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Volume 26, Issue 1; January 1, 2006

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AnnouncementBack


Arterioscler Thromb Vasc Biol. 2006;26:1, doi:10.1161/01.ATV.0000200224.48947.a6
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EditorialsBack

Arteriosclerosis, Thrombosis, and Vascular Biology, 2006

Donald D. Heistad
Arterioscler Thromb Vasc Biol. 2006;26:2-4, doi:10.1161/01.ATV.0000198400.82143.3b
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Lipoprotein-Associated Phospholipase A2 and Cardiovascular Risk: State of the Evidence and Future Directions

Carlos Iribarren
Arterioscler Thromb Vasc Biol. 2006;26:5-6, doi:10.1161/01.ATV.0000196545.32393.13
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HIV Protease Inhibitors and Hyperlipidemia: A Fatty Acid Connection

Arthur A. Spector
Arterioscler Thromb Vasc Biol. 2006;26:7-9, doi:10.1161/01.ATV.0000198749.28422.29
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Tightening the Barrier: Mechanical Forces and the Control of Endothelial Permeability

Jeremy D. Pearson
Arterioscler Thromb Vasc Biol. 2006;26:10-11, doi:10.1161/01.ATV.0000197858.50074.c6
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Brief ReviewsBack

Linda K. Curtiss, David T. Valenta, Neil J. Hime, and Kerry-Anne Rye
Arterioscler Thromb Vasc Biol. 2006;26:12-19; published online before print November 3 2005, doi:10.1161/01.ATV.0000194291.94269.5a
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In this brief review, we propose that spherical apoAI is derived from HDL by remodeling events that are accomplished by proteins secreted by cholesteryl ester-loaded foam cells, including the lipid transfer proteins, phospholipid transfer protein, and cholesteryl ester transfer protein, and the triglyceride hydrolases hepatic lipase and lipoprotein lipase.  

Shinji Yokoyama
Arterioscler Thromb Vasc Biol. 2006;26:20-27; published online before print November 10 2005, doi:10.1161/01.ATV.0000195789.39418.e8
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HDL is generated by the interaction of helical apolipoproteins with cellular lipid. The reaction is mediated by ABCA1 as one of the major pathways for somatic cells to export cellular cholesterol for its homeostasis. Phospholipid is primarily recruited for the HDL assembly and its cholesterol enrichment is regulated independently.  

Florian Blaschke, Yasunori Takata, Evren Caglayan, Ronald E. Law, and Willa A. Hsueh
Arterioscler Thromb Vasc Biol. 2006;26:28-40; published online before print October 20 2005, doi:10.1161/01.ATV.0000191663.12164.77
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Obesity and the interrelated disorders of the metabolic syndrome have become a major worldwide health problem. In this review, we summarize the critical role of PPARs in regulating inflammation, lipoprotein metabolism, and glucose homeostasis and their potential implications for the treatment of obesity, diabetes, and atherosclerosis.  

Dougald M. Monroe and Maureane Hoffman
Arterioscler Thromb Vasc Biol. 2006;26:41-48; published online before print October 27 2005, doi:10.1161/01.ATV.0000193624.28251.83
Abstract | Full Text | PDF
The coagulation process has been conceptualized as being primarily dependent on adequate levels of the coagulation proteins. This concept was based on the clear relationship between the bleeding tendency and factor levels in hemophilia. Our understanding of how specific cellular features control the processes of hemostasis and thrombosis is developing rapidly. This review discusses some aspects of the cellular control of coagulation.  

 

Vascular BiologyBack

Mariska G. Rondaij, Ruben Bierings, Astrid Kragt, Karina A. Gijzen, Erica Sellink, Jan A. van Mourik, Mar Fernandez-Borja, and Jan Voorberg
Arterioscler Thromb Vasc Biol. 2006;26:49-55; published online before print October 20 2005, doi:10.1161/01.ATV.0000191639.08082.04
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Perinuclear clustering is observed for several different organelles and illustrates dynamic regulation of the secretory pathway and organelle distribution. Previously, we observed that a subset of Weibel-Palade bodies (WPBs), endothelial cell-specific storage organelles, undergo centralization when endothelial cells are stimulated with cAMP-raising agonists of von Willebrand factor secretion. In this study, we investigated this phenomenon of WPB clustering in more detail.  

