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Volume 26, Issue 12; December 1, 2006

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EditorialsBack

Origin of Neointimal Smooth Muscle: We’ve Come Full Circle

Mark H. Hoofnagle, James A. Thomas, Brian R. Wamhoff, and Gary K. Owens
Arterioscler Thromb Vasc Biol. 2006;26:2579-2581, doi:10.1161/01.ATV.0000249623.79871.bc.
Full Text | PDF  

Regulation of TLR4 Expression Is a Tale About Tail

Zhong-qun Yan
Arterioscler Thromb Vasc Biol. 2006;26:2582-2584, doi:10.1161/01.ATV.0000250933.92917.dd.
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Coupling eNOS Uncoupling to the Innate Immune Response

Ton J. Rabelink and Anton-Jan van Zonneveld
Arterioscler Thromb Vasc Biol. 2006;26:2585-2587, doi:10.1161/01.ATV.0000250932.24151.50.
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Brief ReviewsBack

Frederick F. Samaha and Mark L. Kahn
Arterioscler Thromb Vasc Biol. 2006;26:2588-2593; published online before print October 5 2006, doi:10.1161/01.ATV.0000248734.89782.37.
Abstract | Full Text | PDF
Recent studies have revealed novel and diverse roles for immunoreceptor signaling in vascular biology. In the present review we discuss immunoreceptor signaling downstream of platelet collagen receptors and in hematopoietic cells that contribute to the developing lymphatic vascular system, as well as future clinical and scientific directions of this field.  

Olivier Morel, Florence Toti, Bénédicte Hugel, Babé Bakouboula, Laurence Camoin-Jau, Françoise Dignat-George, and Jean-Marie Freyssinet
Arterioscler Thromb Vasc Biol. 2006;26:2594-2604; published online before print September 21 2006, doi:10.1161/01.ATV.0000246775.14471.26.
Abstract | Full Text | PDF
Plasma membrane-derived microparticles are at the crossroad of atherothrombosis processes involving vascular inflammation, remodeling, endothelial dysfunction, and plaque thrombogenicity. After plaque disruption, trapped and circulating microparticles provide the concentration of tissue factor allowing blood coagulation to be triggered. The pharmacological modulation of microparticle release appears a promising preventive approach.  

Jonathan Golledge, Juanita Muller, Alan Daugherty, and Paul Norman
Arterioscler Thromb Vasc Biol. 2006;26:2605-2613; published online before print September 14 2006, doi:10.1161/01.ATV.0000245819.32762.cb.
Abstract | Full Text | PDF
Abdominal aortic aneurysm is associated with significant morbidity and mortality. Presently medical therapy for this condition has been neglected. This article summarises efforts to better understand the pathology of AAA to develop such treatments.  

 

Vascular BiologyBack

Shu-ichi Saitoh, Cuihua Zhang, Johnathan D. Tune, Barry Potter, Takahiko Kiyooka, Paul A. Rogers, Jarrod D. Knudson, Gregory M. Dick, Albert Swafford, and William M. Chilian
Arterioscler Thromb Vasc Biol. 2006;26:2614-2621; published online before print October 5 2006, doi:10.1161/01.ATV.0000249408.55796.da.
Abstract | Full Text | PDF
We tested the hypothesis that H2O2 couples myocardial oxygen consumption to coronary flow. Isolated myocytes produced O2{middle dot}- and H2O2 in proportion to metabolism, and produced dilation that was eliminated by catalase. In intact animals tissue concentrations of H2O2 were linearly related to myocardial oxygen consumption and directly linked to coronary blood flow. We conclude that H2O2 couples coronary blood flow to myocardial oxygen consumption.  

