Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [6])

Volume 25, Issue 6; June 1, 2005

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

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	Editorials
	Toll To Be Paid at the Gateway to the Vessel Wall Göran K. Hansson and Kristina Edfeldt Arterioscler Thromb Vasc Biol. 2005;25:1085-1087, doi:10.1161/01.ATV.0000168894.43759.47. Full Text \| PDF
	CD40 Ligand: Not Bad to the Bone (Marrow), After All Olujimi A. Ajijola, Pascal J. Goldschmidt-Clermont, and Lisa L. Satterwhite Arterioscler Thromb Vasc Biol. 2005;25:1088-1090, doi:10.1161/01.ATV.0000169538.64914.70. Full Text \| PDF
	CRP or not CRP? That Is the Question Mark B. Pepys Arterioscler Thromb Vasc Biol. 2005;25:1091-1094, doi:10.1161/01.ATV.0000169644.88847.28. Full Text \| PDF
	Antiatherogenic Properties of Fibrates P.J. Barter Arterioscler Thromb Vasc Biol. 2005;25:1095-1096, doi:10.1161/01.ATV.0000168895.21726.20. Full Text \| PDF
	ApoA-V: The Regulation of a Regulator of Plasma Triglycerides Sven-Olof Olofsson Arterioscler Thromb Vasc Biol. 2005;25:1097-1099, doi:10.1161/01.ATV.0000167518.27125.b1. Full Text \| PDF
	Quest for Genes Regulating Plasma Fibrinogen Concentration: Still a Long Way to Go Anders Hamsten, Maria Nastase Mannila, and Angela Silveira Arterioscler Thromb Vasc Biol. 2005;25:1100-1101, doi:10.1161/01.ATV.0000167519.47426.83. Full Text \| PDF
	Brief Reviews
	Myeloperoxidase and Cardiovascular Disease Stephen J. Nicholls and Stanley L. Hazen Arterioscler Thromb Vasc Biol. 2005;25:1102-1111; published online before print March 24 2005, doi:10.1161/01.ATV.0000163262.83456.6d. Abstract \| Full Text \| PDF Myeloperoxidase-catalyzed reactions have been attributed to potentially proatherogenic biological activities throughout the evolution of cardiovascular disease, including during initiation, propagation, and acute complication phases of the atherosclerotic process. As a result, myeloperoxidase and its downstream inflammatory pathways represent attractive targets for both prognostication and therapeutic intervention in the prophylaxis of atherosclerotic cardiovascular disease.
	ACAT2 Is a Target for Treatment of Coronary Heart Disease Associated With Hypercholesterolemia Lawrence L. Rudel, Richard G. Lee, and Paolo Parini Arterioscler Thromb Vasc Biol. 2005;25:1112-1118; published online before print April 14 2005, doi:10.1161/01.ATV.0000166548.65753.1e. Abstract \| Full Text \| PDF The inhibition of intracellular esterification of cholesterol as a means to prevent the arterial cholesteryl ester accumulation in atherosclerosis has been a strategy considered to have potential throughout the scientific community for many years. Presently, the bulk of the available data suggest that the strategy seeming to bear the most potential for treatment of coronary heart disease associated with hypercholesterolemia would be to specifically inhibit ACAT2.
	Extracellular Proteases in Atherosclerosis and Restenosis Arturo Garcia-Touchard, Timothy D. Henry, Giuseppe Sangiorgi, Luigi Giusto Spagnoli, Alessandro Mauriello, Cheryl Conover, and Robert S. Schwartz Arterioscler Thromb Vasc Biol. 2005;25:1119-1127; published online before print March 31 2005, doi:10.1161/01.ATV.0000164311.48592.da. Abstract \| Full Text \| PDF Extracellular proteases are a complex and heterogeneous family of enzymes involved in many important biological functions. This review discusses the extracellular proteases relevant to the vasculature, their functions, and how protease disorders can contribute to plaque growth, including chronic atherosclerosis, acute coronary syndromes, restenosis, and vascular remodeling.