Eser Adiguzel, Guangpei Hou, Diane Mulholland, Ulrike Hopfer, Naomi Fukai, Bjorn Olsen, and Michelle Bendeck
Arterioscler Thromb Vasc Biol. 2006;26:56-61; published online before print November 3 2005, doi:10.1161/01.ATV.0000194155.96456.b7
Abstract | Full Text | PDF | Data Supplement
Type VIII collagen is upregulated after vascular injury and in atherosclerosis. Using smooth muscle cells from wild-type and type VIII collagen knockout mice, we show that cells that are able to produce endogenous type VIII collagen, proliferate, spread, and migrate more when the cells are plated on a type I collagen matrix.  

Nora T. Collins, Philip M. Cummins, Olga C. Colgan, Gail Ferguson, Yvonne A. Birney, Ronan P. Murphy, Gerardene Meade, and Paul A. Cahill
Arterioscler Thromb Vasc Biol. 2006;26:62-68; published online before print November 3 2005, doi:10.1161/01.ATV.0000194097.92824.b3
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The objective of this study was to investigate the effects of cyclic strain on the expression, modification, and function of 2 pivotal endothelial tight junction components: occludin and ZO-1. Our findings indicate that cyclic strain modulates the expression and phosphorylation of both proteins with consequences for their association and subcellular localization at the cell-cell border and, ultimately, for endothelial barrier integrity.  

Jonathan T. Butcher, Sarah Tressel, Tiffany Johnson, Debi Turner, George Sorescu, Hanjoong Jo, and Robert M. Nerem
Arterioscler Thromb Vasc Biol. 2006;26:69-77; published online before print November 17 2005, doi:10.1161/01.ATV.0000196624.70507.0d
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Aortic and aortic valve endothelial cell gene expression was compared in static and steady shear environments. Transcriptional profiles suggested that valvular endothelial cells are similar in some respects but distinct in other ways that may have important implications for the understanding of valvular pathology and therapeutic strategies.  

Xin Tang, Blythe B. Holmes, Kasem Nithipatikom, Cecilia J. Hillard, Hartmut Kuhn, and William B. Campbell
Arterioscler Thromb Vasc Biol. 2006;26:78-84; published online before print October 20 2005, doi:10.1161/01.ATV.0000191640.73313.ad
Abstract | Full Text | PDF | Data Supplement
15-LO-I is expressed in rabbit aorta. 15-LO regulates vasodilatory eicosanoid synthesis and vascular tone.  

Xiaoping Yang, D. Paul Thomas, Xiaochun Zhang, Bruce W. Culver, Brenda M. Alexander, William J. Murdoch, Mysore N.A. Rao, David A. Tulis, Jun Ren, and Nair Sreejayan
Arterioscler Thromb Vasc Biol. 2006;26:85-90; published online before print October 20 2005, doi:10.1161/01.ATV.0000191635.00744.b6
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Curcumin, the major component of the food additive turmeric, inhibits PDGF-stimulated smooth muscle cell proliferation, migration, and collagen synthesis. Curcumin attenuates neointima development, collagen accumulation, and upregulation of PDGF receptors in a rat arterial balloon-injury model. These effects may be attributed to the inhibition of PDGF signal transduction by curcumin.  

Kwang-il Kim, Hyun-Ju Cho, Joo-Yong Hahn, Tae-Youn Kim, Kyung-Woo Park, Bon-Kwon Koo, Chan Soo Shin, Cheol-Ho Kim, Byung-Heeh Oh, Myoung-Mook Lee, Young-Bae Park, and Hyo-Soo Kim
Arterioscler Thromb Vasc Biol. 2006;26:91-98; published online before print October 27 2005, doi:10.1161/01.ATV.0000193569.12490.4b
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The role of ß-catenin in endothelial cells and myocytes has not been studied. We show that ß-catenin overexpression augments angiogenesis and skeletal muscle regeneration through not only vascular endothelial growth factor-mediated endothelial cell proliferation but also through progenitor cell mobilization or activation. These results implicate ß-catenin as an important regulator in ischemic tissue.  