Feng-Yen Lin, Yung-Hsiang Chen, Yi-Wen Lin, Jen-Sung Tsai, Jaw-Wen Chen, Hsiao-Jung Wang, Yuh-Lien Chen, Chi-Yuan Li, and Shing-Jong Lin
Arterioscler Thromb Vasc Biol. 2006;26:2622-2629; published online before print September 21 2006, doi:10.1161/01.ATV.0000246779.78003.cf.
Abstract | Full Text | PDF | Data Supplement
We investigated the posttranscriptional regulation in LPS-induced TLR4 expression in HASMCs and balloon-injured rabbit aorta. These results demonstrate that activation of NADPH oxidase and the MAPK-signaling pathway contribute to HuR-mediated stabilization of TLR4 mRNA induced by LPS in smooth muscle cells.  

Feng-Yen Lin, Yung-Hsiang Chen, Jen-Sung Tasi, Jaw-Wen Chen, Tung-Lin Yang, Hsiao-Jung Wang, Chi-Yuan Li, Yuh-Lien Chen, and Shing-Jong Lin
Arterioscler Thromb Vasc Biol. 2006;26:2630-2637; published online before print September 28 2006, doi:10.1161/01.ATV.0000247259.01257.b3.
Abstract | Full Text | PDF | Data Supplement
We investigated the mechanisms in LPS-induced TLR4 expression in HASMCs and balloon-injured rabbit aorta. These results demonstrate that NADPH oxidase activation, mRNA stabilization, and MAPK signaling pathways play critical roles in LPS-increased TLR4 expression in HASMCs that involved in vascular inflammation.  

Lixin Li and Balz Frei
Arterioscler Thromb Vasc Biol. 2006;26:2638-2643; published online before print September 14 2006, doi:10.1161/01.ATV.0000245820.34238.da.
Abstract | Full Text | PDF | Data Supplement
This study shows that the iron chelator, desferrioxamine (DFO), but not iron-loaded DFO, inhibits NF-{kappa}B activation and cellular adhesion molecule expression in a murine model of local inflammation by inhibiting p22phox protein expression, NADPH oxidase activity, and oxidant production. Therefore, chelation of excess iron may help attenuate inflammation and atherosclerosis.  

Kai Kappert, Jan Sparwel, Åsa Sandin, Alexander Seiler, Udo Siebolts, Olli Leppänen, Stephan Rosenkranz, and Arne Östman
Arterioscler Thromb Vasc Biol. 2006;26:2644-2651; published online before print September 21 2006, doi:10.1161/01.ATV.0000246777.30819.85.
Abstract | Full Text | PDF | Data Supplement
Growth factor- and reactive oxygen species-induced activation of VSMCs is involved in vascular disease. This study demonstrates that inhibitory oxidation of protein tyrosine phosphatases (PTPs) contributes to signaling in VSMCs in vitro and in vivo, and that antioxidants can effectively reactivate oxidized PTPs and thereby reduce PDGF signaling and neointima formation.  

Kenji Inoue, Mika Kobayashi, Kiichiro Yano, Mai Miura, Akashi Izumi, Chikage Mataki, Takeshi Doi, Takao Hamakubo, Patrick C. Reid, David A. Hume, Minoru Yoshida, William C. Aird, Tatsuhiko Kodama, and Takashi Minami
Arterioscler Thromb Vasc Biol. 2006;26:2652-2659; published online before print September 28 2006, doi:10.1161/01.ATV.0000247247.89787.e7.
Abstract | Full Text | PDF | Data Supplement
A global-survey of TNF-{alpha}-signaling in ECs revealed that VCAM-1 expression is highly induced in a process dependent on PI3-K, GATA, HDAC, and new protein synthesis. HDAC inhibition abrogated monocyte adhesion to inflamed endothelium suggesting that HDAC, specifically HDAC3, might be useful for the attenuation of the inflammatory response in ECs.  

