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About This Cover
Volume 27, Issue 6; June 1, 2007
Announcement
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
Abstracts of the Arteriosclerosis, Thrombosis, and Vascular Biology Annual Conference 2007
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Announcement
June 1, 2007, Notice of Editorial Office Transition
Arterioscler Thromb Vasc Biol. 2007;27:1223, doi:10.1161/ATVBAHA.107.111222
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Editorials
Apolipoprotein A-V Genetic Variation and Plasma Lipoprotein Response to Fibrates
Robert A. Hegele and Rebecca L. Pollex
Arterioscler Thromb Vasc Biol. 2007;27:1224-1227, doi:10.1161/ATVBAHA.107.144980
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LDL Cholesteryl Oleate: A Biomarker for Atherosclerosis?
Arthur A. Spector and William G. Haynes
Arterioscler Thromb Vasc Biol. 2007;27:1228-1230, doi:10.1161/ATVBAHA.107.147082
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Brief Reviews
Vascular Functions of the Plasminogen Activation System
William P. Fay, Nadish Garg, and Madhavi Sunkar
Arterioscler Thromb Vasc Biol. 2007;27:1231-1237; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.140046
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The plasminogen activator (PA) system plays key roles in modulating fibrinolysis, vascular remodeling, and atherosclerosis development. This article reviews the use of murine models to elucidate the in vivo functions of the PA system and the roles of specific PA system components in pathologic vascular processes.
Oral, Direct Factor Xa Inhibitors in Development for the Prevention and Treatment of Thromboembolic Diseases
Alexander G.G. Turpie
Arterioscler Thromb Vasc Biol. 2007;27:1238-1247; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.139402
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Anticoagulants are recommended in a wide variety of indications. There is a need for novel oral anticoagulants that do not require frequent monitoring or dose adjustment. Factor Xa is an attractive target for novel anticoagulants.
Developmental Basis of Vascular Smooth Muscle Diversity
Mark W. Majesky
Arterioscler Thromb Vasc Biol. 2007;27:1248-1258; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.141069
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The origins of vascular smooth muscle are far more diverse than previously thought. A closer look at the diversity of smooth muscle origins in vascular development provides new perspectives about how blood vessels differ from one another and why they respond in disparate ways to common risk factors associated with vascular disease.
Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury
Jean-Baptiste Michel, Olivier Thaunat, Xavier Houard, Olivier Meilhac, Giuseppina Caligiuri, and Antonino Nicoletti
Arterioscler Thromb Vasc Biol. 2007;27:1259-1268; published online before print March 29 2007, doi:10.1161/ATVBAHA.106.137851
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The present review focuses on involvement of the adventitia in the response to arterial injury leading to vascular remodeling. The initial luminal insult lead to the genesis of (neo-) mediators that are centrifugally conveyed towards the adventitia. These mediators trigger local adventitial responses including angiogenesis, immuno-inflammation, and fibrosis.
Vascular Biology
TNF-
Contributes to Endothelial Dysfunction by Upregulating Arginase in Ischemia/Reperfusion Injury
Xue Gao, Xiangbin Xu, Souad Belmadani, Yoonjung Park, Zhonghua Tang, Arthur M. Feldman, William M. Chilian, and Cuihua Zhang
Arterioscler Thromb Vasc Biol. 2007;27:1269-1275; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.142521
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We tested whether TNF-{alpha} increases arginase expression in endothelial cells as one of the primary mechanisms by which this inflammatory cytokine compromises endothelial function during I/R injury. Our data demonstrate TNF-{alpha} upregulates expression of arginase in endothelial cells, which leads to O2- production, then induces endothelial dysfunction in I/R injury.
Expression of Heme Oxygenase-1 in Human Vascular Cells Is Regulated by Peroxisome Proliferator-Activated Receptors
Gerhard Krönke, Alexandra Kadl, Elena Ikonomu, Stefan Blüml, Alexander Fürnkranz, Ian J. Sarembock, Valery N. Bochkov, Markus Exner, Bernd R. Binder, and Norbert Leitinger
Arterioscler Thromb Vasc Biol. 2007;27:1276-1282; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.142638
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We investigated if the vasculoprotective activity of PPARs could be mediated by expression of HO-1. We found that PPAR{alpha} and PPAR{gamma} ligands upregulate HO-1 expression in vascular cells via 2 PPAR responsive elements. In addition, PPAR-induced HO-1 mediated anti-inflammatory and antiproliferative action of PPAR{alpha}-ligands in smooth muscle cells.