Clara De Palma, Elisabetta Meacci, Cristiana Perrotta, Paola Bruni, and Emilio Clementi
Arterioscler Thromb Vasc Biol. 2006;26:99-105; published online before print November 3 2005, doi:10.1161/01.ATV.0000194074.59584.42
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How tumor necrosis factor (TNF)-activates endothelial NO synthase to generate NO in the endothelium was not known. This study shows that TNF- activates endothelial NO synthase via Sph1P. Because Sph1P and NO interact to regulate important aspects of endothelial cell activation by TNF-, their link with TNF- in a same signaling pathway is of biological relevance.  

Eric H. Yang, Joseph P. McConnell, Ryan J. Lennon, Gregory W. Barsness, Geralyn Pumper, Stacy J. Hartman, Charanjit S. Rihal, Lilach O. Lerman, and Amir Lerman
Arterioscler Thromb Vasc Biol. 2006;26:106-111; published online before print October 20 2005, doi:10.1161/01.ATV.0000191655.87296.ab
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Coronary endothelial dysfunction can be considered a marker for early atherosclerosis and has been shown to be associated with an increased risk of ischemic cardiac events and stroke. The results of the current study show that Lp-PLA2, an enzyme involved in the metabolism of oxidized phospholipids, is independently associated with coronary artery endothelial dysfunction and is a strong predictor of endothelial dysfunction in humans.  

Nikos Werner, Sven Wassmann, Patrick Ahlers, Sonja Kosiol, and Georg Nickenig
Arterioscler Thromb Vasc Biol. 2006;26:112-116; published online before print October 20 2005, doi:10.1161/01.ATV.0000191634.13057.15
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Endothelial function may be influenced by the degree of endothelial cell apoptosis. Endothelial function and endothelial cell apoptosis was assessed in patients with coronary artery disease. Increased apoptotic microparticle counts correlated with impairment of invasively measured coronary endothelial function. Endothelial-dependent vasodilatation closely relies on the degree of endothelial cell apoptosis.  

Vicenta Llorente-Cortés, Marta Otero-Viñas, Sandra Camino-López, Paula Costales, and Lina Badimon
Arterioscler Thromb Vasc Biol. 2006;26:117-123; published online before print October 27 2005, doi:10.1161/01.ATV.0000193618.32611.8b
Abstract | Full Text | PDF | Data Supplement
LRP1-mediated aggregated low-density lipoprotein (agLDL) uptake induces intracellular cholesteryl ester (CE) accumulation. Our aim was to characterize the mechanism of agLDL internalization in human vascular smooth muscle cells (VSMCs). Results demonstrate that LRP1 mediates the selective uptake of CE from agLDL and that CE derived from agLDL is not intracellularly processed but stored in lipid droplets in human VSMCs.  

Marion A.M. den Boer, Jimmy F.P. Berbée, Peter Reiss, Marc van der Valk, Peter J. Voshol, Folkert Kuipers, Louis M. Havekes, Patrick C.N. Rensen, and Johannes A. Romijn
Arterioscler Thromb Vasc Biol. 2006;26:124-129; published online before print November 3 2005, doi:10.1161/01.ATV.0000194073.87647.10
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We investigated the mechanism underlying the hypertriglyceridemia associated with ritonavir treatment in APOE*3-Leiden mice. Ritonavir increased the postprandial triglyceride response and decreased the clearance of glycerol tri[3H]oleatelabeled very low density lipoprotein-like emulsion particles, as related to decreased plasma lipoprotein lipase activity. These effects were accompanied by decreased fatty acid flux into adipose tissue.  

Mariam Rodríguez-Lee, Gunnel Östergren-Lundén, Boel Wallin, Jonatan Moses, Göran Bondjers, and Germán Camejo
Arterioscler Thromb Vasc Biol. 2006;26:130-135; published online before print October 20 2005, doi:10.1161/01.ATV.0000191659.94059.62
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We examined the effects of increased NEFA and insulin on the proteoglycans secreted by hASMC and whether these effects might affect LDL binding. The results indicate that increased fatty acids could induce qualitative and quantitative alterations of the intima extracellular matrix proteoglycans favoring LDL retention and possibly atherogenesis.  

