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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 28, Issue 2; February 1, 2008

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EditorialsBack

Adding Complexity to Fibronectin-Platelet Interactions

Deane F. Mosher
Arterioscler Thromb Vasc Biol. 2008;28:203-204, doi:10.1161/ATVBAHA.107.159798
Extract | Full Text | PDF  

New Direction for WE Thrombin

Michael C. Berndt and Robert K. Andrews
Arterioscler Thromb Vasc Biol. 2008;28:205-207, doi:10.1161/ATVBAHA.107.159301
Extract | Full Text | PDF  

 

Brief ReviewsBack

Stefanie Dimmeler, Jana Burchfield, and Andreas M. Zeiher
Arterioscler Thromb Vasc Biol. 2008;28:208-216; published online before print October 19 2007, doi:10.1161/ATVBAHA.107.155317
Abstract | Full Text | PDF
Cell based therapy is a promising option for treatment of ischemic diseases. Several cell types have been shown to increase the functional recovery of the heart after ischemia. The present review article summarizes the results of the experimental and clinical studies and discusses open questions in cell-based therapies.  

Daniel C. Rafii, Bethan Psaila, Jason Butler, David K. Jin, and David Lyden
Arterioscler Thromb Vasc Biol. 2008;28:217-222; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.151159
Abstract | Full Text | PDF
Platelets are major delivery vehicles for pro- and antiangiogenic growth factors. During the formation of new blood vessels, platelet-deployed factors support the recruitment and differentiation of bone marrow-derived cells. Therapeutic manipulation of the site-specific deployment of these factors by platelets may be used to inhibit tumor growth or promote tissue restoration.  

Dietmar Vestweber
Arterioscler Thromb Vasc Biol. 2008;28:223-232; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.158014
Abstract | Full Text | PDF  

James T.B. Crawley and David A. Lane
Arterioscler Thromb Vasc Biol. 2008;28:233-242; published online before print October 19 2007, doi:10.1161/ATVBAHA.107.141606
Abstract | Full Text | PDF  

 

Integrative Physiology/Experimental MedicineBack

AL gif  CX3CR1 Deficiency Impairs Dendritic Cell Accumulation in Arterial Intima and Reduces Atherosclerotic Burden

Peng Liu, Yen-Rei A. Yu, Jessica A. Spencer, Ashley E. Johnson, Christopher T. Vallanat, Alan M. Fong, Cam Patterson, and Dhavalkumar D. Patel
Arterioscler Thromb Vasc Biol. 2008;28:243-250; published online before print December 13 2007, doi:10.1161/ATVBAHA.107.158675
Abstract | Full Text | PDF | Data Supplement
Dendritic cells (DCs) and the chemokine receptor CX3CR1 have been implicated in the pathogenesis of atherosclerosis. In mouse aortas, CX3CR1 was expressed on intimal DCs that increased abundance in aged and ApoE-/- aortas. CX3CR1 deficiency impairs the accumulation of DCs in the aortic wall and reduces the atherosclerotic burden.  

AL gif  CXCR3 Antagonist NBI-74330 Attenuates Atherosclerotic Plaque Formation in LDL Receptor–Deficient Mice

Eva J.A. van Wanrooij, Saskia C.A. de Jager, Thomas van Es, Paula de Vos, Helen L. Birch, David A. Owen, Robbert J. Watson, Erik A.L. Biessen, Gayle A. Chapman, Theo J.C. van Berkel, and Johan Kuiper
Arterioscler Thromb Vasc Biol. 2008;28:251-257; published online before print November 29 2007, doi:10.1161/ATVBAHA.107.147827
Abstract | Full Text | PDF | Data Supplement
Antagonizing CXCR3 using NBI-74330 reduced atherogenesis not only by blocking direct migration of effector cells from the circulation to the atherosclerotic plaque, but also by beneficially modulating the inflammatory response in lymph nodes draining from the atherosclerotic lesion.  

