Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [4])

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Volume 25, Issue 4; April 1, 2005

Editorials
Special Article
Brief Reviews
Vascular Biology
Atherosclerosis & Lipoproteins
Thrombosis
Special Reports
Letters to the Editor
Corrections

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	Editorials
	Inorganic Pyrophosphate: A Paracrine Regulator of Vascular Calcification and Smooth Muscle Phenotype Dwight A. Towler Arterioscler Thromb Vasc Biol. 2005;25:651-654, doi:10.1161/01.ATV.0000158943.79580.9d. Full Text \| PDF
	When Interleukin-18 Conducts, the Preludio Sounds the Same no Matter Who Plays Giuseppina Caligiuri, Srini Kaveri, and Antonino Nicoletti Arterioscler Thromb Vasc Biol. 2005;25:655-657, doi:10.1161/01.ATV.0000154921.49792.ef. Full Text \| PDF
	Special Article
	Leukocytosis and Ischemic Vascular Disease Morbidity and Mortality: Is It Time to Intervene? Barry S. Coller Arterioscler Thromb Vasc Biol. 2005;25:658-670; published online before print January 20 2005, doi:10.1161/01.ATV.0000156877.94472.a5. Abstract \| Full Text \| PDF This article reviews the epidemiological evidence of an association between leukocytosis and increased morbidity and mortality from ischemic vascular disease, focusing on whether the data are consistent with a causal role for leukocytes in vascular events. It then discusses whether the existing data justify selectively entering to lower the leukocyte count.
	Brief Reviews
	Redox Modulation of Vascular Tone: Focus of Potassium Channel Mechanisms of Dilation David D. Gutterman, Hiroto Miura, and Yanping Liu Arterioscler Thromb Vasc Biol. 2005;25:671-678; published online before print February 10 2005, doi:10.1161/01.ATV.0000158497.09626.3b. Abstract \| Full Text \| PDF Opening of potassium channels on vascular smooth muscle cells with resultant hyperpolarization plays a central role in several mechanisms of vasodilation. Disease states such as coronary atherosclerosis and its risk factors are associated with elevated levels of reactive oxygen (ROS) and nitrogen species that have well-defined inhibitory effects on nitric oxide-mediated vasodilation. Depending on the oxidative species, ROS can activate, inhibit, or leave unaltered potassium channel function in blood vessels. Therefore, discerning the activity of enzymes regulating production or degradation of ROS is important when assessing tissue perfusion in health and disease.
	Transcriptional Control of COX-2 via C/EBPß Kenneth K. Wu, Jun-Yang Liou, and Katarzyna Cieslik Arterioscler Thromb Vasc Biol. 2005;25:679-685; published online before print January 27 2005, doi:10.1161/01.ATV.0000157899.35660.61. Abstract \| Full Text \| PDF Cyclooxygenase-2 (COX-2) is a highly inducible enzyme exerting diverse actions on cell functions, including proliferation, migration, and DNA damage. Enhanced COX-2 expression may be protective, but excessive expression may be harmful, causing inflammation, atheromatous plaque instability, and intimal hyperplasia. In this review, the role of C/EBP in regulating COX-2 transcription is highlighted.
	Vascular Biology
	Chondrogenesis Mediated by PP_i Depletion Promotes Spontaneous Aortic Calcification in NPP1–/– Mice Kristen Johnson, Monika Polewski, Deborah van Etten, and Robert Terkeltaub Arterioscler Thromb Vasc Biol. 2005;25:686-691; published online before print December 29 2004, doi:10.1161/01.ATV.0000154774.71187.f0. Abstract \| Full Text \| PDF Human "idiopathic" infantile arterial media calcification is linked to deficient PPi-generating PC-1/nucleotide pyrophosphatase phosphodiesterase 1 (NPP1). We demonstrate that NPP1 and extracellular PPi deficiencies promote chondrogenic differentiation in mesenchymal precursors and vascular smooth muscle cells. Therefore, NPP1 and PPi deficiencies promote active rather than simply dystrophic artery calcification, mediated partly by primary alterations in cell differentiation.