 

Atherosclerosis and LipoproteinsBack

Anne-Louise Hemdahl, Anders Gabrielsen, Chaoyong Zhu, Per Eriksson, Ulf Hedin, Jens Kastrup, Peter Thorén, and Göran K. Hansson
Arterioscler Thromb Vasc Biol. 2006;26:136-142; published online before print October 27 2005, doi:10.1161/01.ATV.0000193567.88685.f4
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NGAL protects MMP-9 from inactivation but has not been described previously in atherosclerosis. Our study shows that NGAL and its mouse homolog are increased in atherosclerosis and after myocardial infarction and colocalize with MMP-9 in atherosclerotic areas with high-proteolytic activity, suggesting a modulating role for NGAL in atherosclerosis.  

Paul P. Lau, Lan Li, Aksam J. Merched, Alan L. Zhang, Kerry W.S. Ko, and Lawrence Chan
Arterioscler Thromb Vasc Biol. 2006;26:143-149; published online before print October 27 2005, doi:10.1161/01.ATV.0000193510.19000.10
Abstract | Full Text | PDF | Data Supplement
We investigated the molecular mechanism of nicotine-accelerated atherosclerosis in the hyperlipidemic LDLR-/- mouse model. Our findings reveal a novel mechanism of nicotine-mediated atherogenesis. Nicotine directly activates macrophages via the nicotinic acetylcholine receptor, activating multiple downstream events, leading to NF-{kappa}B-mediated inflammation in the arterial wall and accelerated atherosclerosis.  

Hong Yu, Wenwu Zhang, Patricia G. Yancey, Mark J. Koury, Youmin Zhang, Sergio Fazio, and MacRae F. Linton
Arterioscler Thromb Vasc Biol. 2006;26:150-156; published online before print November 3 2005, doi:10.1161/01.ATV.0000194096.89476.73
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Mice null for apolipoprotein E and scavenger receptor class BI develop severe hypercholesterolemia, occlusive coronary atherosclerosis, myocardial infarction, and premature death, The current study indicates that macrophage apolipoprotein E is able to rescue the lethal phenotype of apolipoprotein E-/- scavenger receptor class BI-/- mice by preventing severe dyslipidemia and atherosclerotic lesion development.  

Zhi H. Huang, Michael L. Fitzgerald, and Theodore Mazzone
Arterioscler Thromb Vasc Biol. 2006;26:157-162; published online before print October 27 2005, doi:10.1161/01.ATV.0000193627.12516.1d
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These studies establish 2 separate pathways for lipid efflux mediated by the endogenous expression of cellular apoE. One is mediated by the extracellular accumulation of endogenous apolipoprotein E and depends on the expression of ABCA1. The second requires the intracellular synthesis and transport of apolipoprotein E and is independent of ABCA1.  

Makoto Ayaori, Shojiro Sawada, Atsushi Yonemura, Noriyuki Iwamoto, Masatsune Ogura, Nobukiyo Tanaka, Kazuhiro Nakaya, Masatoshi Kusuhara, Haruo Nakamura, and Fumitaka Ohsuzu
Arterioscler Thromb Vasc Biol. 2006;26:163-168; published online before print October 27 2005, doi:10.1161/01.ATV.0000193513.29074.52
Abstract | Full Text | PDF | Data Supplement
Several nuclear receptors regulate ABCA1 expression to maintain intracellular cholesterol. The present study showed that glucocorticoid receptor (GR) agonist and antagonist, respectively, attenuated and stimulated cholesterol efflux from macrophages by apolipoprotein and ABCA1 expression, which are regulated by GR at a transcriptional level through an LXR-independent mechanism.  

Patrick C.N. Rensen, Leo A.J.M. Sliedregt, Peter J. van Santbrink, Michiel Ferns, Hendrik N.J. Schifferstein, Steven H. van Leeuwen, John H.M. Souverijn, Theo J.C. van Berkel, and Erik A.L. Biessen
Arterioscler Thromb Vasc Biol. 2006;26:169-175; published online before print October 27 2005, doi:10.1161/01.ATV.0000193620.98587.40
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A bifunctional glycolipid with a high affinity for the asialoglycoprotein receptor on hepatocytes dramatically induced the hepatic uptake of lipoproteins and evoked strong and persistent cholesterol-lowering effects in mice. This glycolipid may be of added value in the treatment of patients who do not respond to conventional cholesterol-lowering therapies.  