Hisanori Kosuge, Jun-ichi Suzuki, Go Haraguchi, Noritaka Koga, Yasuhiro Maejima, Manabu Inobe, Mitsuaki Isobe, and Toshimitsu Uede
Arterioscler Thromb Vasc Biol. 2006;26:2660-2665; published online before print September 21 2006, doi:10.1161/01.ATV.0000245805.52081.ca.
Abstract | Full Text | PDF | Data Supplement
The role of the ICOS pathway in SMC proliferation has not yet been evaluated. We demonstrate that blockade of the ICOS pathway significantly suppressed SMC proliferation and neointimal thickening.  

P. Christian Schulze, Heling Liu, Elizabeth Choe, Jun Yoshioka, Anath Shalev, Kenneth D. Bloch, and Richard T. Lee
Arterioscler Thromb Vasc Biol. 2006;26:2666-2672; published online before print October 5 2006, doi:10.1161/01.ATV.0000248914.21018.f1.
Abstract | Full Text | PDF | Data Supplement
Cellular redox balance is tightly regulated and nitric oxide (NO) promotes antioxidative mechanisms. We show the NO-dependent transcriptional regulation of the antioxidative thioredoxin system through suppression of Txnip and induction of thioredoxin reductase. NO also increased thioredoxin activity. These findings represent a novel antioxidative mechanism of NO.  

Hideto Sano, Kohei Hosokawa, Hiroyasu Kidoya, and Nobuyuki Takakura
Arterioscler Thromb Vasc Biol. 2006;26:2673-2680; published online before print September 14 2006, doi:10.1161/01.ATV.0000245821.77155.c3.
Abstract | Full Text | PDF | Data Supplement
Angiopoietin-1 (Ang1) suppresses VEGF-mediated hyperpermeability. We found that ACE expression in Endothelial cells was negatively or positively regulated by Ang1 or VEGF, respectively, and VEGF-mediated hyperpermeability was suppressed by Angiotensin II type1 receptor blocker (ARB) suggesting availability of ARB for minimizing the risk of edema in therapeutic angiogenesis using VEGF.  

Alexandra Buehler, Marc A.M.J. van Zandvoort, Bram J. Stelt, Tilman M. Hackeng, Bianca H.G.J. Schrans-Stassen, Abdelkader Bennaghmouch, Leo Hofstra, Jack P.M. Cleutjens, Adriaan Duijvestijn, Mirjam B. Smeets, Dominique P.V. de Kleijn, Mark J. Post, and Ebo D. de Muinck
Arterioscler Thromb Vasc Biol. 2006;26:2681-2687; published online before print September 21 2006, doi:10.1161/01.ATV.0000245807.65714.0b.
Abstract | Full Text | PDF | Data Supplement
In murine myocardial infarcts we show that the cell surface marker CD13/APN (aminopeptidase N) is selectively upregulated on angiogenic endothelium. Using in vivo fluorescence imaging and ex vivo 2-photon scanning electron microscopy, we show that angiogenic CD13/APN can be targeted and imaged specifically with the synthetic targeting peptide cNGR.  

 

Atherosclerosis and LipoproteinsBack

Jian Xu, Zhonglin Xie, Richard Reece, David Pimental, and Ming-Hui Zou
Arterioscler Thromb Vasc Biol. 2006;26:2688-2695; published online before print October 5 2006, doi:10.1161/01.ATV.0000249394.94588.82.
Abstract | Full Text | PDF
Endothelial nitric oxide synthase (eNOS) uncoupling is observed in cardiovascular diseases, but its mechanisms remain elusive. Here we reported that hypochlorous acid activated PKC-{zeta}-dependent NAD(P)H oxidase and generated kindling radicals (O2{middle dot}-) and oxidants (ONOO-), which further oxidizes the zinc-thiolate center, dissociates the enzyme-active dimers, and uncouples the enzyme.  