	Mesoangioblasts, Vessel-Associated Multipotent Stem Cells, Repair the Infarcted Heart by Multiple Cellular Mechanisms: A Comparison With Bone Marrow Progenitors, Fibroblasts, and Endothelial Cells Daniela Galli, Anna Innocenzi, Lidia Staszewsky, Lucia Zanetta, Maurilio Sampaolesi, Antonio Bai, Elena Martinoli, Eleonora Carlo, Giovanna Balconi, Fabio Fiordaliso, Stefano Chimenti, Gabriella Cusella, Elisabetta Dejana, Giulio Cossu, and Roberto Latini Arterioscler Thromb Vasc Biol. 2005;25:692-697; published online before print January 20 2005, doi:10.1161/01.ATV.0000156402.52029.ce. Abstract \| Full Text \| PDF \| Data Supplement Mesoangioblasts (Mabs), vessel-associated stem cells, were compared with bone marrow progenitor cells (BMPCs), fibroblasts, and embryonic stem cell-derived endothelial cells in their ability to ameliorate cardiac function after infarction, aiming to identify putative cellular mechanisms. Mabs appeared as effective as BMPCs in reducing postinfarction damage, likely through production of antiapoptotic and angiogenic factors.
	Hyperglycemia Reduces Survival and Impairs Function of Circulating Blood-Derived Progenitor Cells Nicolle Kränkel, Volker Adams, Axel Linke, Stephan Gielen, Sandra Erbs, Karsten Lenk, Gerhard Schuler, and Rainer Hambrecht Arterioscler Thromb Vasc Biol. 2005;25:698-703; published online before print January 20 2005, doi:10.1161/01.ATV.0000156401.04325.8f. Abstract \| Full Text \| PDF In circulating progenitor cells (CPC), hyperglycemia induces cell-cycle arrest, impaired NO synthesis, and decreased migrational and integrative capacity. These mechanisms might contribute to the decline of CPC amount and function in diabetes mellitus.
	Selective Blockade of the Intermediate-Conductance Ca²⁺-Activated K⁺ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo Ivica Grgic, Ines Eichler, Philipp Heinau, Han Si, Susanne Brakemeier, Joachim Hoyer, and Ralf Köhler Arterioscler Thromb Vasc Biol. 2005;25:704-709; published online before print January 20 2005, doi:10.1161/01.ATV.0000156399.12787.5c. Abstract \| Full Text \| PDF We tested whether Ca2+-activated K+ (KCa) channels contribute to endothelial cell (EC) proliferation induced by proangiogenic factors. Angiogenic factors augmented mRNA expression and function of intermediate-conductance KCa channel (IKCa1). EC proliferation in vitro and angiogenesis in vivo was abolished by IKCa1 blockers, which might be of therapeutic value to prevent tumor angiogenesis.
	15-Deoxy- ${Delta}$ ^12,14-Prostaglandin J₂ (15d-PGJ2) Signals Through Retinoic Acid Receptor–Related Orphan Receptor- ${alpha}$ but Not Peroxisome Proliferator–Activated Receptor- ${gamma}$ in Human Vascular Endothelial Cells: The Effect of 15d-PGJ2 on Tumor Necrosis Factor- ${alpha}$ –Induced Gene Expression Hideyuki Migita and John Morser Arterioscler Thromb Vasc Biol. 2005;25:710-716; published online before print January 20 2005, doi:10.1161/01.ATV.0000156482.76228.d1. Abstract \| Full Text \| PDF 15-Deoxy-{Delta}12,14-PG J2 (15d-PGJ2) inhibits proinflammatory gene expression, but its signaling mechanisms remain unclear. Because retinoic acid receptor-related orphan receptor-{alpha} (ROR{alpha}) suppresses proinflammatory gene expression, we hypothesized that 15d-PGJ2 induces ROR{alpha} expression, resulting in inhibition of proinflammatory gene expression. Our results provide a novel insight into anti-inflammatory actions of 15d-PGJ2.
	C-Reactive Protein and Annexin A5 Bind to Distinct Sites of Negatively Charged Phospholipids Present in Oxidized Low-Density Lipoprotein Lambertus van Tits, Jacqueline de Graaf, Helga Toenhake, Waander van Heerde, and Anton Stalenhoef Arterioscler Thromb Vasc Biol. 2005;25:717-722; published online before print February 3 2005, doi:10.1161/01.ATV.0000157979.51673.2c. Abstract \| Full Text \| PDF We investigated interactions of C-reactive protein (CRP), annexin A5, and low-density lipoprotein (LDL) with U937 cells. CRP binds to oxidized LDL, and via subsequent interaction with Fc{gamma} receptors it enhances binding of the particle to U937 cells. Annexin A5 also binds to oxidized LDL but does not interfere with CRP.