Fabien Hyafil, Jean-Pierre Laissy, Mikael Mazighi, Didier Tchétché, Liliane Louedec, Homa Adle-Biassette, Sylvie Chillon, Dominique Henin, Marie-Paule Jacob, Didier Letourneur, and Laurent J. Feldman
Arterioscler Thromb Vasc Biol. 2006;26:176-181; published online before print November 3 2005, doi:10.1161/01.ATV.0000194098.82677.57
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We evaluated the ability of ferumoxtran-10-enhanced MRI to quantify macrophage infiltration in the aortic wall of hypercholesterolemic rabbits. Ferumoxtran-10-induced magnetic susceptibility artifacts were detected by in vivo MRI only in macrophage-rich aortic segments. Magnetic susceptibility artifact-related luminal narrowing on MRI correlated with macrophage infiltration on corresponding aortic cross-sections.  

Philippe O. Szapary, LeAnne T. Bloedon, Frederick F. Samaha, Danielle Duffy, Megan L. Wolfe, Daniel Soffer, Muredach P. Reilly, Jesse Chittams, and Daniel J. Rader
Arterioscler Thromb Vasc Biol. 2006;26:182-188; published online before print November 10 2005, doi:10.1161/01.ATV.0000195790.24531.4f
Abstract | Full Text | PDF
We performed a detailed evaluation of the lipid effects of pioglitazone (PIO) in nondiabetic patients with metabolic syndrome. The primary finding was that PIO raised high-density lipoprotein cholesterol by 14% compared with placebo, without significant changes triglycerides or low-density lipoprotein cholesterol. Our results suggest that PIO may be useful as an antiatherosclerotic strategy in this nondiabetic population.  

Philip B. Mellen, William T. Cefalu, and David M. Herrington
Arterioscler Thromb Vasc Biol. 2006;26:189-193; published online before print October 20 2005, doi:10.1161/01.ATV.0000191656.71812.7c
Abstract | Full Text | PDF
Although the metabolic syndrome (MS) is associated with increased cardiovascular risk, its relationship with atherosclerotic progression is less well defined. We sought to determine whether the MS predicts angiographic progression of coronary heart disease in a cohort of postmenopausal women. Among postmenopausal women with coronary heart disease, the presence of diabetes predicted disease progression, but the MS did not.  

Dietrich Rothenbacher, Sylvia Müller-Scholze, Christian Herder, Wolfgang Koenig, and Hubert Kolb
Arterioscler Thromb Vasc Biol. 2006;26:194-199; published online before print October 20 2005, doi:10.1161/01.ATV.0000191633.52585.14
Abstract | Full Text | PDF
In this large, case-control study including patients with angiographically defined stable CHD, we found evidence of a differential expression of chemokines associated with the risk for CHD.  

Kirsten B. Holven, Jan K. Damås, Arne Yndestad, Torgun Wæhre, Thor Ueland, Bente Halvorsen, Lars Heggelund, Wiggo J. Sandberg, Anne G. Semb, Stig S. Frøland, Leiv Ose, Marit S. Nenseter, and Pål Aukrust
Arterioscler Thromb Vasc Biol. 2006;26:200-205; published online before print October 27 2005, doi:10.1161/01.ATV.0000193619.67288.ed
Abstract | Full Text | PDF | Data Supplement
Herein we show that children with heterozygous familial hypercholesterolemia are characterized by enhanced expression of RANTES but not of the other measured chemokines in peripheral blood mononuclear cells. Our findings support a role for inflammation also in the early stages of atherogenesis possibly involving RANTES as an important mediator.  

Thor Edvardsen, Robert Detrano, Boaz D. Rosen, J. Jeffrey Carr, Kiang Liu, Shenghan Lai, Steven Shea, Li Pan, David A. Bluemke, and João A.C. Lima
Arterioscler Thromb Vasc Biol. 2006;26:206-211; published online before print November 3 2005, doi:10.1161/01.ATV.0000194077.23234.ae
Abstract | Full Text | PDF
Participants of the Multiethnic Study of Atherosclerosis without history of previous heart disease were studied by MRI tagging and computed tomography. Greater coronary calcification in all coronary arteries were related to worse function in their respective perfusion territories. These results indicate a link between atherosclerosis and subclinical regional left ventricular dysfunction.  