Glutaredoxin Mediates Akt and eNOS Activation by Flow in a Glutathione Reductase-Dependent Manner
Jing Wang, Shi Pan, and Bradford C. Berk
Arterioscler Thromb Vasc Biol. 2007;27:1283-1288; published online before print April 12 2007, doi:10.1161/ATVBAHA.107.144659
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The role of a thioltransferase, glutaredoxin was studied in flow stimulation of the Akt-eNOS signaling pathway in endothelial cells. Flow activates glutaredoxin via a mechanism dependent on glutathione reductase. Glutaredoxin maintains Akt in the reduced form, which enables its activation, and stimulation of the eNOS-NO signaling pathway.
Cyclic Strain Regulates the Notch/CBF-1 Signaling Pathway in Endothelial Cells: Role in Angiogenic Activity
David Morrow, John P. Cullen, Paul A. Cahill, and Eileen M. Redmond
Arterioscler Thromb Vasc Biol. 2007;27:1289-1296; published online before print March 29 2007, doi:10.1161/ATVBAHA.107.142778
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A relationship exists between hemodynamic forces and angiogenesis, but details of the signaling involved are scant. We report that cyclic strain stimulates endothelial cell angiogenic activity in vitro, in part, through a Notch-dependent, Angiopoietin1/Tie2 signaling pathway.
A Role for the Aryl Hydrocarbon Receptor in Regulation of Ischemia-Induced Angiogenesis
Sahoko Ichihara, Yoshiji Yamada, Gaku Ichihara, Tamie Nakajima, Ping Li, Takahisa Kondo, Frank J. Gonzalez, and Toyoaki Murohara
Arterioscler Thromb Vasc Biol. 2007;27:1297-1304; published online before print April 5 2007, doi:10.1161/ATVBAHA.106.138701
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Ischemia-induced angiogenesis was markedly enhanced in aryl hydrocarbon receptor (AHR)-null mice. This effect may be attributable to an increased association of hypoxia-inducible factor-1{alpha} with the AHR nuclear translocator and a consequent increased production of vascular endothelial growth factor in AHR-null mice.
c-Myb–Dependent Inositol 1,4,5-Trisphosphate Receptor Type-1 Expression in Vascular Smooth Muscle Cells
Talat Afroze, Al Muktafi Sadi, M. Abdul Momen, Steven Gu, Scott Heximer, and Mansoor Husain
Arterioscler Thromb Vasc Biol. 2007;27:1305-1311; published online before print March 15 2007, doi:10.1161/ATVBAHA.107.142059
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The IP3R1 promoter contains several putative binding sites for the c-Myb transcription factor, two of which are shown by gel shift and ChIP to bind c-Myb. Point mutations in these abolished promoter activity in immortalized and primary VSMCs. These data provide a mechanism for cell cycle- and c-Myb-responsive IP3R1 expression.
Induction of Vascular Permeability by the Sphingosine-1-Phosphate Receptor–2 (S1P2R) and its Downstream Effectors ROCK and PTEN
Teresa Sanchez, Athanasia Skoura, Ming Tao Wu, Brian Casserly, Elizabeth O. Harrington, and Timothy Hla
Arterioscler Thromb Vasc Biol. 2007;27:1312-1318; published online before print April 12 2007, doi:10.1161/ATVBAHA.107.143735
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We tested the hypothesis that S1P2R signaling via Rho-ROCK-PTEN pathway is a critical modulator of vascular permeability. Our results show that activation of S1P2R in endothelial cells results in Rho-, p160-Rho-associated kinase (ROCK)- and PTEN-dependent disruption of endothelial cell-cell junctions, profound modulation of actin cytoskeletal dynamics, and increased paracellular permeability.