AL gif  Combined Deletion of Macrophage ABCA1 and ABCG1 Leads to Massive Lipid Accumulation in Tissue Macrophages and Distinct Atherosclerosis at Relatively Low Plasma Cholesterol Levels

Ruud Out, Menno Hoekstra, Kim Habets, Illiana Meurs, Vivian de Waard, Reeni B. Hildebrand, Yanan Wang, Giovanna Chimini, Johan Kuiper, Theo J.C. Van Berkel, and Miranda Van Eck
Arterioscler Thromb Vasc Biol. 2008;28:258-264; published online before print November 15 2007, doi:10.1161/ATVBAHA.107.156935
Abstract | Full Text | PDF | Data Supplement
To assess the combined role of macrophage ABCA1 and ABCG1 in atherosclerosis, we generated LDL receptor knockout mice that are selectively deficient in ABCA1 and ABCG1 by using bone marrow transfer. Despite relatively low plasma cholesterol levels these mice show distinct atherosclerosis and massive accumulation of lipids in tissue macrophages.  

AL gif  p38 MAPK Inhibition Reduces Aortic Ultrasmall Superparamagnetic Iron Oxide Uptake in a Mouse Model of Atherosclerosis: MRI Assessment

Joanne B. Morris, Alan R. Olzinski, Roberta E. Bernard, Karpagam Aravindhan, Rosanna C. Mirabile, Rogely Boyce, Robert N. Willette, and Beat M. Jucker
Arterioscler Thromb Vasc Biol. 2008;28:265-271; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.151175
Abstract | Full Text | PDF | Data Supplement
The purpose of this study was to noninvasively evaluate USPIO uptake in aorta of Ang II-administered apoE-/- mice treated with a p38 MAPK inhibitor (SB-239063). MRI assessment of USPIO uptake, as a marker for inflammation in atherosclerotic plaque, is feasible and p38 MAPK inhibition attenuates the uptake of USPIO in aorta of Ang II-infused apoE-/- mice.  

TH gif  Antiinflammatory and Antiatherogenic Effects of the NF-{kappa}B Inhibitor Acetyl-11-Keto-β-Boswellic Acid in LPS-Challenged ApoE–/– Mice

Clarisse Cuaz-Pérolin, Ludivine Billiet, Eric Baugé, Corinne Copin, Daniel Scott-Algara, Felicitas Genze, Berhold Büchele, Tatiana Syrovets, Thomas Simmet, and Mustapha Rouis
Arterioscler Thromb Vasc Biol. 2008;28:272-277; published online before print November 21 2007, doi:10.1161/ATVBAHA.107.155606
Abstract | Full Text | PDF | Data Supplement
We studied the effect of acetyl-11-keto-β-boswellic acid (AKβBA), a natural antiinflammatory molecule isolated from the oleogum resin of Boswellia carterii, on LPS-induced atherosclerotic lesion in apoE-/- mice. The results showed a significant reduction in the expression of several proatherogenic genes, NF-{kappa}B activity, and lesion size in AKβBA-treated mice.  

TH gif  Human ApoA-I Transfer Attenuates Transplant Arteriosclerosis via Enhanced Incorporation of Bone marrow–derived Endothelial Progenitor Cells

Yingmei Feng, Frank Jacobs, Eline Van Craeyveld, Christine Brunaud, Jan Snoeys, Marc Tjwa, Sophie Van Linthout, and Bart De Geest
Arterioscler Thromb Vasc Biol. 2008;28:278-283; published online before print December 6 2007, doi:10.1161/ATVBAHA.107.158741
Abstract | Full Text | PDF | Data Supplement
Endothelial progenitor cells (EPCs) contribute to endothelial regeneration in allografts. Increased HDL cholesterol after human apoA-I transfer in C57BL/6 apoE-/- mice increases EPC number, improves EPC function in vitro, enhances EPC incorporation in allografts, stimulates endothelial regeneration, and attenuates neointima formation in a murine model of transplant arteriosclerosis.  

TH gif  Tumor Necrosis Factor Receptor-2 Signaling Attenuates Vein Graft Neointima Formation by Promoting Endothelial Recovery

Lisheng Zhang, Perumal Sivashanmugam, Jiao-Hui Wu, Leigh Brian, Sabrina T. Exum, Neil J. Freedman, and Karsten Peppel
Arterioscler Thromb Vasc Biol. 2008;28:284-289; published online before print November 15 2007, doi:10.1161/ATVBAHA.107.151613
Abstract | Full Text | PDF | Data Supplement
In murine IVC grafts implanted into congenic recipient mice, TNF receptor-2 deficiency significantly augmented neointimal hyperplasia, medial expansion, and adhesion molecule expression, while delaying endothelial resurfacing of the graft lumen. As opposed to TNF receptor-1 signaling, activation of TNF receptor-2 does not change SMC proliferation and chemotaxis.  