	Tissue-Engineered Blood Vessels: Alternative to Autologous Grafts? Michel R. Hoenig, Gordon R. Campbell, Barbara E. Rolfe, and Julie H. Campbell Arterioscler Thromb Vasc Biol. 2005;25:1128-1134; published online before print February 10 2005, doi:10.1161/01.ATV.0000158996.03867.72. Abstract \| Full Text \| PDF Several laboratories have produced tissue-engineered blood vessels using molds or prosthetic or biodegradable scaffolds, but each has significant problems. Recently, autologous vascular conduits, derived from cells of bone marrow origin, have been grown in the peritoneal cavity of animals. This technology opens new possibilities in vascular modeling and remodeling.
	Vascular Implications of the Krüppel-Like Family of Transcription Factors Toru Suzuki, Kenichi Aizawa, Takayoshi Matsumura, and Ryozo Nagai Arterioscler Thromb Vasc Biol. 2005;25:1135-1141; published online before print April 7 2005, doi:10.1161/01.ATV.0000165656.65359.23. Abstract \| Full Text \| PDF The Kruppel-like factor (KLF) family is a recently highlighted group of zinc finger transcription factors given their important biological roles, which include the vasculature. KLF2, KLF4, KLF5, and KLF6 are notable factors that have been implicated in developmental as well as pathological vascular processes. In this brief review, we aim to provide a working view for understanding the pathological actions of KLFs in the vasculature.
	Vascular Biology
	Mechanisms of Reactive Oxygen Species–Dependent Downregulation of Insulin Receptor Substrate-1 by Angiotensin II Yoshihiro Taniyama, Hirofumi Hitomi, Anand Shah, R. Wayne Alexander, and Kathy K. Griendling Arterioscler Thromb Vasc Biol. 2005;25:1142-1147; published online before print March 31 2005, doi:10.1161/01.ATV.0000164313.17167.df. Abstract \| Full Text \| PDF \| Data Supplement Angiotensin II and reactive oxygen species (ROS) mediate insulin resistance, but the underlying mechanisms are unclear. In vascular smooth muscle cells, angiotensin II induces IRS-1 phosphorylation and degradation via Src, PDK1, and ROS. These events impair insulin signaling and may explain the role of angiotensin II in diabetic vasculopathy.
	A New Cellular Signaling Mechanism for Angiotensin II Activation of NF- ${kappa}$ B: An I ${kappa}$ B–Independent, RSK–Mediated Phosphorylation of p65 Liping Zhang, Yewei Ma, Jiqiang Zhang, Jizhong Cheng, and Jie Du Arterioscler Thromb Vasc Biol. 2005;25:1148-1153; published online before print March 31 2005, doi:10.1161/01.ATV.0000164624.00099.e7. Abstract \| Full Text \| PDF \| Data Supplement We examined an intracellular mechanism whereby Ang II activates NF-{kappa}B. Ang II caused no significant increase in I{kappa}B phosphorylation or protein levels. Instead, we found a nonclassical signaling pathway, Ras/MEK1/ERK/RSK, that activated NF-{kappa}B via phosphorylation of p65, leading to IL-6 production and suggesting a mechanism by which Ang II causes vascular inflammation.
	Regulation of Endothelial Cell and Endothelial Progenitor Cell Survival and Vasculogenesis by Integrin-Linked Kinase Hyun-Jai Cho, Seock-Won Youn, Soo-In Cheon, Tae-Youn Kim, Jin Hur, Shu-Ying Zhang, Seung Pyo Lee, Kyung-Woo Park, Myoung-Mook Lee, Yun-Shik Choi, Young-Bae Park, and Hyo-Soo Kim Arterioscler Thromb Vasc Biol. 2005;25:1154-1160; published online before print March 31 2005, doi:10.1161/01.ATV.0000164312.20008.93. Abstract \| Full Text \| PDF \| Data Supplement Neovascularization is a dynamic process of detachment and reattachment of ECs and EPCs. Endogenous integrin-linked kinase (ILK) expression was decreased in various stress conditions, and the gene transfer of ILK protected ECs and EPCs from temporary anchorage or nutrient deprivation. Futhermore, ILK gene transfer in EPCs significantly enhanced neovascularization in vivo.