Acrolein Induces Cyclooxygenase-2 and Prostaglandin Production in Human Umbilical Vein Endothelial Cells: Roles of p38 MAP Kinase
Yong Seek Park, Jayoung Kim, Yoshiko Misonou, Rina Takamiya, Motoko Takahashi, Michael R. Freeman, and Naoyuki Taniguchi
Arterioscler Thromb Vasc Biol. 2007;27:1319-1325; published online before print March 15 2007, doi:10.1161/ATVBAHA.106.132837
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The present study demonstrates that acrolein, a known toxin in tobacco smoke, stimulates expression of COX-2 and enhances PG synthesis in endothelial cells through activation of PKC, p38 MAPK, and CREB pathway. Our finding suggests that acrolein may play a role in progression of atherosclerosis.
Synchrotron Radiation Coronary Microangiography for Morphometric and Physiological Evaluation of Myocardial Neovascularization Induced by Endothelial Progenitor Cell Transplantation
Hiroto Iwasaki, Kazuhito Fukushima, Atsuhiko Kawamoto, Keiji Umetani, Akira Oyamada, Saeko Hayashi, Tomoyuki Matsumoto, Masakazu Ishikawa, Toshihiko Shibata, Hiromi Nishimura, Hidekazu Hirai, Yutaka Mifune, Miki Horii, Kazuro Sugimura, Shigefumi Suehiro, and Takayuki Asahara
Arterioscler Thromb Vasc Biol. 2007;27:1326-1333; published online before print March 15 2007, doi:10.1161/ATVBAHA.106.137141
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Therapeutic effect of stem cell transplantation (SCTx) for myocardial neovascularization has been evaluated by histological capillary density in small animals. However, it has been technically difficult to obtain imaging evidence of collateral formation by conventional angiography. The present results indicate that the synchrotron radiation microangiography (SRM) may be useful to both morphologically and physiologically evaluate therapeutic neovascularization by SCTx in small animals. The novel imaging system may be an essential tool in future preclinical/translational research of stem cell biology. Further development of in vivo imaging system in future may lead to clinical application of the SRM.
(6R)-5,6,7,8-Tetrahydro-L-Biopterin and Its Stereoisomer Prevent Ischemia Reperfusion Injury in Human Forearm
Lila Mayahi, Simon Heales, David Owen, Juan P. Casas, Joanne Harris, Raymond J. MacAllister, and Aroon D. Hingorani
Arterioscler Thromb Vasc Biol. 2007;27:1334-1339; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.142257
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6R-BH4, the NOS cofactor, corrected ischemia reperfusion injury in the human forearm arterioles, an effect shared by 6S-BH4 and NH4. This may be a result of radical scavenging action rather than NOS catalysis. This study shows that insulin and angiotensin II have a major role in HDL metabolism in vivo. These hormones induce redistribution of SR-BI to the plasma membrane in adipose tissue. This will then lead to an increase in LXR binding activity in an insulin and angiotensin II dependent fashion.
Atherosclerosis and Lipoproteins
In Vivo Evidence for a Role of Adipose Tissue SR-BI in the Nutritional and Hormonal Regulation of Adiposity and Cholesterol Homeostasis
Laurent Yvan-Charvet, Alexandre Bobard, Pascale Bossard, Florence Massiéra, Xavier Rousset, Gérard Ailhaud, Michèle Teboul, Pascal Ferré, Georges Dagher, and Annie Quignard-Boulangé
Arterioscler Thromb Vasc Biol. 2007;27:1340-1345; published online before print March 15 2007, doi:10.1161/ATVBAHA.106.136382
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This study shows that insulin and angiotensin II have a major role in HDL metabolism in vivo. These hormones induce redistribution of SR-BI to the plasma membrane in adipose tissue. This will then lead to an increase in LXR binding activity in an insulin and angiotensin II dependent fashion.
High-Density Lipoprotein Modulates Oxidized Phospholipid Signaling in Human Endothelial Cells From Proinflammatory to Anti-inflammatory
Nima M. Gharavi, Peter S. Gargalovic, Irene Chang, Jesus A. Araujo, Michael J. Clark, Wan Lam Szeto, Andrew D. Watson, Aldons J. Lusis, and Judith A. Berliner
Arterioscler Thromb Vasc Biol. 2007;27:1346-1353; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.141283
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Previously, we demonstrated that oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycero-phosphorylcholine and component lipids caused induction of genes regulating chemotaxis, sterol biosynthesis, the unfolded protein response, and redox homeostasis in human aortic endothelial cells. Taken together, these studies demonstrated that high-density lipoprotein inhibits the pro-inflammatory effects of oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycero-phosphorylcholine and phospholipid, 1-palmitoyl-2-(5,6 epoxyisoprostanoyl)-sn-glycero-3-phosphocholine, while maintaining the antioxidant activities of these lipids.