Mark P.S. Sie, Fakhredin A. Sayed-Tabatabaei, Hok-Hay S. Oei, André G. Uitterlinden, Hubert A.P. Pols, Albert Hofman, Cornelia M. van Duijn, and Jacqueline C.M. Witteman
Arterioscler Thromb Vasc Biol. 2006;26:212-217; published online before print November 3 2005, doi:10.1161/01.ATV.0000194099.65024.17
Abstract | Full Text | PDF | Data Supplement
Inflammation plays an important role in atherosclerosis. The association of the inflammatory interleukin 6 -174 G/C polymorphism and risk of coronary heart disease was investigated in a population-based study and additional meta-analysis. No association was found; we conclude the polymorphism is not a suitable marker for increased risk.  

Sammy Al-Benna, Carlene A. Hamilton, John D. McClure, Paul N. Rogers, Geoffrey A. Berg, Ian Ford, Christian Delles, and Anna F. Dominiczak
Arterioscler Thromb Vasc Biol. 2006;26:218-223; published online before print October 27 2005, doi:10.1161/01.ATV.0000193626.22269.45
Abstract | Full Text | PDF | Data Supplement
We examined the role of oxidative stress in the relationship between endothelial dysfunction of saphenous veins and cardiovascular disease. Low-density lipoprotein cholesterol was the major determinant of endothelial dysfunction and oxidative stress in patients with coronary artery disease. These results support intensive low-density lipoprotein cholesterol-lowering therapy as suggested by recent clinical trials.  

 

ThrombosisBack

Hisashi Kato, Hirokazu Kashiwagi, Masamichi Shiraga, Seiji Tadokoro, Tsuyoshi Kamae, Hidetoshi Ujiie, Shigenori Honda, Shigeki Miyata, Yoshinobu Ijiri, Junichiro Yamamoto, Norikazu Maeda, Tohru Funahashi, Yoshiyuki Kurata, Iichiro Shimomura, Yoshiaki Tomiyama, and Yuzuru Kanakura
Arterioscler Thromb Vasc Biol. 2006;26:224-230; published online before print November 3 2005, doi:10.1161/01.ATV.0000194076.84568.81
Abstract | Full Text | PDF | Data Supplement
We demonstrated an enhanced thrombus formation and platelet aggregation in adiponectin knockout mice and that adenovirus-mediated supplementation of adiponectin attenuated the enhanced thrombus formation. In wild-type mice, overexpression of adiponectin attenuated thrombus formation. These findings reveal a new role of adiponectin as an endogenous antithrombotic factor.  

 

Letters to the EditorBack

High Plasma Levels of Osteopontin in Patients With Restenosis After Percutaneous Coronary Intervention

Ryuichi Kato, Yukihiko Momiyama, Reiko Ohmori, Nobukiyo Tanaka, Hiroaki Taniguchi, Koh Arakawa, Masatoshi Kusuhara, Haruo Nakamura, and Fumitaka Ohsuzu
Arterioscler Thromb Vasc Biol. 2006;26:e1-e2, doi:10.1161/01.ATV.0000194157.26665.e6
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Impaired Endothelium-Dependent and -Independent Vasodilation in Young Female Athletes With Exercise-Associated Amenorrhea

Noriko Yoshida, Hisao Ikeda, Kenzo Sugi, and Tsutomu Imaizumi
Arterioscler Thromb Vasc Biol. 2006;26:231-232, doi:10.1161/01.ATV.0000199102.60747.18
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Aldosterone Promotes Thrombosis Formation After Arterial Injury in Mice

P.F. Bodary, C. Sambaziotis, K.J. Wickenheiser, S. Rajagopalan, B. Pitt, and D.T. Eitzman
Arterioscler Thromb Vasc Biol. 2006;26:233, doi:10.1161/01.ATV.0000195782.07637.44
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Acknowledgement of ReviewersBack

Acknowledgement of Reviewers


Arterioscler Thromb Vasc Biol. 2006;26:e3-e9
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