Jacob F. Bentzon, Charlotte Weile, Claus S. Sondergaard, Johnny Hindkjaer, Moustapha Kassem, and Erling Falk
Arterioscler Thromb Vasc Biol. 2006;26:2696-2702; published online before print September 28 2006, doi:10.1161/01.ATV.0000247243.48542.9d.
Abstract | Full Text | PDF | Data Supplement
Recent studies have concluded that SMCs in atherosclerosis can originate from circulating progenitor cells. In contrast to this hypothesis, we showed by a series of bone marrow and vessel transplantations that SMCs in atherosclerotic plaques are derived entirely from the local vessel wall in apoE knockout mice  

Brian W. Parks, Aldons J. Lusis, and Janusz H.S. Kabarowski
Arterioscler Thromb Vasc Biol. 2006;26:2703-2709; published online before print September 21 2006, doi:10.1161/01.ATV.0000246774.02426.71.
Abstract | Full Text | PDF | Data Supplement
The G2A receptor mediates chemotactic and apoptotic effects of lysophosphatidylcholine in vitro. Loss of G2A suppressed aortic atherosclerosis, reduced macrophage accumulation at lesion-prone sites of the aorta, and elevated circulating HDL cholesterol levels in LDLR knockout mice. A pleiotropy of effects may contribute to the pro-atherogenic action of G2A.  

L. Hu, L.S.M. Boesten, P. May, J. Herz, N. Bovenschen, M.V. Huisman, J.F.P. Berbée, L.M. Havekes, B.J.M. van Vlijmen, and J.T. Tamsma
Arterioscler Thromb Vasc Biol. 2006;26:2710-2715; published online before print October 12 2006, doi:10.1161/01.ATV.0000249641.96896.e6.
Abstract | Full Text | PDF | Data Supplement
We investigated the role of macrophage specific LRP deficiency in the development of atherosclerosis independent of its role in lipoprotein metabolism. Specific deletion of macrophage LRP in mice resulted in more advanced atherosclerosis and in lesions that contain more collagen and less relative numbers of CD3+ T cells. This indicates that macrophage LRP has an atheroprotective potential.  

Chiara Cuccurullo, Annalisa Iezzi, Maria Luigia Fazia, Domenico De Cesare, Andrea Di Francesco, Raffaella Muraro, Roberto Bei, Sante Ucchino, Francesco Spigonardo, Francesco Chiarelli, Ann Marie Schmidt, Franco Cuccurullo, Andrea Mezzetti, and Francesco Cipollone
Arterioscler Thromb Vasc Biol. 2006;26:2716-2723; published online before print October 12 2006, doi:10.1161/01.ATV.0000249630.02085.12.
Abstract | Full Text | PDF | Data Supplement
The aim of this study was to characterize the effect of simvastatin on the expression of RAGE and RAGE-dependent plaque-destabilizing genes in human atherosclerotic plaques. We found that simvastatin inhibits macrophage RAGE expression by decreasing myeloperoxidase-dependent AGE generation. This effect in turn might contribute to plaque stabilization by inhibiting the release of PGE2-dependent MMPs responsible for plaque rupture.  

Sabine M. Post, Martine Groenendijk, Caroline C. van der Hoogt, Catherine Fievet, Gérald Luc, Menno Hoekstra, Hans M.G. Princen, Bart Staels, and Patrick C.N. Rensen
Arterioscler Thromb Vasc Biol. 2006;26:2724-2730; published online before print September 28 2006, doi:10.1161/01.ATV.0000247260.42560.e1.
Abstract | Full Text | PDF | Data Supplement
High levels of plasma HDL-cholesterol are correlated with a low risk of cardiovascular disease. We show that strongly reduced bile acid formation in APOE*3-Leiden transgenic mice by cholesterol 7{alpha}-hydroxylase (Cyp7a1)-deficiency increases HDL-cholesterol. The clearance of HDL was not changed but hepatic ABCA1 mRNA expression was increased, suggesting an increased rate of cholesterol efflux from the liver to HDL.  