Low Levels of Nogo-B in Human Carotid Atherosclerotic Plaques Are Associated With an Atheromatous Phenotype, Restenosis, and Stenosis Severity
Juan A. Rodriguez-Feo, Willem E. Hellings, Bart A.N. Verhoeven, Frans L. Moll, Dominique P.V. de Kleijn, Jay Prendergast, Yuan Gao, Yolanda van der Graaf, George Tellides, William C. Sessa, and Gerard Pasterkamp
Arterioscler Thromb Vasc Biol. 2007;27:1354-1360; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.140913
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Nogo B protects arteries from lumen loss by reducing smooth muscle cell migration and intimal thickening. We report that low levels of Nogo B are associated with atheromatous plaques and stenotic lesions. Therefore, reduction of Nogo B in atherosclerotic tissue might contribute to plaque formation and/or instability triggering luminal narrowing.
Grb2 Is Required for Atherosclerotic Lesion Formation
Brandon M. Proctor, Jie Ren, Zhouji Chen, Jochen G. Schneider, Trey Coleman, Traian S. Lupu, Clay F. Semenkovich, and Anthony J. Muslin
Arterioscler Thromb Vasc Biol. 2007;27:1361-1367; published online before print March 15 2007, doi:10.1161/ATVBAHA.106.134007
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We tested the role of Grb2 in atherosclerosis using Grb2+/- apoE-/- mice. Grb2+/- apoE-/- mice were resistant to atherosclerosis, and Grb2 haploinsufficiency in blood-borne cells conferred resistance to lesion formation. Also, Grb2 was required for foam cell formation. These results implicate a fundamental role for Grb2 in atherosclerotic lesion formation.
Adenovirus-Mediated Expression of Human Paraoxonase 3 Protects Against the Progression of Atherosclerosis in Apolipoprotein E–Deficient Mice
Carey J. Ng, Noam Bourquard, Susan Y. Hama, Diana Shih, Victor R. Grijalva, Mohamad Navab, Alan M. Fogelman, and Srinivasa T. Reddy
Arterioscler Thromb Vasc Biol. 2007;27:1368-1374; published online before print April 19 2007, doi:10.1161/ATVBAHA.106.134189
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The objective of this study was to determine whether PON3 can protect against the progression of atherosclerosis in vivo. PON3 overexpression enhances the cholesterol efflux potential of serum, increases the antiinflammatory properties of HDL, and protects against the progression of atherosclerosis in vivo.
Increased Expression of Glutathione Reductase in Macrophages Decreases Atherosclerotic Lesion Formation in Low-Density Lipoprotein Receptor–Deficient Mice
Mu Qiao, Marta Kisgati, Jill M. Cholewa, Weifei Zhu, Eric J. Smart, Melanie S. Sulistio, and Reto Asmis
Arterioscler Thromb Vasc Biol. 2007;27:1375-1382; published online before print March 15 2007, doi:10.1161/ATVBAHA.107.142109
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Thiol oxidative stress leads to macrophage dysfunction and cell injury, and has been implicated in the development of atherosclerotic lesions. We show that overexpression of mitochondrial or cytosolic glutathione reductase in macrophages decreases the severity of atherosclerosis, providing direct evidence that the glutathione-dependent antioxidant system in macrophages plays a critical role in atherogenesis.
Plasmin Triggers Cytokine Induction in Human Monocyte-Derived Macrophages
Qun Li, Yves Laumonnier, Tatiana Syrovets, and Thomas Simmet
Arterioscler Thromb Vasc Biol. 2007;27:1383-1389; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.142901
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Plasmin, but not catalytically blocked plasmin, induces cytokines such as TNF-{alpha} and IL-6 in human monocyte-derived macrophages. The plasmin-induced signaling utilizes the annexin A2 heterotetramer as receptor that triggers downstream signaling via JAK/STAT, Akt-dependent NF-{kappa}B activation, as well as ERK1/2 and the p38 MAPK, leading to proinflammatory gene induction.
