984-1985, doi:10.1161/ATVBAHA.109.196683 Extract \| Full Text \| PDF
	Brief Reviews
	Tissue Factor: Past, Present, and Future Nigel Mackman and Mark Taubman Arterioscler Thromb Vasc Biol. 2009;29:1986-1988, doi:10.1161/ATVBAHA.109.198929 Extract \| Full Text \| PDF
	Tissue Factor in Coagulation: Which? Where? When? Saulius Butenas, Thomas Orfeo, and Kenneth G. Mann Arterioscler Thromb Vasc Biol. 2009;29:1989-1996; published online before print July 10 2009, doi:10.1161/ATVBAHA.108.177402 Abstract \| Full Text \| PDF Reports related to TF structure-function and to the role of TF during various phases of the blood coagulation process are presented. Controversies concerning the presence, expression, and activation of TF on various cells and in blood in normal and pathological states are also discussed.
	What Is Wrong With the Allosteric Disulfide Bond Hypothesis? Ronald R. Bach and Dougald Monroe Arterioscler Thromb Vasc Biol. 2009;29:1997-1998, doi:10.1161/ATVBAHA.109.194985 Extract \| Full Text \| PDF
	Tissue Factor and PAR2 Signaling in the Tumor Microenvironment Florence Schaffner and Wolfram Ruf Arterioscler Thromb Vasc Biol. 2009;29:1999-2004; published online before print August 6 2009, doi:10.1161/ATVBAHA.108.177428 Abstract \| Full Text \| PDF Tumor cell TF-VIIa-PAR2 signaling shapes the tumor microenvironment by inducing proangiogenic and immune modulating cytokines, chemokines, and growth factors. Selective inhibition of TF-PAR2 signaling is sufficient to reduce tumor angiogenesis and primary breast cancer growth, demonstrating that coagulation signaling can be targeted for therapeutic benefit.
	Tissue Factor and Cancer Stem Cells: Is There a Linkage? Chloe Milsom, Nathalie Magnus, Brian Meehan, Khalid Al-Nedawi, Delphine Garnier, and Janusz Rak Arterioscler Thromb Vasc Biol. 2009;29:2005-2014; published online before print July 23 2009, doi:10.1161/ATVBAHA.108.177444 Abstract \| Full Text \| PDF
	Protein S as Cofactor for TFPI Tilman M. Hackeng and Jan Rosing Arterioscler Thromb Vasc Biol. 2009;29:2015-2020; published online before print August 6 2009, doi:10.1161/ATVBAHA.108.177436 Abstract \| Full Text \| PDF
	Integrative Physiology/Experimental Medicine
	Fn14-Fc Fusion Protein Regulates Atherosclerosis in ApoE^–/– Mice and Inhibits Macrophage Lipid Uptake In Vitro Kitty Schapira, Linda C. Burkly, Timothy S. Zheng, Ping Wu, Mathijs Groeneweg, Mat Rousch, Mark M. Kockx, Mat J.A.P. Daemen, and Sylvia Heeneman Arterioscler Thromb Vasc Biol. 2009;29:2021-2027; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.195040 Abstract \| Full Text \| PDF \| Data Supplement The role of TWEAK and its receptor Fn14 were investigated in a mouse model of atherosclerosis. Treatment with an Fn14-Fc fusion protein to inhibit TWEAK resulted in advanced plaques with an increased abundance of macrophages and smaller macrophage size. Blocking TWEAK inhibited macrophage uptake of modified lipids in vitro.
	Acipimox, an Inhibitor of Lipolysis, Attenuates Atherogenesis in LDLR-Null Mice Treated With HIV Protease Inhibitor Ritonavir Wen Guo, Siu Wong, Jeffrey Pudney, Ravi Jasuja, Ning Hua, Lan Jiang, Andrew Miller, Paul W. Hruz, James A. Hamilton, and Shalender Bhasin Arterioscler Thromb Vasc Biol. 2009;29:2028-2032; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.191304 Abstract \| Full Text \| PDF \| Data Supplement This work provides the first evidence that lipolysis inhibitor acipimox antagonizes premature atherogenesis in LDLR-null mice induced by ritonavir, and supports the hypothesis that dysregulation of adipose tissue lipolysis attributable to impaired insulin action may contribute to the proatherogenic side effects of selected HIV protease inhibitors.