Fanny Lalloyer, Catherine Fiévet, Sophie Lestavel, Gérard Torpier, Jelske van der Veen, Véronique Touche, Stéphanie Bultel, Saïd Yous, Folkert Kuipers, Réjane Paumelle, Jean-Charles Fruchart, Bart Staels, and Anne Tailleux
Arterioscler Thromb Vasc Biol. 2006;26:2731-2737; published online before print September 28 2006, doi:10.1161/01.ATV.0000248101.93488.84.
Abstract | Full Text | PDF | Data Supplement
In human apolipoprotein E2-knockin mice, the rexinoid bexarotene inhibits atherosclerotic lesion development in association with decreased intestinal cholesterol absorption, resulting in lower circulating atherogenic lipoprotein concentrations. Bexarotene enhances the capacity of macrophages to efflux cellular lipids, whereas it has only modest effects on inflammation in the vascular wall.  

Cara L. Carty, Patrick Heagerty, Karen Nakayama, E. Clair McClung, Julieann Lewis, Dawn Lum, Erin Boespflug, Carrie McCloud-Gehring, Behrooz R. Soleimani, Jane Ranchalis, Tamara J. Bacus, Clement E. Furlong, and Gail P. Jarvik
Arterioscler Thromb Vasc Biol. 2006;26:2738-2744; published online before print October 5 2006, doi:10.1161/01.ATV.0000248534.30057.b5.
Abstract | Full Text | PDF
Influenza vaccination results in acute phase response (APR) in men with and without severe carotid artery disease. Increased serum amyloid A (SAA) APR predicted severe vascular disease. APR magnitude may be a marker of CAAD.  

Wolfgang Koenig, Natalie Khuseyinova, Jens Baumert, Barbara Thorand, Hannelore Loewel, Lloyd Chambless, Christa Meisinger, Andrea Schneider, Stephan Martin, Hubert Kolb, and Christian Herder
Arterioscler Thromb Vasc Biol. 2006;26:2745-2751; published online before print September 28 2006, doi:10.1161/01.ATV.0000248096.62495.73.
Abstract | Full Text | PDF | Data Supplement
Within the MONICA/KORA Augsburg case-cohort study, concentrations of IL-18 were measured in 382 cases with incident coronary heart disease (CHD) and 1980 noncases. We found no statistically significant association between increased IL-18 concentrations and incident CHD, whereas CRP and IL-6 were independent predictors of future cardiovascular risk in this population.  

Takashi Kawai, Tsunekata Ito, Kazuo Ohwada, Yasuko Mera, Mutsuyoshi Matsushita, and Hitonobu Tomoike
Arterioscler Thromb Vasc Biol. 2006;26:2752-2757; published online before print September 21 2006, doi:10.1161/01.ATV.0000245808.12493.40.
Abstract | Full Text | PDF
Postprandial hypertriglyceridemic (PHT) rabbit shows hyperinsulinemia, glucose intolerance, and central obesity. This rabbit provides a model of inherited metabolic syndrome.  

Peter M. Nilsson, Gunnar Engström, Bo Hedblad, Jan Frystyk, Margaretha M. Persson, Göran Berglund, and Allan Flyvbjerg
Arterioscler Thromb Vasc Biol. 2006;26:2758-2762; published online before print October 12 2006, doi:10.1161/01.ATV.0000249638.01416.4b.
Abstract | Full Text | PDF
Plasma adiponectin is a marker of glucose metabolism and obesity and shows an inverse age-adjusted association with carotid ultrasound IMT in men, but not in women, selected for varying degree of insulin resistance (HOMA) in a population-based study (n=887). This association is attenuated after adjustment for metabolic risk factors.  