TH gif  The Role of Osteopontin in Recovery from Hind Limb Ischemia

Craig L. Duvall, Daiana Weiss, Scott T. Robinson, Fadi M.F. Alameddine, Robert E. Guldberg, and W. Robert Taylor
Arterioscler Thromb Vasc Biol. 2008;28:290-295; published online before print November 15 2007, doi:10.1161/ATVBAHA.107.158485
Abstract | Full Text | PDF
We investigated the role of osteopontin (OPN) in recovery from hind limb ischemia. OPN-/- mice exhibited delayed ischemic limb recovery, which may be attributable to defective response of OPN-/- monocytes/macrophages to chemoattraction. These results provide the first evidence that a role exists for OPN during ischemic limb revascularization in vivo.  

TH gif   Prothrombotic Effects of Fibronectin Isoforms Containing the EDA Domain

Anil K. Chauhan, Janka Kisucka, Maria R. Cozzi, Meghan T. Walsh, Federico A. Moretti, Monica Battiston, Mario Mazzucato, Luigi De Marco, Francisco E. Baralle, Denisa D. Wagner, and Andrés F. Muro
Arterioscler Thromb Vasc Biol. 2008;28:296-301; published online before print November 8 2007, doi:10.1161/ATVBAHA.107.149146
Abstract | Full Text | PDF | Data Supplement
EDA+FN is absent in normal plasma but elevated levels are observed in several pathological conditions. We found that EDA+FN has prothrombotic potential that is revealed at arterial shear rates. Thus the presence of EDA+FN in plasma may aggravate peripheral arterial disease, coronary artery disease, stroke, and other conditions.  

 

Cell Biology/SignalingBack

TH gif  Forkhead Factor, FOXO3a, Induces Apoptosis of Endothelial Cells Through Activation of Matrix Metalloproteinases

Hae-Young Lee, Hyun-Jung You, Joo-Yun Won, Seock-Won Youn, Hyun-Jai Cho, Kyung-Woo Park, Woong-Yang Park, Jeong-Sun Seo, Young-Bae Park, Kenneth Walsh, Byung-Hee Oh, and Hyo-Soo Kim
Arterioscler Thromb Vasc Biol. 2008;28:302-308; published online before print December 6 2007, doi:10.1161/ATVBAHA.107.150664
Abstract | Full Text | PDF | Data Supplement
The forkhead factor, FOXO3a, is known to induce apoptosis in endothelial cells. Here, we evaluated the role of FOXO3a on endothelial cells-extracellular matrix interactions. We found activation of MMPs and possible ECM disruption represent novel mechanisms of FOXO3a-mediated apoptosis in endothelial cells.  

TH gif  Activated Mast Cells Induce Endothelial Cell Apoptosis by a Combined Action of Chymase and Tumor Necrosis Factor-{alpha}

Hanna M. Heikkilä, Soili Lätti, Markus J. Leskinen, Jukka K. Hakala, Petri T. Kovanen, and Ken A. Lindstedt
Arterioscler Thromb Vasc Biol. 2008;28:309-314; published online before print December 13 2007, doi:10.1161/ATVBAHA.107.151340
Abstract | Full Text | PDF | Data Supplement
Activated mast cells are present in the subendothelial space of coronary atheromas, colocalize with plaque erosions and parietal microthrombi, and induce endothelial cell apoptosis in vitro by a combined action of chymase and TNF-{alpha}. Thus, activated mast cells may contribute to plaque erosion with the progression of atherosclerosis and its complications.  

TH gif  Suppression of Pro-inflammatory Adhesion Molecules by PPAR-{delta} in Human Vascular Endothelial Cells

Yanbo Fan, Ying Wang, Zhihui Tang, Hong Zhang, Xiaomei Qin, Yi Zhu, Youfei Guan, Xian Wang, Bart Staels, Shu Chien, and Nanping Wang
Arterioscler Thromb Vasc Biol. 2008;28:315-321; published online before print November 29 2007, doi:10.1161/ATVBAHA.107.149815
Abstract | Full Text | PDF | Data Supplement
By using the selective agonists and siRNA-mediated gene silencing, we have demonstrated that ligand-activation of PPAR-{delta} in primary-cultured human endothelial cells has a potent antiinflammatory effect via a novel binary mechanism involving the induction of antioxidative genes and the release of nuclear corepressors.  