	Absence of Akt1 Reduces Vascular Smooth Muscle Cell Migration and Survival and Induces Features of Plaque Vulnerability and Cardiac Dysfunction During Atherosclerosis Carlos Fernández-Hernando, Levente József, Deborah Jenkins, Annarita Di Lorenzo, and William C. Sessa Arterioscler Thromb Vasc Biol. 2009;29:2033-2040; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.196394 Abstract \| Full Text \| PDF \| Data Supplement Deletion of Akt1 leads to severe atherosclerosis and occlusive coronary artery disease. Here, we report that Akt1 is essential for VSMC proliferation, migration, and protection against oxidative stress-induced apoptosis. Moreover, we show that absence of Akt1 in mice induces features of plaque vulnerability such as enlarged necrotic core formation and reduced fibrous cap.
	Increased PAFAH and Oxidized Lipids Are Associated With Inflammation and Atherosclerosis in Hypercholesterolemic Pigs Dieuwke De Keyzer, Sonia-Athina Karabina, Wenhzong Wei, Benjamine Geeraert, Dominique Stengel, Judit Marsillach, Jordi Camps, Paul Holvoet, and Ewa Ninio Arterioscler Thromb Vasc Biol. 2009;29:2041-2046; published online before print October 1 2009, doi:10.1161/ATVBAHA.109.196592 Abstract \| Full Text \| PDF \| Data Supplement In hypercholesterolemic minipigs, increased PAFAH activity was associated with increased circulating oxidized LDL. This association was further supported by our cell experiments, in which oxidized LDL induced PAFAH gene expression. The increase in PAFAH was also associated with an increase in proinflammatory gene expression in plaque macrophages and with accelerated atherosclerosis.
	Expression of Human ApoAII in Transgenic Rabbits Leads to Dyslipidemia: A New Model for Combined Hyperlipidemia Tomonari Koike, Shuji Kitajima, Ying Yu, Ying Li, Kazutoshi Nishijima, Enqi Liu, Huijun Sun, Ahmed Bilal Waqar, Nobumitsu Shibata, Tomoriho Inoue, Yao Wang, Bo Zhang, Junji Kobayashi, Masatoshi Morimoto, Keijiro Saku, Teruo Watanabe, and Jianglin Fan Arterioscler Thromb Vasc Biol. 2009;29:2047-2053; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.190264 Abstract \| Full Text \| PDF \| Data Supplement In this study, we generated transgenic rabbits expressing human apoAII and found that expression of human apoAII resulted in elevated plasma levels of triglycerides, total cholesterol, and phospholipids accompanied by reduced plasma HDL-C. Human apoAII transgenic rabbits may become a useful model for the study of combined hyperlipidemia.
	Increased HDL Cholesterol and ApoA-I in Humans and Mice Treated With a Novel SR-BI Inhibitor David Masson, Masahiro Koseki, Minako Ishibashi, Christopher J. Larson, Stephen G. Miller, Bernard D. King, and Alan R. Tall Arterioscler Thromb Vasc Biol. 2009;29:2054-2060; published online before print October 8 2009, doi:10.1161/ATVBAHA.109.191320 Abstract \| Full Text \| PDF \| Data Supplement ITX5061 initially characterized as a p38 MAPK inhibitor increased HDL-C and apo A-I in humans and mice. In vivo and in vitro experiments indicated that ITX5061 raised HDL cholesterol levels by inhibition of SR-BI activity. Finally, ITX5061 reduced atherosclerotic lesions in the aortic arch in Ldlr+/- mice fed the Paigen diet for 18 weeks.
	Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) Enhances Vascular and Renal Damage Induced by Hyperlipidemic Diet in ApoE-Knockout Mice Begoña Muñoz-García, Juan Antonio Moreno, Oscar López-Franco, Ana Belén Sanz, José Luis Martín-Ventura, Julia Blanco, Aniela Jakubowski, Linda C. Burkly, Alberto Ortiz, Jesús Egido, and Luis Miguel Blanco-Colio Arterioscler Thromb Vasc Biol. 2009;29:2061-2068; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.194852 Abstract \| Full Text \| PDF \| Data Supplement