Farnesyltransferase Inhibitor, Manumycin A, Prevents Atherosclerosis Development and Reduces Oxidative Stress in Apolipoprotein E-Deficient Mice
Michiko Sugita, Hiroki Sugita, and Masao Kaneki
Arterioscler Thromb Vasc Biol. 2007;27:1390-1395; published online before print March 15 2007, doi:10.1161/ATVBAHA.107.140673
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Farnesyltransferase inhibitor, manumycin A, prevented the development of atherosclerosis with concomitant decreases in oxidative stress and Ras activation, with unaltered plasma cholesterol level. These results highlight farnesyltransferase as a molecular target to prevent atherogenesis and suggest that inhibition of farnesylation may be involved in lipid-lowering-independent beneficial effects of statins.
Dietary Fat–Induced Alterations in Atherosclerosis Are Abolished by ACAT2-Deficiency in ApoB100 Only, LDLr
–/–
Mice
Thomas A. Bell, III, Kathryn Kelley, Martha D. Wilson, Janet K. Sawyer, and Lawrence L. Rudel
Arterioscler Thromb Vasc Biol. 2007;27:1396-1402; published online before print April 12 2007, doi:10.1161/ATVBAHA.107.142802
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When ACAT2 was removed by gene deletion in apoB100 only,LDLr-/- mice, the ability of any of several types of dietary fat to induce atherosclerosis was prevented. LDL concentration, CE composition, and particle size were modified in ACAT2-/- mice; these changes appeared to play an important role in limiting atherogenesis.
Repetition of Ischemic Preconditioning Augments Endothelium-Dependent Vasodilation in Humans: Role of Endothelium-Derived Nitric Oxide and Endothelial Progenitor Cells
Masashi Kimura, Keiko Ueda, Chikara Goto, Daisuke Jitsuiki, Kenji Nishioka, Takashi Umemura, Kensuke Noma, Masao Yoshizumi, Kazuaki Chayama, and Yukihito Higashi
Arterioscler Thromb Vasc Biol. 2007;27:1403-1410; published online before print April 19 2007, doi:10.1161/ATVBAHA.107.143578
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We evaluated forearm blood flow responses to acetylcholine and to sodium nitroprusside before and after ischemic preconditioning (IPC) stimulus in 30 young healthy men. Repetition of late IPC stimulus augments endothelium-dependent vasodilation in humans through increases in nitric oxide production and number of endothelial progenitor cells under a local condition.
Elevated Lp-PLA
2
Levels Add Prognostic Information to the Metabolic Syndrome on Incidence of Cardiovascular Events Among Middle-Aged Nondiabetic Subjects
Margaretha Persson, Bo Hedblad, Jeanenne J. Nelson, and Göran Berglund
Arterioscler Thromb Vasc Biol. 2007;27:1411-1416; published online before print April 12 2007, doi:10.1161/ATVBAHA.107.142679
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To explore potential interrelationship between Lp-PLA2 and the Metabolic syndrome, in 4480 subjects from the Malmo Diet and Cancer Study, and incident cardiovascular disease. Lp-PLA2 is associated to MetS but increases risk for incident CVD regardless of MetS. Presence of both elevated Lp-PLA2 and MetS may identify an especially high risk individual.
Fenofibrate Effect on Triglyceride and Postprandial Response of Apolipoprotein A5 Variants: The GOLDN Study
Chao-Qiang Lai, Donna K. Arnett, Dolores Corella, Robert J. Straka, Michael Y. Tsai, James M. Peacock, Xian Adiconis, Laurence D. Parnell, James E. Hixson, Michael A. Province, and Jose M. Ordovas
Arterioscler Thromb Vasc Biol. 2007;27:1417-1425; published online before print April 12 2007, doi:10.1161/ATVBAHA.107.140103
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We examined association between variants at APOA5 and TG and HDL-C response to fenofibrate and a postprandial lipid challenge in 791 men and women participating in the GOLDN study, and observed that the 56G carriers benefited more from the fenofibrate treatment than noncarriers in lowering TG and increasing HDL-C levels
Expression of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor-1, and CXCR4 in Human Limb Muscle With Acute and Chronic Ischemia
Vincent van Weel, Leonard Seghers, Margreet R. de Vries, Esther J. Kuiper, Reinier O. Schlingemann, Ingeborg M. Bajema, Jan H.N. Lindeman, Pien M. Delis-van Diemen, Victor W.M. van Hinsbergh, J. Hajo van Bockel, and Paul H.A. Quax
Arterioscler Thromb Vasc Biol. 2007;27:1426-1432; published online before print March 15 2007, doi:10.1161/ATVBAHA.107.139642
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In amputated limbs of patients with peripheral artery disease, expression patterns of VEGF, SDF-1, and CXCR4 suggest a coordinated role of these factors in ischemia-induced angiogenesis, which were downregulated in chronic ischemia versus upregulated in more acute ischemia. This pathway is a promising target to treat chronic ischemic disease.
