Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (26 [10])

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Volume 26, Issue 10; October 1, 2006

Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor

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	Editorials
	Is Two out of Three Enough for ABCG1? Linda K. Curtiss Arterioscler Thromb Vasc Biol. 2006;26:2175-2177, doi:10.1161/01.ATV.0000243741.89303.27 Full Text \| PDF
	Epidemiology Complements Immunology in the Heart Göran K. Hansson Arterioscler Thromb Vasc Biol. 2006;26:2178-2180, doi:10.1161/01.ATV.0000242906.04522.5f Full Text \| PDF
	Perplexity of Plaque Proteinases Peter Libby Arterioscler Thromb Vasc Biol. 2006;26:2181-2182, doi:10.1161/01.ATV.0000240249.88921.d8 Full Text \| PDF
	A Role for Plasminogen Activator Inhibitor-1 in Obesity: From Pie to PAI? Marcelo L.G. Correia and William G. Haynes Arterioscler Thromb Vasc Biol. 2006;26:2183-2185, doi:10.1161/01.ATV.0000244018.24120.70 Full Text \| PDF
	Summary of American Heart Association Diet and Lifestyle Recommendations Revision 2006 Alice H. Lichtenstein, Lawrence J. Appel, Michael Brands, Mercedes Carnethon, Stephen Daniels, Harold A. Franch, Barry Franklin, Penny Kris-Etherton, William S. Harris, Barbara Howard, Njeri Karanja, Michael Lefevre, Lawrence Rudel, Frank Sacks, Linda Van Horn, Mary Winston, and Judith Wylie-Rosett Arterioscler Thromb Vasc Biol. 2006;26:2186-2191, doi:10.1161/01.ATV.0000238352.25222.5e Full Text \| PDF
	Brief Reviews
	Selective Agonists of Estrogen Receptor Isoforms: New Perspectives for Cardiovascular Disease Chiara Bolego, Elisabetta Vegeto, Christian Pinna, Adriana Maggi, and Andrea Cignarella Arterioscler Thromb Vasc Biol. 2006;26:2192-2199; published online before print August 17 2006, doi:10.1161/01.ATV.0000242186.93243.25 Abstract \| Full Text \| PDF Despite a wealth of encouraging preclinical and epidemiological research, estrogenic hormones have not shown cardiovascular benefit in clinical trials. Based on molecular pharmacology studies, selective agonists of individual estrogen receptor isoforms targeted to the vessel wall represent a promising and safe strategy to bypass the limitations of endogenous hormones.
	PAI-1 and the Metabolic Syndrome: Links, Causes, and Consequences Marie-Christine Alessi and Irène Juhan-Vague Arterioscler Thromb Vasc Biol. 2006;26:2200-2207; published online before print August 24 2006, doi:10.1161/01.ATV.0000242905.41404.68 Abstract \| Full Text \| PDF The metabolic syndrome is associated with overexpression of PAI-1; the mechanisms involved are complex. Besides its role in atherothrombosis, PAI-1 is also implicated in obesity and insulin resistance. The development of PAI-1 inhibitors is a challenge.
	Vascular Biology
	Blockade of Angiotensin II Receptors Reduces the Expression of Receptors for Advanced Glycation End Products in Human Endothelial Cells Masashi Fujita, Hiroko Okuda, Osamu Tsukamoto, Yoshihiro Asano, Yulin Liao Akio Hirata, Jiyoong Kim, Takeshi Miyatsuka, Seiji Takashima, Tetsuo Minamino, Hitonobu Tomoike, and Masafumi Kitakaze Arterioscler Thromb Vasc Biol. 2006;26:e138-e139; published online before print August 3 2006, doi:10.1161/01.ATV.0000239569.99126.37 Abstract \| Full Text \| PDF We investigated whether an angiotensin II type-1 receptor blocker (ARB) exerts antiatherosclerotic effects via inhibiting TNF{alpha}-RAGE interaction. ARBs decreased TNF{alpha}-induced RAGE expression in human endothelial cells along with the decrease in the activity of NF-{kappa}B and the expression of inflammatory mediators. ARBs exert antiatherosclerotic effects via reducing TNF{alpha}-RAGE interaction.