	Effect of Leptin on Vascular Calcification in Apolipoprotein E–Deficient Mice Melec Zeadin, Martin Butcher, Geoff Werstuck, Mohammad Khan, Colin K. Yee, and Stephen G. Shaughnessy Arterioscler Thromb Vasc Biol. 2009;29:2069-2075; published online before print October 1 2009, doi:10.1161/ATVBAHA.109.195255 Abstract \| Full Text \| PDF ApoE-deficient mice placed on a high-fat diet were given daily i.p injections of saline or recombinant leptin. Leptin-treated mice demonstrated an increase in valvular and atherosclerotic lesion calcification. The increase in calcification was accompanied by an increase in the expression of osteoblast-specific markers, alkaline phosphatase, osteopontin, and osteocalcin.
	Combined Therapy With Simvastatin and Bone Marrow–Derived Mesenchymal Stem Cells Increases Benefits in Infarcted Swine Hearts Yue-Jin Yang, Hai-Yan Qian, Ji Huang, Jian-Jun Li, Run-Lin Gao, Ke-Fei Dou, Guo-Sheng Yang, James T. Willerson, and Yong-Jian Geng Arterioscler Thromb Vasc Biol. 2009;29:2076-2082; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.189662 Abstract \| Full Text \| PDF \| Data Supplement Extensive transplanted cell death hampers the efficacy of cellular cardiomyoplasty in treating myocardial infarction. Based on the pleiotropic effects of statins, we hypothesized and tested that statins can improve the postinfarction myocardial microenvironment to improve the survival and bioactivities of implanted mesenchymal stem cells after myocardial infarction.
	Discrete Contributions of Elastic Fiber Components to Arterial Development and Mechanical Compliance Luca Carta, Jessica E. Wagenseil, Russell H. Knutsen, Boubacar Mariko, Gilles Faury, Elaine C. Davis, Barry Starcher, Robert P. Mecham, and Francesco Ramirez Arterioscler Thromb Vasc Biol. 2009;29:2083-2089; published online before print October 22 2009, doi:10.1161/ATVBAHA.109.193227 Abstract \| Full Text \| PDF Mice with discrete deficiencies in elastic fiber components demonstrate the unique role of elastin in baseline blood pressure and vessel morphology, the discrete mechanical functions and overlapping material properties of fibrillin-1 and elastin in arterial tissues, and the involvement of fibrillin-1 in the hypertension-promoted remodeling of the elastin-deficient aorta.
	Mapping 3-Dimensional Neovessel Organization Steps Using Micro-Computed Tomography in a Murine Model of Hindlimb Ischemia–Brief Report Pierre Oses, Marie-Ange Renault, Rémi Chauvel, Lionel Leroux, Cécile Allières, Benjamin Séguy, Jean-Marie Daniel Lamazière, Pascale Dufourcq, Thierry Couffinhal, and Cécile Duplàa Arterioscler Thromb Vasc Biol. 2009;29:2090-2092; published online before print September 10 2009, doi:10.1161/ATVBAHA.109.192732 Abstract \| Full Text \| PDF \| Data Supplement We evaluated using microcomputed tomography (mCT) method mouse hindlimb postischemic neovascularization. We uncovered a predominant arteriogenesis and angiogenesis-related processes respectively in the thigh an tibiofibular regions. We provided new mCT data on the rapid and potent angiogenic effects of mesenchymal stem cell therapy on vessel formation and organization.
	Actin-Binding Rho Activating Protein (Abra) Is Essential for Fluid Shear Stress-Induced Arteriogenesis Kerstin Troidl, Inka Rüding, Wei-Jun Cai, Yvonne Mücke, Leonie Grossekettler, Izabela Piotrowska, Hanna Apfelbeck, Wilma Schierling, Oscar L. Volger, Anton J. Horrevoets, Karsten Grote, Thomas Schmitz-Rixen, Wolfgang Schaper, and Christian Troidl Arterioscler Thromb Vasc Biol. 2009;29:2093-2101; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.195305 Abstract \| Full Text \| PDF \| Data Supplement In a rat model of chronically elevated fluid shear stress we show that Actin-binding Rho activating protein (Abra) is upregulated in growing collaterals and serves as an inducer of arteriogenesis. Our results indicate that FSS-induced Abra expression during arteriogenesis is triggered by NO and leads to stimulation of collateral growth by smooth muscle cell proliferation.