Endotoxemia, Immune Response to Periodontal Pathogens, and Systemic Inflammation Associate With Incident Cardiovascular Disease Events
Pirkko J. Pussinen, Karolina Tuomisto, Pekka Jousilahti, Aki S. Havulinna, Jouko Sundvall, and Veikko Salomaa
Arterioscler Thromb Vasc Biol. 2007;27:1433-1439; published online before print March 15 2007, doi:10.1161/ATVBAHA.106.138743
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We investigated the connection between serum inflammation markers, antibody levels to major periodontal pathogens, endotoxin concentration, and CVD events in a prospective case-cohort study. Our results suggest that endotoxemia or systemic immune response to periodontal pathogens together with high concentrations of inflammation markers indicate a high risk of incident CVD.
Identification of Atherosclerotic Lipid Deposits by Diffusion-Weighted Imaging
Ye Qiao, Itamar Ronen, Jason Viereck, Frederick L. Ruberg, and James A. Hamilton
Arterioscler Thromb Vasc Biol. 2007;27:1440-1446; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.141028
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Compared with detection of triglyceride in fat depots, MRI of mobile atherosclerotic plaque lipids (mainly CE) is difficult because CE is relatively dilute and present in a heterogeneous environment. DWI is superior to commonly used imaging protocols because it confers very high contrast of the fluid lipid.
Thrombosis
Modulation of Tissue Factor–Factor VIIa Signaling by Lipid Rafts and Caveolae
Vineet Awasthi, Samir K. Mandal, Veena Papanna, L. Vijaya Mohan Rao, and Usha R. Pendurthi
Arterioscler Thromb Vasc Biol. 2007;27:1447-1455; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.143438
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The present study was undertaken to investigate the role of lipid rafts and caveolae in modulating the coagulant and signaling functions of tissue factor. Caveolar localization of tissue factor does not influence its ability to support coagulation but is essential to activate PAR2-mediated cell signaling.
Role of Protease Activated Receptor 1 and 2 Signaling in Hypoxia-Induced Angiogenesis
Hannele Uusitalo-Jarvinen, Toru Kurokawa, Barbara M. Mueller, Patricia Andrade-Gordon, Martin Friedlander, and Wolfram Ruf
Arterioscler Thromb Vasc Biol. 2007;27:1456-1462; published online before print March 15 2007, doi:10.1161/ATVBAHA.107.142539
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The TF pathway regulates angiogenesis through direct TF-VIIa signaling and potentially downstream coagulation activation and thrombin signaling. TF-VIIa-driven angiogenesis in TF cytoplasmic domain deleted mice is shown to be dependent on PAR2 signaling without significant contributions from downstream coagulation activation or mouse PAR1 signaling in vivo.
Platelets Recruit Human Dendritic Cells Via Mac-1/JAM-C Interaction and Modulate Dendritic Cell Function In Vitro
Harald F. Langer, Karin Daub, Gregor Braun, Tanja Schönberger, Andreas E. May, Martin Schaller, Gerburg M. Stein, Konstantinos Stellos, Andreas Bueltmann, Dorothea Siegel-Axel, Hans P. Wendel, Hermann Aebert, Martin Roecken, Peter Seizer, Sentot Santoso, Sebastian Wesselborg, Peter Brossart, and Meinrad Gawaz
Arterioscler Thromb Vasc Biol. 2007;27:1463-1470; published online before print March 22 2007, doi:10.1161/ATVBAHA.107.141515
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Thrombotic events and immunoinflammatory processes take place next to each other in atherosclerotic lesion formation. We show that recruitment of dendritic cells is mediated by platelets in vitro and in vivo and lead to DC activation and apoptosis. This process may be of importance for atherosclerotic lesion progression.