	Autocrine and Paracrine Transcriptional Regulation of Type IIA Secretory Phospholipase A2 Gene in Vascular Smooth Muscle Cells Amandine Jaulmes, Brigitte Janvier, Marise Andreani, and Michel Raymondjean Arterioscler Thromb Vasc Biol. 2005;25:1161-1167; published online before print March 31 2005, doi:10.1161/01.ATV.0000164310.67356.a9. Abstract \| Full Text \| PDF \| Data Supplement A cell supernatant containing human sPLA2-IIA proteins increases the transcription of the sPLA2-IIA gene in rat and human VSMCs. This effect, independent of the sPLA2 catalytic activity, could involve a sPLA2 receptor and heparan sulfate proteoglycans binding. We thus describe a new autocrine role of sPLA2-IIA in VSMCs.
	Vascular Endothelial Growth Factor–Expressing Mesenchymal Stem Cell Transplantation for the Treatment of Acute Myocardial Infarction Ryo Matsumoto, Takashi Omura, Minoru Yoshiyama, Tetsuya Hayashi, Sakiko Inamoto, Ki-Ryang Koh, Kensuke Ohta, Yasukatsu Izumi, Yasuhiro Nakamura, Kaname Akioka, Yasushi Kitaura, Kazuhide Takeuchi, and Junichi Yoshikawa Arterioscler Thromb Vasc Biol. 2005;25:1168-1173; published online before print April 14 2005, doi:10.1161/01.ATV.0000165696.25680.ce. Abstract \| Full Text \| PDF \| Data Supplement We studied cell transplantation of VEGF-expressing mesenchymal stem cells (MSCs) on rat myocardial infarction (MI). Infarct size, left ventricular dimensions, ejection fraction, E wave/A wave ratio, and capillary density were most improved in the VEGF-expressing MSCs group. In conclusion, this cell transplantation with gene therapy could be a useful treatment for MI.
	Systemic Endothelial Dysfunction as an Early Predictor of Adverse Outcome in Heart Failure Thomas Heitzer, Stephan Baldus, Yskert von Kodolitsch, Volker Rudolph, and Thomas Meinertz Arterioscler Thromb Vasc Biol. 2005;25:1174-1179; published online before print April 14 2005, doi:10.1161/01.ATV.0000166516.52477.81. Abstract \| Full Text \| PDF Endothelium-dependent and endothelium-independent vasodilatation was assessed in 289 patients with mild heart failure by measuring forearm blood flow with and without vitamin C administered at pharmacological doses using venous occlusion plethysmography. During follow-up, patients experiencing adverse events had lower vasodilator responses to acetylcholine and sodium nitroprusside, but similar beneficial effects of vitamin C.
	Atherosclerosis and Lipoproteins
	Activation of ATP-Binding Cassette Transporter A1 Transcription by Chromatin Remodeling Complex Jarkko Huuskonen, Meeta Vishnu, Phoebe E. Fielding, and Christopher J. Fielding Arterioscler Thromb Vasc Biol. 2005;25:1180-1185; published online before print March 17 2005, doi:10.1161/01.ATV.0000163186.58462.c5. Abstract \| Full Text \| PDF \| Data Supplement Catalytic subunits of SWI/SNF chromatin remodeling complex, BRG-1 and brahma, enhanced ABCA1 transcription via the promoter DR-4 element. Physical interaction of LXR/RXR and BRG-1 and recruitment of BRG-1 to ABCA1 promoter was demonstrated. These results indicate that chromatin remodeling regulates ABCA1 transcription.
	Transcriptional Regulation of Apolipoprotein A5 Gene Expression by the Nuclear Receptor ROR ${alpha}$ Annelise Genoux, Hélène Dehondt, Audrey Helleboid-Chapman, Christian Duhem, Dean W. Hum, Geneviève Martin, Len A. Pennacchio, Bart Staels, Jamila Fruchart-Najib, and Jean-Charles Fruchart Arterioscler Thromb Vasc Biol. 2005;25:1186-1192; published online before print March 24 2005, doi:10.1161/01.ATV.0000163841.85333.83. Abstract \| Full Text \| PDF Apolipoprotein A5 has recently been identified as a crucial determinant of plasma triglyceride levels. Our results showed that ROR{alpha} upregulates human APOA5 but has no effect on mouse apoa5 gene. These data suggest an additional important physiological role for ROR{alpha} in the regulation of genes involved in lipid homeostasis in human and probably in the development of atherosclerosis.