	Powerful Inflammatory Properties of Large Vein Endothelium In Vivo Einar E. Eriksson, Eva Karlof, Karin Lundmark, Pierre Rotzius, Ulf Hedin, and Xun Xie Arterioscler Thromb Vasc Biol. 2005;25:723-728; published online before print January 27 2005, doi:10.1161/01.ATV.0000157578.51417.6f. Abstract \| Full Text \| PDF \| Data Supplement The inflammatory capacity of large vein endothelium is unclear. Here, we show that endothelium in the mouse IVC holds powerful inflammatory properties that are equally potent as that in postcapillary venules and distinct from that in arteries. The data emphasize the endothelium as target for treatment of vein disease.
	Involvement of JAM-A in Mononuclear Cell Recruitment on Inflamed or Atherosclerotic Endothelium: Inhibition by Soluble JAM-A Georg Ostermann, Line Fraemohs, Thomas Baltus, Andreas Schober, Michael Lietz, Alma Zernecke, Elisa A. Liehn, and Christian Weber Arterioscler Thromb Vasc Biol. 2005;25:729-735; published online before print January 27 2005, doi:10.1161/01.ATV.0000157154.14474.3b. Abstract \| Full Text \| PDF We studied the effect of soluble JAM-A (sJAM-A.Fc) on atherogenic recruitment of mononuclear cells. Because sJAM-A.Fc can inhibit distinct steps of mononuclear cell recruitment, ie, adhesion and transendothelial chemotaxis, on inflamed and atherosclerotic endothelium, our data suggest a functional contribution of JAM-A to atherogenesis.
	Antiangiogenic Activity of a Domain Deletion Mutant of Tissue Plasminogen Activator Containing Kringle 2 Veronica A. Carroll, Leonid L. Nikitenko, Roy Bicknell, and Adrian L. Harris Arterioscler Thromb Vasc Biol. 2005;25:736-741; published online before print February 3 2005, doi:10.1161/01.ATV.0000157980.15710.2b. Abstract \| Full Text \| PDF \| Data Supplement In this study, we report that wound healing and angiogenesis are compromised with the fibrinolytic drug, Reteplase, and show that these effects are critically dependent on the kringle 2 domain. These data provide new mechanistic insights into the bleeding complications that can occur in some patients with this drug.
	Activated Forkhead Transcription Factor Inhibits Neointimal Hyperplasia After Angioplasty Through Induction of p27 Kyung-Woo Park, Dae-Hee Kim, Hyun-Jung You, Jung-Ju Sir, Soo-In Jeon, Seock-Won Youn, Han-Mo Yang, Carsten Skurk, Young-Bae Park, Kenneth Walsh, and Hyo-Soo Kim Arterioscler Thromb Vasc Biol. 2005;25:742-747; published online before print January 20 2005, doi:10.1161/01.ATV.0000156288.70849.26. Abstract \| Full Text \| PDF The role of FKHRL1 (forkhead transcription factor in rhabdomyosarcoma like-1) in VSMC biology and in neointimal hyperplasia after balloon angioplasty has not been studied. Here, we show that the inactivation of the forkhead transcription factor is required for neointimal hyperplasia after angioplasty, and that overexpression of FKHRL1 leads to the induction of p27 resulting in inhibition of neointimal hyperplasia.
	Inhibition of Neointima Formation by a Novel Drug-Eluting Stent System That Allows for Dose-Adjustable, Multiple, and On-Site Stent Coating Rainer Wessely, Jörg Hausleiter, Cornelia Michaelis, Birgit Jaschke, Michael Vogeser, Stefan Milz, Boris Behnisch, Thomas Schratzenstaller, Magdalena Renke-Gluszko, Michael Stöver, Erich Wintermantel, Adnan Kastrati, and Albert Schömig Arterioscler Thromb Vasc Biol. 2005;25:748-753; published online before print January 27 2005, doi:10.1161/01.ATV.0000157579.52566.ee. Abstract \| Full Text \| PDF In-stent neointima formation can be successfully attenuated by drug-eluting stents. We introduce a novel conceptual approach for stent-coating that allows for dose-adjustable, on-site stent coating process if desired with multiple compounds. Microporous stents coated with rapamycin proved safe and effective for the limitation of neointima formation in a porcine coronary stent model.