Fluvastatin Alters Platelet Aggregability in Patients With Hypercholesterolemia: Possible Improvement of Intraplatelet Redox Imbalance via HMG-CoA Reductase
Nobuya Haramaki, Hisao Ikeda, Katsuhiko Takenaka, Atsushi Katoh, Ryo Sugano, Sho-ichi Yamagishi, Hidehiro Matsuoka, and Tsutomu Imaizumi
Arterioscler Thromb Vasc Biol. 2007;27:1471-1477; published online before print March 22 2007, doi:10.1161/ATVBAHA.106.128793
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This study examined whether statins inhibit platelet aggregation. Twelve patients with hypercholesterolemia were randomized in a crossover design to receive either fluvastatin or colestimide for 12 weeks. Fluvastatin altered platelet aggregability in hypercholesterolemic patients in a cholesterol-lowering independent manner, which was partly mediated by the improvement of intraplatelet redox imbalance.
Platelets Possess and Require an Active Protein Palmitoylation Pathway for Agonist-Mediated Activation and In Vivo Thrombus Formation
Derek S. Sim, James R. Dilks, and Robert Flaumenhaft
Arterioscler Thromb Vasc Biol. 2007;27:1478-1485; published online before print February 15 2007, doi:10.1161/ATVBAHA.106.139287
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Several platelet proteins are palmitoylated, but whether protein palmitoylation functions in platelet activation is unknown. We sought to determine the role of platelet protein palmitoylation in platelet activation and thrombus formation. Our studies show that platelets possess a protein palmitoylation machinery that is required for both platelet activation and platelet accumulation into thrombi. These studies show that inhibition of platelet protein palmitoylation blocks platelet aggregation and granule secretion. In a murine model of thrombus formation, inhibition of protein palmitoylation markedly inhibits platelet accumulation into thrombi at sites of vascular injury.
Haplotypes of
IL1B
,
IL1RN
,
IL1R1
, and
IL1R2
and the Risk of Venous Thrombosis
Rick van Minkelen, Marieke C.H. de Visser, Jeanine J. Houwing-Duistermaat, Hans L. Vos, Rogier M. Bertina, and Frits R. Rosendaal
Arterioscler Thromb Vasc Biol. 2007;27:1486-1491; published online before print April 5 2007, doi:10.1161/ATVBAHA.107.140384
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Data Supplement
The effect of variations in IL1B, IL1RN, IL1R1, and IL1R2 on venous thrombosis risk was investigated by a haplotype-based approach. Homozygous carriership of haplotype 5 of IL1RN (tagged by SNP 13888T/G, rs2232354) was associated with an increased risk of venous thrombosis (OR=3.9; 95% CI:1.6 to 9.7; P=0.002).
Letters to the Editor
Serum Levels of Soluble Form of Receptor for Advanced Glycation End Products (sRAGE) May Reflect Tissue RAGE Expression In Diabetes
Sho-ichi Yamagishi and Tsutomu Imaizumi
Arterioscler Thromb Vasc Biol. 2007;27:e32, doi:10.1161/ATVBAHA.107.139923
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Assaying Soluble Forms of Receptor for Advanced Glycation End Products
Yasuhiko Yamamoto, Junnosuke Miura, Shigeru Sakurai, Takuo Watanabe, Hideto Yonekura, Hironori Tamei, Hirokazu Matsuki, Ken-ichi Obata, Yasuko Uchigata, Yasuhiko Iwamoto, Hidenori Koyama, and Hiroshi Yamamoto
Arterioscler Thromb Vasc Biol. 2007;27:e33-e34, doi:10.1161/ATVBAHA.107.144337
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Abstracts of the Arteriosclerosis, Thrombosis, and Vascular Biology Annual Conference 2007
Arteriosclerosis, Thrombosis, and Vascular Biology Annual Conference 2007
Arterioscler Thromb Vasc Biol. 2007;27:e35-e137
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Spotlight
TOC Spotlight File
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