	Ablation of Angiotensin IV Receptor Attenuates Hypofibrinolysis via PAI-1 Downregulation and Reduces Occlusive Arterial Thrombosis Yasushi Numaguchi, Masakazu Ishii, Ryuji Kubota, Yasuhiro Morita, Koji Yamamoto, Tadashi Matsushita, Kenji Okumura, and Toyoaki Murohara Arterioscler Thromb Vasc Biol. 2009;29:2102-2108; published online before print September 10 2009, doi:10.1161/ATVBAHA.109.195057 Abstract \| Full Text \| PDF \| Data Supplement Knockout mice for insulin-regulated aminopeptidase, identified as the novel angiotensin IV receptor (AT4R), showed accelerated fibrinolysis in an endotoxin-induced microcoagulation model and decreased occlusive thrombosis in a carotid artery double-injury model when compared with control mice, partly because of suppressed induction of plasminogen activator inhibitor type 1 and inhibition of inflammation.
	Cell Biology/Signaling
	Matrix Metalloproteinase-10 Is Upregulated by Thrombin in Endothelial Cells and Increased in Patients With Enhanced Thrombin Generation Josune Orbe, José A. Rodríguez, Olivier Calvayrac, Ricardo Rodríguez-Calvo, Cristina Rodríguez, Carmen Roncal, Sara Martínez de Lizarrondo, Jaione Barrenetxe, Juan C. Reverter, José Martínez-González, and José A. Páramo Arterioscler Thromb Vasc Biol. 2009;29:2109-2116; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.194589 Abstract \| Full Text \| PDF \| Data Supplement Thrombin can interact with extracellular matrix components and promote vascular proinflammatory responses including MMP upregulation. We show that thrombin induces endothelial MMP-10, in vitro and in vivo, through a PAR-1-dependent mechanism mediated by ERK1/2, JNK, and AP-1 activation. Increased MMP-10 can be observed in pathologies with augmented thrombin generation.
	The ADMA/DDAH Pathway Regulates VEGF-Mediated Angiogenesis Lorna R Fiedler, Tiziana Bachetti, James Leiper, Ian Zachary, Lihua Chen, Thomas Renné, and Beata Wojciak-Stothard Arterioscler Thromb Vasc Biol. 2009;29:2117-2124; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.194035 Abstract \| Full Text \| PDF \| Data Supplement The endogenous NO synthase inhibitor and cardiovascular risk factor ADMA inhibits angiogenesis. We show for the first time that ADMA inhibits VEGF-induced endothelial cell motility and angiogenesis by modulating NO-dependent Rho GTPase activity. Further, normal angiogenic responses to VEGF are restored by overexpression of DDAH or active Rac1.
	Shear Stress Increases Expression of the Arterial Endothelial Marker EphrinB2 in Murine ES Cells via the VEGF-Notch Signaling Pathways Tomomi Masumura, Kimiko Yamamoto, Nobutaka Shimizu, Syotaro Obi, and Joji Ando Arterioscler Thromb Vasc Biol. 2009;29:2125-2131; published online before print October 1 2009, doi:10.1161/ATVBAHA.109.193185 Abstract \| Full Text \| PDF We have demonstrated in vitro that shear stress increases expression of the arterial endothelial cell marker ephrinB2 in murine ES cell-derived VEGFR2+ cells. VEGF-Notch signaling pathways, in which VEGF receptor phosphorylation leads to Notch activation, was involved in the upregulation of ephrinB2 expression. Shear stress may have an effect on the arterial-differentiation of ES cell-derived endothelial cells.