	Fenofibric Acid, an Active Form of Fenofibrate, Increases Apolipoprotein A-I–Mediated High-Density Lipoprotein Biogenesis by Enhancing Transcription of ATP-Binding Cassette Transporter A1 Gene in a Liver X Receptor–Dependent Manner Reijiro Arakawa, Norimasa Tamehiro, Tomoko Nishimaki-Mogami, Kazumitsu Ueda, and Shinji Yokoyama Arterioscler Thromb Vasc Biol. 2005;25:1193-1197; published online before print March 24 2005, doi:10.1161/01.ATV.0000163844.07815.c4. Abstract \| Full Text \| PDF Fibrates are widely used drugs to reduce plasma triglyceride and increase high-density lipoprotein. Their active forms, fibric acids, are peroxisome proliferator-activated receptor-{alpha} activators, but no direct evidence has been demonstrated for their activation of ATP-binding cassette transporter A1 (ABCA1) in relation to clinically used fibrates. We investigated the reaction of fenofibric acid in this regard, finding that fenofibric acid increased transcription of ABCA1 gene in n liver X receptor-dependent manner.
	Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1-Deficient Macrophages Omar L. Francone, Lori Royer, Germaine Boucher, Mehrdad Haghpassand, Ann Freeman, Dominique Brees, and Robert J. Aiello Arterioscler Thromb Vasc Biol. 2005;25:1198-1205; published online before print April 14 2005, doi:10.1161/01.ATV.0000166522.69552.99. Abstract \| Full Text \| PDF The ABCA1 role in macrophage morphology, properties, and functional activities was examined in wild-type and Abca1-deficient mice. Our studies demonstrate that the absence of ABCA1 leads to an inflammatory activation of macrophages, accompanied by cholesterol loading, increased expression of scavenger receptors, and synthesis of chemokines, cytokines, and growth factors, resulting in an increased ability of macrophages to respond to a variety of chemotactic factors.
	High-Density Lipoproteins Prevent the Oxidized Low-Density Lipoprotein–Induced Endothelial Growth Factor Receptor Activation and Subsequent Matrix Metalloproteinase-2 Upregulation Fanny Robbesyn, Nathalie Augé, Cécile Vindis, Anne-Valérie Cantero, Ronald Barbaras, Anne Negre-Salvayre, and Robert Salvayre Arterioscler Thromb Vasc Biol. 2005;25:1206-1212; published online before print April 7 2005, doi:10.1161/01.ATV.0000164805.73558.80. Abstract \| Full Text \| PDF \| Data Supplement Oxidized LDLs induce EGFR activation and subsequent MMP-2 activation. HDLs inhibit these events by 2 separate mechanisms, ie, by blocking carbonyl-protein adduct formation and by inhibiting the oxLDL-induced and H2O2-induced intracellular ROS increase, through a catalase-dependent process. This may contribute to reduce cell activation, excessive remodeling, and vascular wall alteration.
	Toll-Like Receptor 4–Dependent and –Independent Cytokine Secretion Induced by Minimally Oxidized Low-Density Lipoprotein in Macrophages Yury I. Miller, Suganya Viriyakosol, Dorothy S. Worrall, Agnès Boullier, Susan Butler, and Joseph L. Witztum Arterioscler Thromb Vasc Biol. 2005;25:1213-1219; published online before print February 17 2005, doi:10.1161/01.ATV.0000159891.73193.31. Abstract \| Full Text \| PDF \| Data Supplement Minimally oxidized LDL (mmLDL) stimulated PI3K activation, Akt, and ERK1/2 phosphorylation, and induced mRNA and protein expression of MIP-2, MCP-1, TNF-{alpha}, and IL-6 in macrophages. MIP-2 but not MCP-1 secretion depended on TLR4/MyD88, ERK1/2, and PI3K signaling. Thus, mmLDL activates TLR4-dependent and independent proinflammatory signaling in macrophages.