TH gif  The Molecular Basis of VEGFR-1 Signal Transduction Pathways in Primary Human Monocytes

Vadim Tchaikovski, Guido Fellbrich, and Johannes Waltenberger
Arterioscler Thromb Vasc Biol. 2008;28:322-328; published online before print December 13 2007, doi:10.1161/ATVBAHA.107.158022
Abstract | Full Text | PDF | Data Supplement
Arteriogenesis and wound healing are largely monocyte- and VEGFR1-dependent. VEGFR-1 intracellular signaling pathways were identified and characterized in primary human monocytes. PI-3K appears to be a central regulator in VEGFR-1 signaling mediating the activation of Akt, p38, and ERK1/2. These pathways are critically involved in VEGFR-1-dependent primary monocyte chemotaxis.  

TH gif   Thrombin Mutant W215A/E217A Acts as a Platelet GPIb Antagonist

Michelle A. Berny, Tara C. White, Erik I. Tucker, Leslie A. Bush-Pelc, Enrico Di Cera, András Gruber, and Owen J.T. McCarty
Arterioscler Thromb Vasc Biol. 2008;28:329-334; published online before print October 25 2007, doi:10.1161/ATVBAHA.107.156273
Abstract | Full Text | PDF | Data Supplement
The thrombin mutant WE selectively activates protein C and has potent antithrombotic effects in primates. We demonstrate that WE, while not activating platelets, retains the ability to interact with platelets through GPIb, and inhibits GPIb-dependent binding to vWF-collagen under shear.  

TH gif   Molecular Basis for Staphylococcus aureus–Mediated Platelet Aggregate Formation Under Arterial Shear In Vitro

Steven W. Kerrigan, Niamh Clarke, Anthony Loughman, Gerardene Meade, Timothy J. Foster, and Dermot Cox
Arterioscler Thromb Vasc Biol. 2008;28:335-340; published online before print December 6 2007, doi:10.1161/ATVBAHA.107.152058
Abstract | Full Text | PDF
Both Staphylococcus aureus clumping factor A (Clf A) and fibronectin-binding protein A (Fnbp A) mediate rapid platelet aggregation. However, only Clf A can induce rapid aggregate formation under arterial shear conditions that is dependent on antibody and fibrinogen binding. The corresponding platelet receptors are GPIIb/IIIa and Fc{gamma}RIIa.  

 

Clinical and Population StudiesBack

AL gif  Vitamin E Supplementation Reduces Cardiovascular Events in a Subgroup of Middle-Aged Individuals With Both Type 2 Diabetes Mellitus and the Haptoglobin 2-2 Genotype: A Prospective Double-Blinded Clinical Trial

Uzi Milman, Shany Blum, Chen Shapira, Doron Aronson, Rachel Miller-Lotan, Yefim Anbinder, Junia Alshiek, Lawrence Bennett, Maria Kostenko, Michele Landau, Shlomo Keidar, Yishai Levy, Alexander Khemlin, Arman Radan, and Andrew P. Levy
Arterioscler Thromb Vasc Biol. 2008;28:341-347; published online before print November 21 2007, doi:10.1161/ATVBAHA.107.153965
Abstract | Full Text | PDF | Data Supplement
We sought to determine whether vitamin E could reduce cardiovascular events in DM individuals with the Hp 2-2 genotype. The primary composite outcome was myocardial infarction, stroke, and cardiovascular death. Cardiovascular events were significantly reduced in individuals receiving vitamin E (2.2%) compared with placebo (4.7%; P=0.01).  