	Inhibition of Prolyl Hydroxylase Domain-Containing Protein Suppressed Lipopolysaccharide-Induced TNF- ${alpha}$ Expression Kotaro Takeda, Toshihiro Ichiki, Eriko Narabayashi, Keita Inanaga, Ryohei Miyazaki, Toru Hashimoto, Hirohide Matsuura, Jiro Ikeda, Toshio Miyata, and Kenji Sunagawa Arterioscler Thromb Vasc Biol. 2009;29:2132-2137; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.196071 Abstract \| Full Text \| PDF \| Data Supplement Prolyl hydroxylase domain-containing proteins (PHDs) play pivotal roles in oxygen-sensing system. We demonstrated here that PHD is also a key regulator of inflammation. PHD inhibition strongly attenuated lipopolysaccharide-induced tumor necrosis factor {alpha} expression in macrophages. Therefore, PHD inhibition may be a novel strategy for the treatment of inflammatory diseases.
	Tumor Necrosis Factor- ${alpha}$ Potentiates RhoA-Mediated Monocyte Transmigratory Activity In Vivo at a Picomolar Level Sunny Lim, Jewon Ryu, Jin-Ae Shin, Min-Jung Shin, Yeong Ki Ahn, Jae Joong Kim, and Ki Hoon Han Arterioscler Thromb Vasc Biol. 2009;29:2138-2145; published online before print September 10 2009, doi:10.1161/ATVBAHA.109.195735 Abstract \| Full Text \| PDF \| Data Supplement In response to picomolar levels of TNF-{alpha} detected in serum under inflammatory conditions, human monocytes display enhanced translocation of RhoA to the plasma membrane via ezrin/radixin/moesin complex that is phosphorylated by TNFRI-derived PKC{zeta}. Monocytes pretreated with picomolar TNF-{alpha} eventually display more potent RhoA-mediated transmigration in response to MCP-1 in vivo.
	Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells Md Saha Jamaluddin, Xinwen Wang, Hao Wang, Cubas Rafael, Qizhi Yao, and Changyi Chen Arterioscler Thromb Vasc Biol. 2009;29:2146-2152; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.194134 Abstract \| Full Text \| PDF \| Data Supplement Eotaxin, a newly discovered chemokine (CCL11), significantly increases vascular permeability through the downregulation of tight junction proteins, increase of oxidative stress, and activation of MAPK p38, Stat3, and NF-{kappa}B in human coronary artery endothelial cells, suggesting an important role for eotaxin in endothelial dysfunction during the vascular lesion formation.
	PKA-Dependent Phosphorylation of Serum Response Factor Inhibits Smooth Muscle–Specific Gene Expression Alicia L. Blaker, Joan M. Taylor, and Christopher P. Mack Arterioscler Thromb Vasc Biol. 2009;29:2153-2160; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.197285 Abstract \| Full Text \| PDF \| Data Supplement By screening SRF mutations in an SRF-/- ES model of SMC differentiation, we identified T159 as a phosphorylation site that inhibits SMC-specific gene expression. T159 was phosphorylated by PKA in vitro and in vivo, and this modification inhibited SRF activity by attenuating SRF binding to the SMC-specific CArG elements.
	Identification and Functional Characterization of Phosphorylation Sites on GTP Cyclohydrolase I Jianhai Du, Na Wei, Hao Xu, Ying Ge, Jeannette Vásquez-Vivar, Tongju Guan, Keith T. Oldham, Kirkwood A. Pritchard, Jr, and Yang Shi Arterioscler Thromb Vasc Biol. 2009;29:2161-2168; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.194464 Abstract \| Full Text \| PDF \| Data Supplement The regulation of GCH-1 is not fully understood. We identified 8 putative phosphorylation sites on GCH-1. Our study suggests that GCH-1 is phosphorylated at S51, S167, and T231 and GCH-1 activity is regulated by phosphorylation positively at sites S51, S72, T85, T91, T103, and S130 and negatively at site T231.