	Adipocyte Fatty Acid–Binding Protein Expression and Lipid Accumulation Are Increased During Activation of Murine Macrophages by Toll-Like Receptor Agonists Mahmood R. Kazemi, Carol M. McDonald, Judy K. Shigenaga, Carl Grunfeld, and Kenneth R. Feingold Arterioscler Thromb Vasc Biol. 2005;25:1220-1224; published online before print February 10 2005, doi:10.1161/01.ATV.0000159163.52632.1b. Abstract \| Full Text \| PDF Given the key role of macrophage aP2 in atherosclerosis, we studied aP2 expression in macrophages stimulated with LPS and 2 other TLR ligands: zymosan and poly I:C. Treatment with LPS or zymosan, but not poly I:C, leads to significant increases in aP2 mRNA and protein, which parallel cholesteryl ester and triglyceride accumulation.
	C-Reactive Protein–Induced In Vitro Endothelial Cell Activation Is an Artefact Caused by Azide and Lipopolysaccharide Karolina E. Taylor, John C. Giddings, and Carmen W. van den Berg Arterioscler Thromb Vasc Biol. 2005;25:1225-1230; published online before print March 31 2005, doi:10.1161/01.ATV.0000164623.41250.28. Abstract \| Full Text \| PDF We investigated the validity of the numerous responses of endothelial cells attributed to CRP and demonstrate here that the reported effects are caused by low molecular weight contaminants, like azide and LPS, which are present in commercial CRP preparations.
	Statins Reduce Interleukin-6–Induced C-Reactive Protein in Human Hepatocytes: New Evidence for Direct Antiinflammatory Effects of Statins Claire Arnaud, Fabienne Burger, Sabine Steffens, Niels R. Veillard, Tuan Huy Nguyen, Didier Trono, and François Mach Arterioscler Thromb Vasc Biol. 2005;25:1231-1236; published online before print March 24 2005, doi:10.1161/01.ATV.0000163840.63685.0c. Abstract \| Full Text \| PDF C-reactive protein (CRP), mainly produced by hepatocytes in response to interleukin-6 (IL-6), is a powerful independent predictor of future cardiovascular events. In this study, we demonstrate that statins reduce IL-6-induced CRP production directly in hepatocytes. This effect is mimicked by an inhibitor of the geranylgeranyltransferase and we further demonstrate that statins act via reduction of STAT3 phosphorylation.
	Elevated Serum C-Reactive Protein Levels and Advanced Atherosclerosis in Youth Arthur W. Zieske, Russell P. Tracy, C. Alex McMahan, Edward E. Herderick, Satoki Homma, Gray T. Malcom, Henry C. McGill, Jr, Jack P. Strong for the Pathobiological Determinants of Atherosclerosis in Youth Research Group Arterioscler Thromb Vasc Biol. 2005;25:1237-1243; published online before print March 31 2005, doi:10.1161/01.ATV.0000164625.93129.64. Abstract \| Full Text \| PDF In young subjects 15 to 34 years of age, serum CRP concentration was associated with raised lesions in the abdominal aorta and right coronary artery, and with American Heart Association grade 5 lesions in the proximal left anterior descending coronary artery, independently of traditional coronary heart disease risk factors.
	Atherogenesis in Mice Does Not Require CD40 Ligand From Bone Marrow–Derived Cells Udo Bavendiek, Andreas Zirlik, Samantha LaClair, Lindsey MacFarlane, Peter Libby, and Uwe Schönbeck Arterioscler Thromb Vasc Biol. 2005;25:1244-1249; published online before print March 3 2005, doi:10.1161/01.ATV.0000161420.55482.ef. Abstract \| Full Text \| PDF Although previous studies established CD40L as a mediator of atherogenesis, its relevant cellular source remains unknown. The present study demonstrates that CD40L modulates atherogenesis in mice, primarily by its expression on nonhematopoietic cell types in bone marrow chimeras. This surprising finding has important pathophysiologic and therapeutic implications.