	Stent-Based Delivery of Tissue Inhibitor of Metalloproteinase-3 Adenovirus Inhibits Neointimal Formation in Porcine Coronary Arteries Thomas W. Johnson, Yin Xiong Wu, Christian Herdeg, Andreas Baumbach, Andrew C. Newby, Karl R. Karsch, and Martin Oberhoff Arterioscler Thromb Vasc Biol. 2005;25:754-759; published online before print January 27 2005, doi:10.1161/01.ATV.0000157582.33180.a9. Abstract \| Full Text \| PDF We developed eluting-stent technology to deliver an adenovirus capable of TIMP-3 overexpression and investigated its effect on restenosis. The technology resulted in effective in vitro and in vivo transduction. TIMP-3 overexpression increased apoptosis and reduced neointimal formation. Our results demonstrate for the first time to our knowledge the feasibility of adenovirus-eluting stent technology.
	Insulin Signaling in Arteries Prevents Smooth Muscle Apoptosis T. Nakazawa, T. Chiba, E. Kaneko, K. Yui, M. Yoshida, and K. Shimokado Arterioscler Thromb Vasc Biol. 2005;25:760-765; published online before print February 3 2005, doi:10.1161/01.ATV.0000158307.66945.b4. Abstract \| Full Text \| PDF Insulin is antiapoptotic for cultured vascular smooth muscle, but it is not clear whether insulin is antiapoptotic in vivo. We report here that insulin is antiapoptotic in vitro and in vivo. Decreased insulin action on the artery may cause unstable plaque formation in diabetes by increasing smooth muscle apoptosis.
	Endothelium-Derived Hydrogen Peroxide Accounts for the Enhancing Effect of an Angiotensin-Converting Enzyme Inhibitor on Endothelium-Derived Hyperpolarizing Factor–Mediated Responses in Mice Takako Fujiki, Hiroaki Shimokawa, Keiko Morikawa, Hiroshi Kubota, Makoto Hatanaka, M.A. Hassan Talukder, Tetsuya Matoba, Akira Takeshita, and Kenji Sunagawa Arterioscler Thromb Vasc Biol. 2005;25:766-771; published online before print February 10 2005, doi:10.1161/01.ATV.0000158498.19027.75. Abstract \| Full Text \| PDF This study was designed to examine the involvement of H2O2/EDHF in the effect of an ACE inhibitor in mice. The results showed that endothelium-derived H2O2 is involved in the enhancing effect of temocapril on EDHF-mediated responses in control but not in eNOS-/- mice, thus further supporting our H2O2 theory.
	B1 Kinin Receptor Does Not Contribute to Vascular Tone or Tissue Plasminogen Activator Release in the Peripheral Circulation of Patients With Heart Failure Nicholas L.M. Cruden, George H. Tse, Keith A.A. Fox, Christopher A. Ludlam, Ian Megson, and David E. Newby Arterioscler Thromb Vasc Biol. 2005;25:772-777; published online before print January 27 2005, doi:10.1161/01.ATV.0000157157.78822.25. Abstract \| Full Text \| PDF In contrast to bradykinin, intra-brachial Lys-des-Arg9-bradykinin (B1 agonist) and Lys-[Leu8]-des-Arg9-bradykinin (B1 antagonist) had no effect on vascular tone or tissue plasminogen activator release in patients with heart failure treated with angiotensin-converting enzyme inhibition. The B1 kinin receptor does not have a major vasomotor or fibrinolytic role in patients with heart failure.
	S-Adenosylmethionine and 5-Methyltetrahydrofolate Are Associated With Endothelial Function After Controlling for Confounding by Homocysteine: The Hoorn Study A.M.W. Spijkerman, Y.M. Smulders, P.J. Kostense, R.M.A. Henry, A. Becker, T. Teerlink, C. Jakobs, J.M. Dekker, G. Nijpels, R.J. Heine, L.M. Bouter, and C.D.A. Stehouwer Arterioscler Thromb Vasc Biol. 2005;25:778-784; published online before print February 3 2005, doi:10.1161/01.ATV.0000157981.57694.d2. Abstract \| Full Text \| PDF We explored the associations between homocysteine, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH), total folate, 5-methyltetrahydrofolate (active folate, 5-MTHF), vitamin B12, vitamin B6, and endothelium-dependent flow-mediated vasodilation.
	Atherosclerosis & Lipoproteins
	Serum Amyloid A and Lipoprotein Retention in Murine Models of Atherosclerosis Kevin D. O’Brien, Thomas O. McDonald, Vidya Kunjathoor, KimLi Eng, Eleanor A. Knopp, Katherine Lewis, Roland Lopez, Elizabeth A. Kirk, Alan Chait, Thomas N. Wight, Frederick C. deBeer, and Renee C. LeBoeuf Arterioscler Thromb Vasc Biol. 2005;25:785-790; published online before print February 3 2005, doi:10.1161/01.ATV.0000158383.65277.2b. Abstract \| Full Text \| PDF In chow-fed apoE-/- and LDLR-/- mice, serum amyloid A (SAA) is deposited at all stages of atherosclerotic lesion development and SAA immunoreactive area correlates highly with areas for lesions, apoA-I, apoB, and perlecan. These findings are consistent with the hypothesis that SAA may participate in atherosclerotic lesion lipoprotein retention.
	IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN- ${gamma}$ and CXCL16 Expression Independently of T Cells Charlotta Tenger, Anna Sundborger, Jacek Jawien, and Xinghua Zhou Arterioscler Thromb Vasc Biol. 2005;25:791-796; published online before print December 16 2004, doi:10.1161/01.ATV.0000153516.02782.65. Abstract \| Full Text \| PDF To investigate whether cells other than T cells play a proatherogenic role via secretion of IFN-{gamma}, we used SCID/apoE knockout mice. Administration of IL-18 resulted in larger lesions and elevated IFN-{gamma}. Our data suggest that IFN-{gamma} from macrophages, NK cells, and vascular cells in vivo is sufficient for the disease progression.
	Expression of 12/15-Lipoxygenase Attenuates Intracellular Lipid Deposition During In Vitro Foam Cell Formation Jutta Belkner, Pavlos Chaitidis, Hannelore Stender, Christa Gerth, Ralf J. Kuban, Tanihiro Yoshimoto, and Hartmut Kuhn Arterioscler Thromb Vasc Biol. 2005;25:797-802; published online before print January 27 2005, doi:10.1161/01.ATV.0000157580.26858.2d. Abstract \| Full Text \| PDF Lipoxygenases have been implicated in atherogenesis but their precise roles remain unclear. We tested the impact of 12/15-lipoxygenase on in vitro foam cell formation and found that the enzyme protected macrophages from intracellular lipid deposition. This effect was related to impaired scavenger receptor A expression and to accelerated lipid metabolism.
	Lymphocytes Are Not Required for the Rapid Onset of Coronary Heart Disease in Scavenger Receptor Class B Type I/Apolipoprotein E Double Knockout Mice Sharon L. Karackattu, Michael H. Picard, and Monty Krieger Arterioscler Thromb Vasc Biol. 2005;25:803-808; published online before print February 3 2005, doi:10.1161/01.ATV.0000158310.64498.ac. Abstract \| Full Text \| PDF \| Data Supplement SR-BI/apoE double knockout mice exhibit occlusive atherosclerotic coronary heart disease (CHD) characterized by myocardial infarctions, cardiac dysfunction, and premature death. Analysis of B-cell- and T-cell-deficient SR-BI/apoE/RAG2 triple knockout mice established that B and T lymphocytes do not play a key role in the pathophysiology of this model of human disease.
	Physical Inactivity Increases Oxidative Stress, Endothelial Dysfunction, and Atherosclerosis Ulrich Laufs, Sven Wassmann, Thomas Czech, Thomas Münzel, Marco Eisenhauer, Michael Böhm, and Georg Nickenig Arterioscler Thromb Vasc Biol. 2005;25:809-814; published online before print February 3 2005, doi:10.1161/01.ATV.0000158311.24443.af. Abstract \| Full Text \| PDF \| Data Supplement Sedentary lifestyle predicts vascular risk. To study underlying mechanisms, mice were subjected to physical inactivity or voluntary training on running wheels. Inactivity increased vascular lipid peroxidation, superoxide release, and NADPH oxidase expression and activity. In apoE-/- mice, inactivity significantly impaired endothelium-dependent vasorelaxation and accelerated atherosclerotic lesion formation.
	High Serum Levels of Advanced Glycation End Products Predict Increased Coronary Heart Disease Mortality in Nondiabetic Women but not in Nondiabetic Men: A Population-Based 18-Year Follow-Up Study Bente K. Kilhovd, Auni Juutilainen, Seppo Lehto, Tapani Rönnemaa, Peter A. Torjesen, Kåre I. Birkeland, Tore J. Berg, Kristian F. Hanssen, and Markku Laakso Arterioscler Thromb Vasc Biol. 2005;25:815-820; published online before print February 3 2005, doi:10.1161/01.ATV.0000158380.44231.fe. Abstract \| Full Text \| PDF Serum levels of advanced glycation end products measured at baseline in a random sample of 1141 Finnish middle-aged nondiabetic individuals (535 men and 606 women) predicted all-cause mortality, cardiovascular, and coronary heart disease mortality after 18 years of follow-up in women but not in men.