	HDL3-Mediated Inactivation of LDL-Associated Phospholipid Hydroperoxides Is Determined by the Redox Status of Apolipoprotein A-I and HDL Particle Surface Lipid Rigidity: Relevance to Inflammation and Atherogenesis Amal Zerrad-Saadi, Patrice Therond, Sandrine Chantepie, Martine Couturier, Kerry-Anne Rye, M. John Chapman, and Anatol Kontush Arterioscler Thromb Vasc Biol. 2009;29:2169-2175; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.194555 Abstract \| Full Text \| PDF \| Data Supplement Redox status of apoAI and surface lipid rigidity of dense HDL3 particles are critical to their potent capacity to protect LDL against free radical-induced oxidation. Transfer of LDL-associated phospholipid hydroperoxides to HDL3 with their subsequent reduction to hydroxides by methionine residues of apoAI is central to such antioxidative activity.
	Clinical and Population Studies
	High Factor VIII Levels Independently Predict Venous Thromboembolism in Cancer Patients: The Cancer and Thrombosis Study R. Vormittag, R. Simanek, C. Ay, D. Dunkler, P. Quehenberger, C. Marosi, C. Zielinski, and I. Pabinger Arterioscler Thromb Vasc Biol. 2009;29:2176-2181; published online before print September 24 2009, doi:10.1161/ATVBAHA.109.190827 Abstract \| Full Text \| PDF In the prospective observational Cancer and Thrombosis Study we followed 840 patients over a median observation time of 495 days. 62 events of symptomatic venous thromboembolism (VTE) were observed. High factor VIII levels independently increased the risk of VTE. The risk increase was higher in younger than in older patients.
	Hemostasis, Inflammation, and Fatal and Nonfatal Coronary Heart Disease: Long-Term Follow-Up of the Atherosclerosis Risk in Communities (ARIC) Cohort Anna M. Kucharska-Newton, David J. Couper, James S. Pankow, Ronald J. Prineas, Thomas D. Rea, Nona Sotoodehnia, Aravinda Chakravarti, Aaron R. Folsom, David S. Siscovick, and Wayne D. Rosamond Arterioscler Thromb Vasc Biol. 2009;29:2182-2190; published online before print October 1 2009, doi:10.1161/ATVBAHA.109.192740 Abstract \| Full Text \| PDF Von Willebrand factor and factor VIIIc were associated with an increased risk of cardiac death as compared to the risk of nonfatal MI during an average 12.4 years of follow-up of the ARIC cohort.
	PCSK9 Dominant Negative Mutant Results in Increased LDL Catabolic Rate and Familial Hypobetalipoproteinemia Bertrand Cariou, Khadija Ouguerram, Yassine Zaïr, Raphael Guerois, Cédric Langhi, Sanae Kourimate, Isabelle Benoit, Cédric Le May, Constance Gayet, Khaldia Belabbas, Fabienne Dufernez, Maud Chétiveaux, Patrizia Tarugi, Michel Krempf, Pascale Benlian, and Philippe Costet Arterioscler Thromb Vasc Biol. 2009;29:2191-2197; published online before print September 17 2009, doi:10.1161/ATVBAHA.109.194191 Abstract \| Full Text \| PDF \| Data Supplement We identified a subject with profound hypobetalipoproteinemia heterozygous for 2 PCSK9 R104C and V114A monoallelic mutations. In vitro, this variant is virtually neither processed nor secreted, acting as a dominant negative over wild-type PCSK9. Lipoprotein kinetic studies showed an increased fractional LDL catabolic rate cosegregating with the mutation.
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2009;29:e132, doi:10.1161/01.atv.0000363769.57850.20 Extract \| Full Text \| PDF
	Correction Arterioscler Thromb Vasc Biol. 2009;29:e133, doi:10.1161/01.atv.0000363770.34980.d7 Extract \| Full Text \| PDF
	Correction Arterioscler Thromb Vasc Biol. 2009;29:e134, doi:10.1161/01.atv.0000363771.42603.73 Extract \| Full Text \| PDF
	Editorials Board
	Editorial Board Arterioscler Thromb Vasc Biol. 2009;29:1981, doi:10.1161/01.atv.0000364860.97790.24 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 29, Issue 12; December 1, 2009