	Humoral Immune Response Against Defined Oxidized Low-Density Lipoprotein Antigens Reflects Structure and Disease Activity of Carotid Plaques Isabel Gonçalves, Marie-Louise M. Gronholdt, Ingrid Söderberg, Mikko P.S. Ares, Borge G. Nordestgaard, Jacob F. Bentzon, Gunilla Nordin Fredrikson, and Jan Nilsson Arterioscler Thromb Vasc Biol. 2005;25:1250-1255; published online before print April 14 2005, doi:10.1161/01.ATV.0000166518.96137.38. Abstract \| Full Text \| PDF Immune responses against oxidized low-density lipoprotein (LDL) are important in atherosclerosis. This study demonstrates that IgG and IgM against defined epitopes in oxidized LDL reflects the structure and disease activity of atherosclerotic plaques.
	Phagocytosis of Apoptotic Cells by Macrophages Is Impaired in Atherosclerosis Dorien M. Schrijvers, Guido R.Y. De Meyer, Mark M. Kockx, Arnold G. Herman, and Wim Martinet Arterioscler Thromb Vasc Biol. 2005;25:1256-1261; published online before print April 14 2005, doi:10.1161/01.ATV.0000166517.18801.a7. Abstract \| Full Text \| PDF \| Data Supplement Determination of phagocytosis efficiency of apoptotic cells (ACs) revealed a marked impairment of clearance of ACs in atherosclerotic plaques as compared with tonsils. In vitro studies indicated oxidative stress factors present in the plaque as the major contributors to this impairment.
	Polymorphonuclear Leukocytes May Impair Endothelial Function: Results of Crossover Randomized Study of Lipid-Lowering Therapies Ryo Sugano, Hidehiro Matsuoka, Nobuya Haramaki, Hidekazu Umei, Eiko Murase, Kei Fukami, Shuji Iida, Hisao Ikeda, and Tsutomu Imaizumi Arterioscler Thromb Vasc Biol. 2005;25:1262-1267; published online before print March 24 2005, doi:10.1161/01.ATV.0000163842.91226.ba. Abstract \| Full Text \| PDF Fluvastatin but not colestimide restored endothelium-dependent vasodilation and diminished LDL oxidation and leukocyte activity. PMNs from hypercholesterolemia showed greater cell adhesion and impaired eNOS phosphorylation, which were normalized by fluvastatin. These findings suggest that fluvastatin may improve endothelial function by its anti-inflammatory properties against PMNs, independently of LDL reduction.
	Elevated Interleukin-18 Levels Are Associated With the Metabolic Syndrome Independent of Obesity and Insulin Resistance Joseph Hung, Brendan M. McQuillan, Caroline M. L. Chapman, Peter L. Thompson, and John P. Beilby Arterioscler Thromb Vasc Biol. 2005;25:1268-1273; published online before print March 24 2005, doi:10.1161/01.ATV.0000163843.70369.12. Abstract \| Full Text \| PDF We found in a cross-sectional community population that an elevated serum IL-18 level was associated with increased odds ratio for metabolic syndrome independently of obesity and insulin resistance. The risk relation was not attenuated when adjusted for C-reactive protein and IL-6 levels. Our findings support the hypothesis that activation of IL-18 is involved in the pathogenesis of metabolic syndrome.
	Flow-Mediated Dilatation Is Impaired by a High–Saturated Fat Diet but Not by a High-Carbohydrate Diet Jennifer B. Keogh, Jessica A. Grieger, Manny Noakes, and Peter M. Clifton Arterioscler Thromb Vasc Biol. 2005;25:1274-1279; published online before print March 17 2005, doi:10.1161/01.ATV.0000163185.28245.a1. Abstract \| Full Text \| PDF To determine whether a low-fat diet impaired endothelial vasodilation compared with high saturated or unsaturated fat, 40 subjects were crossed over to 4 diets: high polyunsaturated, monounsaturated, or saturated fat, or low-fat highcarbohydrate. Flow-mediated dilatation was impaired, and P-selectin highest after high saturated fat.