	Hypoadiponectinemia Is Associated With Ischemic Cerebrovascular Disease Miao-Pei Chen, Jack C.-R. Tsai, Fu-Mei Chung, Sheng-Shan Yang, Liang-Lan Hsing, Shyi-Jang Shin, and Yau-Jiunn Lee Arterioscler Thromb Vasc Biol. 2005;25:821-826; published online before print February 3 2005, doi:10.1161/01.ATV.0000157784.25920.a7. Abstract \| Full Text \| PDF Adiponectin, an adipocyte-derived peptide with antiinflammatory and antiatherogenic effects, is known to protect against the initiation and progression of atherosclerosis. In this study, we investigate whether hypoadiponectinemia is present in patients with ischemic cerebrovascular disease (CVD). Our data show that there are significantly lower levels of plasma adiponectin in patients with ischemic CVD.
	Serum Lipid Profiles Poorly Correlate With Chlamydia pneumoniae, Helicobacter pylori, and Cytomegalovirus Seropositivity in Prospectively Followed-Up Healthy Children Iina Volanen, Olli T. Raitakari, Raija Vainionpää, Martti Arffman, Johanna Aarnisalo, Susanna Anglé, Katariina Kallio, and Olli Simell Arterioscler Thromb Vasc Biol. 2005;25:827-832; published online before print February 3 2005, doi:10.1161/01.ATV.0000158382.50942.6a. Abstract \| Full Text \| PDF Because infections have been associated with atherogenic lipid profiles in adults and because atherosclerotic process begins in early childhood, we examined whether Cpn, Hp, or CMV seropositivity is associated with serum lipids in otherwise healthy children. Antibody positivity correlated poorly with lipids, suggesting that other pathways link infection and early atherosclerosis.
	Serum Antibody Levels to Actinobacillus actinomycetemcomitans Predict the Risk for Coronary Heart Disease Pirkko J. Pussinen, Kristiina Nyyssönen, Georg Alfthan, Riitta Salonen, Jari A. Laukkanen, and Jukka T. Salonen Arterioscler Thromb Vasc Biol. 2005;25:833-838; published online before print February 3 2005, doi:10.1161/01.ATV.0000157982.69663.59. Abstract \| Full Text \| PDF The association between serum antibody levels to periodontal pathogens and coronary heart disease (CHD) was analyzed in a prospective population-based study comprising 1023 men in the Kuopio Ischemic Heart Disease Study. High-serum antibody levels to major periodontal pathogens were associated with subclinical, prevalent, and future incidence of CHD.
	Serum Levels of Type II Secretory Phospholipase A2 and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women: The EPIC-Norfolk Prospective Population Study S. Matthijs Boekholdt, Tymen T. Keller, Nicholas J. Wareham, Robert Luben, Sheila A. Bingham, Nicholas E. Day, Manjinder S. Sandhu, J. Wouter Jukema, John J.P. Kastelein, C. Erik Hack, and Kay-Tee Khaw Arterioscler Thromb Vasc Biol. 2005;25:839-846; published online before print February 3 2005, doi:10.1161/01.ATV.0000157933.19424.b7. Abstract \| Full Text \| PDF A prospective case-control study was performed to investigate the relationships between levels of secretory phospholipase A2 and the risk of coronary artery disease (CAD). Adjusted for traditional risk factors and C-reactive protein levels, the odds ratio for future CAD was 1.34 for people in the highest quartile (P for linearity=0.03).
	Adverse Associations Between CX3CR1 Polymorphisms and Risk of Cardiovascular or Cerebrovascular Disease Elise Lavergne, Julien Labreuche, Mehdi Daoudi, Patrice Debré, François Cambien, Philippe Deterre, Pierre Amarenco, Christophe Combadière on Behalf of the GENIC Investigators Arterioscler Thromb Vasc Biol. 2005;25:847-853; published online before print January 27 2005, doi:10.1161/01.ATV.0000157150.23641.36. Abstract \| Full Text \| PDF We analyzed the role of monocyte-recruiting chemokines in cerebrovascular diseases among the subjects of a case-control study of brain infarction (BI). Of the alleles tested, only homozygosity for the CX3CR1 rare alleles was associated with increased risk of BI. The associations may be related to CX3CL1-mediated monocyte adhesion.