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

Editorials

Atherosclerosis: Should We Stop TWEAKing It?

ApoAII Controversy Still in Rabbit?

Brief Reviews

Tissue Factor: Past, Present, and Future

Tissue Factor in Coagulation: Which? Where? When?

What Is Wrong With the Allosteric Disulfide Bond Hypothesis?

Tissue Factor and PAR2 Signaling in the Tumor Microenvironment

Tissue Factor and Cancer Stem Cells: Is There a Linkage?

Protein S as Cofactor for TFPI

Integrative Physiology/Experimental Medicine

Fn14-Fc Fusion Protein Regulates Atherosclerosis in ApoE–/– Mice and Inhibits Macrophage Lipid Uptake In Vitro

Acipimox, an Inhibitor of Lipolysis, Attenuates Atherogenesis in LDLR-Null Mice Treated With HIV Protease Inhibitor Ritonavir

Absence of Akt1 Reduces Vascular Smooth Muscle Cell Migration and Survival and Induces Features of Plaque Vulnerability and Cardiac Dysfunction During Atherosclerosis

Increased PAFAH and Oxidized Lipids Are Associated With Inflammation and Atherosclerosis in Hypercholesterolemic Pigs

Expression of Human ApoAII in Transgenic Rabbits Leads to Dyslipidemia: A New Model for Combined Hyperlipidemia

Increased HDL Cholesterol and ApoA-I in Humans and Mice Treated With a Novel SR-BI Inhibitor

Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) Enhances Vascular and Renal Damage Induced by Hyperlipidemic Diet in ApoE-Knockout Mice

Effect of Leptin on Vascular Calcification in Apolipoprotein E–Deficient Mice

Combined Therapy With Simvastatin and Bone Marrow–Derived Mesenchymal Stem Cells Increases Benefits in Infarcted Swine Hearts

Discrete Contributions of Elastic Fiber Components to Arterial Development and Mechanical Compliance

Mapping 3-Dimensional Neovessel Organization Steps Using Micro-Computed Tomography in a Murine Model of Hindlimb Ischemia–Brief Report

Actin-Binding Rho Activating Protein (Abra) Is Essential for Fluid Shear Stress-Induced Arteriogenesis

Ablation of Angiotensin IV Receptor Attenuates Hypofibrinolysis via PAI-1 Downregulation and Reduces Occlusive Arterial Thrombosis

Cell Biology/Signaling

Matrix Metalloproteinase-10 Is Upregulated by Thrombin in Endothelial Cells and Increased in Patients With Enhanced Thrombin Generation

The ADMA/DDAH Pathway Regulates VEGF-Mediated Angiogenesis

Shear Stress Increases Expression of the Arterial Endothelial Marker EphrinB2 in Murine ES Cells via the VEGF-Notch Signaling Pathways

Inhibition of Prolyl Hydroxylase Domain-Containing Protein Suppressed Lipopolysaccharide-Induced TNF- Expression

Tumor Necrosis Factor- Potentiates RhoA-Mediated Monocyte Transmigratory Activity In Vivo at a Picomolar Level

Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

PKA-Dependent Phosphorylation of Serum Response Factor Inhibits Smooth Muscle–Specific Gene Expression

Identification and Functional Characterization of Phosphorylation Sites on GTP Cyclohydrolase I

HDL3-Mediated Inactivation of LDL-Associated Phospholipid Hydroperoxides Is Determined by the Redox Status of Apolipoprotein A-I and HDL Particle Surface Lipid Rigidity: Relevance to Inflammation and Atherogenesis

Clinical and Population Studies

High Factor VIII Levels Independently Predict Venous Thromboembolism in Cancer Patients: The Cancer and Thrombosis Study

Hemostasis, Inflammation, and Fatal and Nonfatal Coronary Heart Disease: Long-Term Follow-Up of the Atherosclerosis Risk in Communities (ARIC) Cohort

PCSK9 Dominant Negative Mutant Results in Increased LDL Catabolic Rate and Familial Hypobetalipoproteinemia

Corrections

Correction

Correction

Correction

Editorials Board

Editorial Board

Spotlight

Fn14-Fc Fusion Protein Regulates Atherosclerosis in ApoE^–/– Mice and Inhibits Macrophage Lipid Uptake In Vitro

Inhibition of Prolyl Hydroxylase Domain-Containing Protein Suppressed Lipopolysaccharide-Induced TNF- ${alpha}$ Expression

Tumor Necrosis Factor- ${alpha}$ Potentiates RhoA-Mediated Monocyte Transmigratory Activity In Vivo at a Picomolar Level