Olga A. Iakoubova, Carmen H. Tong, Anand P. Chokkalingam, Charles M. Rowland, Todd G. Kirchgessner, Judy Z. Louie, Lynn M. Ploughman, Marc S. Sabatine, Hannia Campos, Joseph J. Catanese, Diane U. Leong, Bradford A. Young, David Lew, Zenta Tsuchihashi, May M. Luke, Christopher J. Packard, Kim E. Zerba, Peter M. Shaw, James Shepherd, James J. Devlin, and Frank M. Sacks
Arterioscler Thromb Vasc Biol. 2006;26:2763-2768; published online before print September 28 2006, doi:10.1161/01.ATV.0000247248.76409.8b.
Abstract | Full Text | PDF | Data Supplement
In CARE, the FCAR 92Asn allele predicted MI (HR=1.68). Pravastatin significantly reduced the risk of MI in carriers of the 92Asn risk allele but not in noncarriers. In WOSCOPS, the 92Asn allele was associated with CHD (OR=1.46), and pravastatin reduced odds of CHD in both carriers and noncarriers.  

Christopher J. O’Donnell, M. Kyla Shea, Paul A. Price, David R. Gagnon, Peter W. F. Wilson, Martin G. Larson, Douglas P. Kiel, Udo Hoffmann, Maros Ferencik, Melvin E. Clouse, Matthew K. Williamson, L. Adrienne Cupples, Bess Dawson-Hughes, and Sarah L. Booth
Arterioscler Thromb Vasc Biol. 2006;26:2769-2774; published online before print September 14 2006, doi:10.1161/01.ATV.0000245793.83158.06.
Abstract | Full Text | PDF
Matrix Gla protein (MGP) is an inhibitor of calcification. MGP concentrations and coronary heart disease (CHD) risk factors were determined in 2 studies of men and women free of clinically apparent CHD. The Framingham CHD risk score was higher across quartiles of circulating MGP.  

Gilles Chironi, Alain Simon, Bénédicte Hugel, Muriel Del Pino, Jérôme Gariepy, Jean-Marie Freyssinet, and Alain Tedgui
Arterioscler Thromb Vasc Biol. 2006;26:2775-2780; published online before print October 12 2006, doi:10.1161/01.ATV.0000249639.36915.04.
Abstract | Full Text | PDF
Circulating leukocyte-derived microparticles (MP) were related to Framingham risk, metabolic syndrome, CRP, and presence and extent of preclinical atherosclerosis in 216 primary prevention subjects. These relationships of leukocyte-derived MP with atherosclerosis were independent of all risk markers, leukocyte count, and concomitant drugs. These data unveil new directions for atherosclerosis research.  

Yoshihide Asato, Keisuke Katsuren, Tadashi Ohshiro, Kazuhide Kikawa, Tadao Shimabukuro, and Takao Ohta
Arterioscler Thromb Vasc Biol. 2006;26:2781-2786; published online before print September 21 2006, doi:10.1161/01.ATV.0000245804.56871.31.
Abstract | Full Text | PDF
Dyslipidemia and insulin resistance (IR) are risk factors for coronary heart disease (CHD) in adults. To help prevent the development of CHD, it may be useful to understand the relationship between lipid abnormalities and IR during childhood. Our results suggest that in addition to controlling body weight, it may be important for school children to characterize lipid phenotypes to prevent progression to CHD and/or type 2 diabetes and to identify subjects who are at high risk for these disorders.  

Florian Bea, Joerg Kreuzer, Michael Preusch, Sandra Schaab, Berend Isermann, Michael E. Rosenfeld, Hugo Katus, and Erwin Blessing
Arterioscler Thromb Vasc Biol. 2006;26:2787-2792; published online before print September 21 2006, doi:10.1161/01.ATV.0000246797.05781.ad.
Abstract | Full Text | PDF | Data Supplement
Effects of chronic thrombin inhibition with melagatran was evaluated in advanced lesions of apoE-deficient mice. Melagatran attenuated lesion progression and promoted plaque stability, possibly through inhibiting activation of proinflammatory transcription factors and reduced synthesis of MMP-9.  