	Allelic Variants of the Human Scavenger Receptor Class B Type 1 and Paraoxonase 1 on Coronary Heart Disease: Genotype-Phenotype Correlations Francisco Rodríguez-Esparragón, José C. Rodríguez-Pérez, Yaridé Hernández-Trujillo, Antonio Macías-Reyes, Alfonso Medina, Araceli Caballero, and Carlos M. Ferrario Arterioscler Thromb Vasc Biol. 2005;25:854-860; published online before print January 27 2005, doi:10.1161/01.ATV.0000157581.88838.03. Abstract \| Full Text \| PDF \| Data Supplement HDL antioxidant properties have been attributed to the genetic-determined paraoxonase activity. Human scavenger receptor class B type 1 plays a central role in HDL-mediated cholesteryl ester hydroperoxides uptake. We tested for a significant contribution of these genes to coronary disease and analyzed the paraoxonase activity and CLA-1/SR-BI receptor functional properties.
	Thrombosis
	Platelet Heterogeneity: Variation in Coagulation Complexes on Platelet Subpopulations Christine L. Kempton, Maureane Hoffman, Harold R. Roberts, and Dougald M. Monroe Arterioscler Thromb Vasc Biol. 2005;25:861-866; published online before print January 13 2005, doi:10.1161/01.ATV.0000155987.26583.9b. Abstract \| Full Text \| PDF Platelets stimulated with convulxin plus thrombin compared with thrombin alone develop a subpopulation with increased surface binding of FV, VIII, IX, and X that is dependent on the concentration of convulxin and is correlated with increases in factor Xa and thrombin generation. These findings suggest that the proportion of platelets in the high-binding subpopulation regulates the degree of thrombin generation in the presence of convulxin.
	Effect of Oxidation on the Platelet-Activating Properties of Low-Density Lipoprotein Suzanne J.A. Korporaal, Gertie Gorter, Herman J.M. van Rijn, and Jan-Willem N. Akkerman Arterioscler Thromb Vasc Biol. 2005;25:867-872; published online before print February 3 2005, doi:10.1161/01.ATV.0000158381.02640.4b. Abstract \| Full Text \| PDF \| Data Supplement OxLDL modulates platelet function via distinct mechanisms. At <15% oxidation, agonist-induced platelet functions are enhanced through activation of a p38MAPK-mediated pathway. At >30% oxidation, oxLDL induces LPA-dependent Ca2+ mobilization, leading to immediate aggregation. At >15% oxidation, p38MAPK-induced sensitization disappears and oxLDL inhibits agonist-induced platelet functions by binding to CD36, thereby interfering with {alpha}IIbß3-mediated outside-in signaling.
	Special Reports
	Clinical Trial Registration: A Statement From the International Committee of Medical Journal Editors Catherine De Angelis, Jeffrey M. Drazen, Frank A. Frizelle, Charlotte Haug, John Hoey, Richard Horton, Sheldon Kotzin, Christine Laine, Ana Marusic, A. John P.M. Overbeke, Torben V. Schroeder, Hal C. Sox, and Martin B. Van Der Weyden Arterioscler Thromb Vasc Biol. 2005;25:873-874, doi:10.1161/01.ATV.0000162428.48796.22. Full Text \| PDF
	Letters to the Editor
	Rho Kinase Inhibition and Vascular Protection: Support From Studies in Bartter and Gitelman Syndrome Lorenzo A. Calò, Elisa Pagnin, Paul A. Davis, Michelangelo Sartori, Andrea Semplicini, Achille C. Pessina, Sebastian Wolfrum, Yoshiyuki Rikitake, James K. Liao, Andreas Dendorfer, Peter Dominiak, Timothy J. Stalker, Yulan Gong, and Rosario Scalia Arterioscler Thromb Vasc Biol. 2005;25:e34-e35, doi:10.1161/01.ATV.0000153089.74997.02. Full Text \| PDF
	Association Between IL-1ß Gene Polymorphism and Myocardial Infarction Yukihiko Momiyama, Reiko Ohmori, and Fumitaka Ohsuzu Arterioscler Thromb Vasc Biol. 2005;25:e36, doi:10.1161/01.ATV.0000159700.18731.d2. Full Text \| PDF
	Oxidative Stress, Antioxidants, and Cardiovascular Disease F. Violi, R. Cangemi, A. Brunelli, Nageswara R. Madamanchi, and Marschall Runge Arterioscler Thromb Vasc Biol. 2005;25:e37, doi:10.1161/01.ATV.0000159889.32537.43. Full Text \| PDF
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2005;25:875. Full Text \| PDF
	Correction Arterioscler Thromb Vasc Biol. 2005;25:875a. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 4; April 1, 2005