	Thrombosis
	Analysis of Gas6 in Human Platelets and Plasma Istvan Balogh, Sassan Hafizi, Jonas Stenhoff, Karin Hansson, and Björn Dahlbäck Arterioscler Thromb Vasc Biol. 2005;25:1280-1286; published online before print March 24 2005, doi:10.1161/01.ATV.0000163845.07146.48. Abstract \| Full Text \| PDF The aim of this study was to analyze the presence of Gas6 in human plasma and platelets. Using sensitive immune-based methods, we detected Gas6 in the human circulation in the sub-nanomolar range, the concentration of which was slightly decreased in warfarin-treated patients. However, we could not detect Gas6 in human platelets.
	A Genome Search for Genetic Determinants That Influence Plasma Fibrinogen Levels José Manuel Soria, Laura Almasy, Juan Carlos Souto, Alfonso Buil, Mark Lathrop, John Blangero, and Jordi Fontcuberta Arterioscler Thromb Vasc Biol. 2005;25:1287-1292; published online before print March 10 2005, doi:10.1161/01.ATV.0000161927.38739.6f. Abstract \| Full Text \| PDF Fibrinogen level is a risk factor for cardiovascular disease, but most of the genetic components are unknown. In a genome-wide linkage scan, 2 loci were detected: 1 on chromosome 12 (most likely the TCF1) and another on chromosome 14, which are important determinants of fibrinogen levels in Spanish families.
	Importance of Platelet Phospholipase C ${gamma}$ 2 Signaling in Arterial Thrombosis as a Function of Lesion Severity Christelle Nonne, Nadège Lenain, Béatrice Hechler, Pierre Mangin, Jean-Pierre Cazenave, Christian Gachet, and François Lanza Arterioscler Thromb Vasc Biol. 2005;25:1293-1298; published online before print March 17 2005, doi:10.1161/01.ATV.0000163184.02484.69. Abstract \| Full Text \| PDF \| Data Supplement This study evaluated the role of adhesion receptors signaling through PLC{gamma}2 in arterial thrombosis. PLC{gamma}2-deficient mice showed resistance to thrombus formation in superficial lesions but productive thrombosis after a more severe laser injury formation. In contrast, resistance to thrombosis was observed in G{alpha}q-/- mice in both levels of injury.
	Platelet Degranulation Is Associated With Progression of Intima-Media Thickness of the Common Carotid Artery in Patients With Diabetes Mellitus Type 2 Suzanne Fateh-Moghadam, Zonyang Li, Simon Ersel, Thomas Reuter, Patrik Htun, Ursula Plöckinger, Wolfgang Bocksch, Rainer Dietz, and Meinrad Gawaz Arterioscler Thromb Vasc Biol. 2005;25:1299-1303; published online before print April 7 2005, doi:10.1161/01.ATV.0000165699.41301.c5. Abstract \| Full Text \| PDF We prospectively examined the relationship between systemic platelet activation and progression of carotid wall thickness within 1 year in 105 patients with type 2 diabetes. Diabetic patients with progression of IMT had a significant increased expression of platelet CD63 compared with patients with stable carotid disease.
	Letters to the Editor
	Association of Cholesterol Subfractions and Carotid Lipid Core Measured by MRI Milind Y. Desai, Annabelle Rodriguez, Bruce A. Wasserman, Gary Gerstenblith, Sachin Agarwal, Margene Kennedy, David A Bluemke, and João A.C. Lima Arterioscler Thromb Vasc Biol. 2005;25:e110-e111, doi:10.1161/01.ATV.0000166599.78182.6c. Full Text \| PDF
	Neutrophil Count and Complex Lesions in Patients With Coronary Artery Disease Juan Carlos Kaski, Pablo Avanzas, Ramón Arroyo-Espliguero, and Barry S. Coller Arterioscler Thromb Vasc Biol. 2005;25:e112, doi:10.1161/01.ATV.0000168419.71423.b8. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 6; June 1, 2005