P.E. Morange, C. Bickel, V. Nicaud, R. Schnabel, H.J. Rupprecht, D. Peetz, K.J. Lackner, F. Cambien, S. Blankenberg, L. Tiret for the AtheroGene Investigators
Arterioscler Thromb Vasc Biol. 2006;26:2793-2799; published online before print October 5 2006, doi:10.1161/01.ATV.0000249406.92992.0d.
Abstract | Full Text | PDF
We examined the association between 5 hemostatic markers and the incidence of fatal cardiovascular events in the prospective Atherogene cohort, including 1057 individuals with coronary artery disease at baseline. Fibrinogen and D-dimer levels are independent predictors of subsequent cardiovascular death. Our data support a role of impaired coagulation/fibrinolysis process in the complications of coronary artery disease.  

 

ThrombosisBack

Gianluca Campo, Marco Valgimigli, Paolo Ferraresi, Patrizia Malagutti, Marcello Baroni, Chiara Arcozzi, Donato Gemmati, Gianfranco Percoco, Giovanni Parrinello, Roberto Ferrari, and Francesco Bernardi
Arterioscler Thromb Vasc Biol. 2006;26:2800-2806; published online before print September 28 2006, doi:10.1161/01.ATV.0000247249.82030.94.
Abstract | Full Text | PDF
Admission FVII and TF antigen, partially predicted by polymorphisms, were independent predictors of composite end point (mortality and reinfarction), which was even worse in patients showing both parameters simultaneously elevated. FVII genotype influenced outcome only in patients with high TF values.  

Nicholas L. Smith, Susan R. Heckbert, Rozenn N. Lemaitre, Alexander P. Reiner, Thomas Lumley, Frits R. Rosendaal, and Bruce M. Psaty
Arterioscler Thromb Vasc Biol. 2006;26:2807-2812; published online before print September 14 2006, doi:10.1161/01.ATV.0000245792.62517.3b.
Abstract | Full Text | PDF
Joint exposure to conjugated equine estrogen (CEE) and prothrombotic genetic variants increase venous thrombotic risk. Esterified estrogen (EE) is not associated with risk and nothing is known about joint risks with prothrombotic variants. Findings suggest EE is associated with less risk than CEE especially among carriers of prothrombotic variants.  

Andreas Schäfer, Ulrike Flierl, Anna Kobsar, Martin Eigenthaler, Georg Ertl, and Johann Bauersachs
Arterioscler Thromb Vasc Biol. 2006;26:2813-2818; published online before print October 5 2006, doi:10.1161/01.ATV.0000249407.92147.12.
Abstract | Full Text | PDF
Diabetes is associated with progressive platelet activation in vivo and thromboembolic complications. Chronic treatment with the direct guanylyl cyclase activator HMR1766 in rats with diabetes improved NO/cGMP signaling and reduced platelet activation in vivo and in vitro.  

Zhenhua Xu, Debasish Maiti, Walter Kisiel, and Elia J. Duh
Arterioscler Thromb Vasc Biol. 2006;26:2819-2825; published online before print October 5 2006, doi:10.1161/01.ATV.0000248731.55781.87.
Abstract | Full Text | PDF
This study investigated the expression and regulation of type-2 tissue factor pathway inhibitor (TFPI-2) in endothelial cells, as well as the regulation of human endothelial cell (EC) function by TFPI-2. Our data suggest that VEGF upregulation of TFPI-2 expression in endothelial cells may represent a mechanism for negative feedback regulation and modulation of its pro-angiogenic action on endothelial cells. TFPI-2 may be a novel therapeutic for treatment of angiogenic disease processes.  

 

Letters to the EditorBack

Evaluation of Differences in Coronary Plaque Mechanical Behavior in Individuals With and Without Type 2 Diabetes Mellitus

James A. Shaw, Anthony J. White, Rodney Reddy, Stephen J. Duffy, Anthony S. Walton, Bronwyn A. Kingwell, and Anthony M. Dart
Arterioscler Thromb Vasc Biol. 2006;26:2826-2827, doi:10.1161/01.ATV.0000246778.32916.f4.
Full Text | PDF | Data Supplement  

 

INDEXBack

Author Index


Arterioscler Thromb Vasc Biol. 2006;26:2828-2837.
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