Editorials

Inorganic Pyrophosphate: A Paracrine Regulator of Vascular Calcification and Smooth Muscle Phenotype

When Interleukin-18 Conducts, the Preludio Sounds the Same no Matter Who Plays

Special Article

Leukocytosis and Ischemic Vascular Disease Morbidity and Mortality: Is It Time to Intervene?

Brief Reviews

Redox Modulation of Vascular Tone: Focus of Potassium Channel Mechanisms of Dilation

Transcriptional Control of COX-2 via C/EBPß

Vascular Biology

Chondrogenesis Mediated by PPi Depletion Promotes Spontaneous Aortic Calcification in NPP1–/– Mice

Mesoangioblasts, Vessel-Associated Multipotent Stem Cells, Repair the Infarcted Heart by Multiple Cellular Mechanisms: A Comparison With Bone Marrow Progenitors, Fibroblasts, and Endothelial Cells

Hyperglycemia Reduces Survival and Impairs Function of Circulating Blood-Derived Progenitor Cells

Selective Blockade of the Intermediate-Conductance Ca2+-Activated K+ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo

15-Deoxy-12,14-Prostaglandin J2 (15d-PGJ2) Signals Through Retinoic Acid Receptor–Related Orphan Receptor- but Not Peroxisome Proliferator–Activated Receptor- in Human Vascular Endothelial Cells: The Effect of 15d-PGJ2 on Tumor Necrosis Factor-–Induced Gene Expression

C-Reactive Protein and Annexin A5 Bind to Distinct Sites of Negatively Charged Phospholipids Present in Oxidized Low-Density Lipoprotein

Powerful Inflammatory Properties of Large Vein Endothelium In Vivo

Involvement of JAM-A in Mononuclear Cell Recruitment on Inflamed or Atherosclerotic Endothelium: Inhibition by Soluble JAM-A

Antiangiogenic Activity of a Domain Deletion Mutant of Tissue Plasminogen Activator Containing Kringle 2

Activated Forkhead Transcription Factor Inhibits Neointimal Hyperplasia After Angioplasty Through Induction of p27

Inhibition of Neointima Formation by a Novel Drug-Eluting Stent System That Allows for Dose-Adjustable, Multiple, and On-Site Stent Coating

Stent-Based Delivery of Tissue Inhibitor of Metalloproteinase-3 Adenovirus Inhibits Neointimal Formation in Porcine Coronary Arteries

Insulin Signaling in Arteries Prevents Smooth Muscle Apoptosis

Endothelium-Derived Hydrogen Peroxide Accounts for the Enhancing Effect of an Angiotensin-Converting Enzyme Inhibitor on Endothelium-Derived Hyperpolarizing Factor–Mediated Responses in Mice

B1 Kinin Receptor Does Not Contribute to Vascular Tone or Tissue Plasminogen Activator Release in the Peripheral Circulation of Patients With Heart Failure

S-Adenosylmethionine and 5-Methyltetrahydrofolate Are Associated With Endothelial Function After Controlling for Confounding by Homocysteine: The Hoorn Study

Atherosclerosis & Lipoproteins

Serum Amyloid A and Lipoprotein Retention in Murine Models of Atherosclerosis

IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN- and CXCL16 Expression Independently of T Cells

Expression of 12/15-Lipoxygenase Attenuates Intracellular Lipid Deposition During In Vitro Foam Cell Formation

Lymphocytes Are Not Required for the Rapid Onset of Coronary Heart Disease in Scavenger Receptor Class B Type I/Apolipoprotein E Double Knockout Mice

Physical Inactivity Increases Oxidative Stress, Endothelial Dysfunction, and Atherosclerosis

High Serum Levels of Advanced Glycation End Products Predict Increased Coronary Heart Disease Mortality in Nondiabetic Women but not in Nondiabetic Men: A Population-Based 18-Year Follow-Up Study

Hypoadiponectinemia Is Associated With Ischemic Cerebrovascular Disease

Serum Lipid Profiles Poorly Correlate With Chlamydia pneumoniae, Helicobacter pylori, and Cytomegalovirus Seropositivity in Prospectively Followed-Up Healthy Children

Serum Antibody Levels to Actinobacillus actinomycetemcomitans Predict the Risk for Coronary Heart Disease

Serum Levels of Type II Secretory Phospholipase A2 and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women: The EPIC-Norfolk Prospective Population Study

Adverse Associations Between CX3CR1 Polymorphisms and Risk of Cardiovascular or Cerebrovascular Disease

Allelic Variants of the Human Scavenger Receptor Class B Type 1 and Paraoxonase 1 on Coronary Heart Disease: Genotype-Phenotype Correlations

Thrombosis

Platelet Heterogeneity: Variation in Coagulation Complexes on Platelet Subpopulations

Effect of Oxidation on the Platelet-Activating Properties of Low-Density Lipoprotein

Special Reports

Clinical Trial Registration: A Statement From the International Committee of Medical Journal Editors

Letters to the Editor

Rho Kinase Inhibition and Vascular Protection: Support From Studies in Bartter and Gitelman Syndrome

Association Between IL-1ß Gene Polymorphism and Myocardial Infarction

Oxidative Stress, Antioxidants, and Cardiovascular Disease

Corrections

Correction

Correction

Spotlight

Chondrogenesis Mediated by PP_i Depletion Promotes Spontaneous Aortic Calcification in NPP1–/– Mice

Selective Blockade of the Intermediate-Conductance Ca²⁺-Activated K⁺ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo

IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN- ${gamma}$ and CXCL16 Expression Independently of T Cells