Editorials

Toll To Be Paid at the Gateway to the Vessel Wall

CD40 Ligand: Not Bad to the Bone (Marrow), After All

CRP or not CRP? That Is the Question

Antiatherogenic Properties of Fibrates

ApoA-V: The Regulation of a Regulator of Plasma Triglycerides

Quest for Genes Regulating Plasma Fibrinogen Concentration: Still a Long Way to Go

Brief Reviews

Myeloperoxidase and Cardiovascular Disease

ACAT2 Is a Target for Treatment of Coronary Heart Disease Associated With Hypercholesterolemia

Extracellular Proteases in Atherosclerosis and Restenosis

Tissue-Engineered Blood Vessels: Alternative to Autologous Grafts?

Vascular Implications of the Krüppel-Like Family of Transcription Factors

Vascular Biology

Mechanisms of Reactive Oxygen Species–Dependent Downregulation of Insulin Receptor Substrate-1 by Angiotensin II

A New Cellular Signaling Mechanism for Angiotensin II Activation of NF-B: An IB–Independent, RSK–Mediated Phosphorylation of p65

Regulation of Endothelial Cell and Endothelial Progenitor Cell Survival and Vasculogenesis by Integrin-Linked Kinase

Autocrine and Paracrine Transcriptional Regulation of Type IIA Secretory Phospholipase A2 Gene in Vascular Smooth Muscle Cells

Vascular Endothelial Growth Factor–Expressing Mesenchymal Stem Cell Transplantation for the Treatment of Acute Myocardial Infarction

Systemic Endothelial Dysfunction as an Early Predictor of Adverse Outcome in Heart Failure

Atherosclerosis and Lipoproteins

Activation of ATP-Binding Cassette Transporter A1 Transcription by Chromatin Remodeling Complex

Transcriptional Regulation of Apolipoprotein A5 Gene Expression by the Nuclear Receptor ROR

Fenofibric Acid, an Active Form of Fenofibrate, Increases Apolipoprotein A-I–Mediated High-Density Lipoprotein Biogenesis by Enhancing Transcription of ATP-Binding Cassette Transporter A1 Gene in a Liver X Receptor–Dependent Manner

Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1-Deficient Macrophages

High-Density Lipoproteins Prevent the Oxidized Low-Density Lipoprotein–Induced Endothelial Growth Factor Receptor Activation and Subsequent Matrix Metalloproteinase-2 Upregulation

Toll-Like Receptor 4–Dependent and –Independent Cytokine Secretion Induced by Minimally Oxidized Low-Density Lipoprotein in Macrophages

Adipocyte Fatty Acid–Binding Protein Expression and Lipid Accumulation Are Increased During Activation of Murine Macrophages by Toll-Like Receptor Agonists

C-Reactive Protein–Induced In Vitro Endothelial Cell Activation Is an Artefact Caused by Azide and Lipopolysaccharide

Statins Reduce Interleukin-6–Induced C-Reactive Protein in Human Hepatocytes: New Evidence for Direct Antiinflammatory Effects of Statins

Elevated Serum C-Reactive Protein Levels and Advanced Atherosclerosis in Youth

Atherogenesis in Mice Does Not Require CD40 Ligand From Bone Marrow–Derived Cells

Humoral Immune Response Against Defined Oxidized Low-Density Lipoprotein Antigens Reflects Structure and Disease Activity of Carotid Plaques

Phagocytosis of Apoptotic Cells by Macrophages Is Impaired in Atherosclerosis

Polymorphonuclear Leukocytes May Impair Endothelial Function: Results of Crossover Randomized Study of Lipid-Lowering Therapies

Elevated Interleukin-18 Levels Are Associated With the Metabolic Syndrome Independent of Obesity and Insulin Resistance

Flow-Mediated Dilatation Is Impaired by a High–Saturated Fat Diet but Not by a High-Carbohydrate Diet

Thrombosis

Analysis of Gas6 in Human Platelets and Plasma

A Genome Search for Genetic Determinants That Influence Plasma Fibrinogen Levels

Importance of Platelet Phospholipase C2 Signaling in Arterial Thrombosis as a Function of Lesion Severity

Platelet Degranulation Is Associated With Progression of Intima-Media Thickness of the Common Carotid Artery in Patients With Diabetes Mellitus Type 2

Letters to the Editor

Association of Cholesterol Subfractions and Carotid Lipid Core Measured by MRI

Neutrophil Count and Complex Lesions in Patients With Coronary Artery Disease

Spotlight

A New Cellular Signaling Mechanism for Angiotensin II Activation of NF- ${kappa}$ B: An I ${kappa}$ B–Independent, RSK–Mediated Phosphorylation of p65

Transcriptional Regulation of Apolipoprotein A5 Gene Expression by the Nuclear Receptor ROR ${alpha}$

Importance of Platelet Phospholipase C ${gamma}$ 2 Signaling in Arterial Thrombosis as a Function of Lesion Severity