TH gif  Time Since Menopause Influences the Acute and Chronic Effect of Estrogens on Endothelial Function

Cristiana Vitale, Giuseppe Mercuro, Elena Cerquetani, Giuseppe Marazzi, Roberto Patrizi, Francesco Pelliccia, Maurizio Volterrani, Massimo Fini, Peter Collins, and Giuseppe M.C. Rosano
Arterioscler Thromb Vasc Biol. 2008;28:348-352; published online before print December 6 2007, doi:10.1161/ATVBAHA.107.158634
Abstract | Full Text | PDF | Data Supplement
To evaluate whether time since menopause influences the effect of Estradiol on flow-mediated dilatation (FMD). Estradiol improved endothelial function in all women and its effect was dependent on time since menopause. The acute and chronic effect of Estradiol on FMD is reduced by a longer time since menopause.  

AL gif  Tea Consumption Is Inversely Associated With Carotid Plaques in Women

Stéphanie Debette, Dominique Courbon, Nathalie Leone, Jérôme Gariépy, Christophe Tzourio, Jean-François Dartigues, Pascale Barberger-Gateau, Karen Ritchie, Annick Alpérovitch, Philippe Amouyel, Pierre Ducimetière, and Mahmoud Zureik
Arterioscler Thromb Vasc Biol. 2008;28:353-359; published online before print December 6 2007, doi:10.1161/ATVBAHA.107.151928
Abstract | Full Text | PDF
Our aim was to assess the relationship of tea consumption with common carotid artery intima-media thickness and carotid plaques in a large population-based sample of elderly subjects. Increasing daily tea consumption was associated with a lower prevalence of carotid plaques in women, independently of vascular risk factors and dietary habits.  

AL gif  Four SNPs on Chromosome 9p21 in a South Korean Population Implicate a Genetic Locus That Confers High Cross-Race Risk for Development of Coronary Artery Disease

Gong-Qing Shen, Lin Li, Shaoqi Rao, Kalil G. Abdullah, Ji Min Ban, Bok-Soo Lee, Jeong Euy Park, and Qing K. Wang
Arterioscler Thromb Vasc Biol. 2008;28:360-365; published online before print November 29 2007, doi:10.1161/ATVBAHA.107.157248
Abstract | Full Text | PDF
A case-control association study in a South Korean population finds that 4 SNPs previously implicated to be associated with CAD in European populations also confer risk in an Asian population. We conclude that chromosome 9p21 is a susceptibility locus associated with increased cross-race risk of development of CAD.  

 

Letters to the EditorBack

The Puzzling Role of TRAIL in Endothelial Cell Biology

Paola Secchiero and Giorgio Zauli
Arterioscler Thromb Vasc Biol. 2008;28:e4, doi:10.1161/ATVBAHA.107.158451
Extract | Full Text | PDF  

The Puzzling Role of TRAIL in Endothelial Cell Biology

Lee A. O’Brien, Mark A. Richardson, David T. Berg, Bruce Gerlitz, Akanksha Gupta, and Brian W. Grinnell
Arterioscler Thromb Vasc Biol. 2008;28:e5-e6, doi:10.1161/ATVBAHA.107.158949
Extract | Full Text | PDF  

Insulin Resistance Affects Gene Expression in Endothelium

Claudia Consoli, Eugenio Martelli, Monica D’Adamo, Rossella Menghini, Diego Arcelli, Ottavia Porzio, Assunta Pandolfi, Giuseppe R. Pistolese, Agostino Consoli, Renato Lauro, Arnaldo Ippoliti, and Massimo Federici
Arterioscler Thromb Vasc Biol. 2008;28:e7-e9, doi:10.1161/ATVBAHA.107.152264
Extract | Full Text | PDF  

 

CorrectionsBack

Correction


Arterioscler Thromb Vasc Biol. 2008;28:e10, doi:10.1161/01.ATV.0000308921.28156.F0
Extract | Full Text | PDF  

Correction


Arterioscler Thromb Vasc Biol. 2008;28:e11, doi:10.1161/01.ATV.0000308922.28156.2B
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Correction


Arterioscler Thromb Vasc Biol. 2008;28:e12, doi:10.1161/01.ATV.0000308925.51027.10
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Correction


Arterioscler Thromb Vasc Biol. 2008;28:e13, doi:10.1161/01.ATV.0000308923.66274.70
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Correction


Arterioscler Thromb Vasc Biol. 2008;28:e14, doi:10.1161/01.ATV.0000308924.73897.E4
Extract | Full Text | PDF  

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