	Blockade of Angiotensin II Receptors Reduces the Expression of Receptors for Advanced Glycation End Products in Human Endothelial Cells Masashi Fujita, Hiroko Okuda, Osamu Tsukamoto, Yoshihiro Asano, Yulin Liao, Akio Hirata, Jiyoong Kim, Takeshi Miyatsuka, Seiji Takashima, Tetsuo Minamino, Hitonobu Tomoike, and Masafumi Kitakaze Arterioscler Thromb Vasc Biol. 2006;26:2208; published online before print July 13 2006, doi:10.1161/01.ATV.0000236203.90331.d0 Abstract \| Full Text \| PDF
	Modulation of Adipose Tissue Development by Pharmacological Inhibition of PAI-1 David L. Crandall, Elaine M. Quinet, Soulaf El Ayachi, Amy L. Hreha, Courtney E. Leik, Dawn A. Savio, Irene Juhan-Vague, and Marie-Christine Alessi Arterioscler Thromb Vasc Biol. 2006;26:2209-2215; published online before print July 6 2006, doi:10.1161/01.ATV.0000235605.51400.9d Abstract \| Full Text \| PDF \| Data Supplement Pharmacological inhibition of PAI-1 was achieved in vitro and in vivo, resulting in effects on adipose tissue differentiation. PAI-1 inhibition may be beneficial in those diseases associated with increased adipose tissue mass, including diabetes and obesity.
	Oxidized Phospholipids Alter Vascular Connexin Expression, Phosphorylation, and Heterocellular Communication Brant E. Isakson, Gerhard Kronke, Alexandra Kadl, Norbert Leitinger, and Brian R. Duling Arterioscler Thromb Vasc Biol. 2006;26:2216-2221; published online before print July 20 2006, doi:10.1161/01.ATV.0000237608.19055.53 Abstract \| Full Text \| PDF \| Data Supplement Atherosclerosis has been associated with oxidized phospholipids (eg, OxPAPC) and changes in connexin expression. We demonstrate that OxPAPC alters connexin expression in endothelial cells and smooth muscle cells and at the in vitro myoendothelial junction. Once more, OxPAPC inhibited heterocellular communication, which coincided with phosphorylation of Cx43 at the myoendothelial junction.
	Atypical GPI-Anchored T-Cadherin Stimulates Angiogenesis In Vitro and In Vivo Maria Philippova, Andrea Banfi, Danila Ivanov, Roberto Gianni-Barrera, Roy Allenspach, Paul Erne, and Thérèse Resink Arterioscler Thromb Vasc Biol. 2006;26:2222-2230; published online before print July 27 2006, doi:10.1161/01.ATV.0000238356.20565.92 Abstract \| Full Text \| PDF \| Data Supplement This study demonstrates that GPI-anchored T-cadherin stimulates angiogenesis in 2-dimensional model of endothelial differentiation, in 3-dimensional endothelial spheroid, and Nicosia tissue assays in vitro. In vivo, T-cad potentiates VEGF effects on neovascularization in mouse skeletal muscle. We conclude that T-cad is a novel modulator of angiogenesis.
	l-Caldesmon Regulates Proliferation and Migration of Vascular Smooth Muscle Cells and Inhibits Neointimal Formation After Angioplasty Kazuhiko Yokouchi, Yasushi Numaguchi, Ryuji Kubota, Masakazu Ishii, Hajime Imai, Ryuichiro Murakami, Yasuhiro Ogawa, Takahisa Kondo, Kenji Okumura, Donald E. Ingber, and Toyoaki Murohara Arterioscler Thromb Vasc Biol. 2006;26:2231-2237; published online before print August 3 2006, doi:10.1161/01.ATV.0000239441.29687.97 Abstract \| Full Text \| PDF \| Data Supplement Light-type caldesmon (l-CaD) is a potent cytostatic protein that inhibits cell tension generation by promoting disassembly of contractile microfilaments in the actin cytoskeleton. Overexpression of l-CaD suppressed cell growth and migration in vascular smooth muscle cells and inhibited neointimal formation in balloon-injured rat carotid arteries, partly by regulating the focal adhesion kinase-extracellular signal regulated-kinase axis.
	Effects of Granulocyte Colony Stimulating Factor on Functional Activities of Endothelial Progenitor Cells in Patients With Chronic Ischemic Heart Disease Joerg Honold, Ralf Lehmann, Christopher Heeschen, Dirk H. Walter, Birgit Assmus, Ken-Ichiro Sasaki, Hans Martin, Judith Haendeler, Andreas M. Zeiher, and Stefanie Dimmeler Arterioscler Thromb Vasc Biol. 2006;26:2238-2243; published online before print August 10 2006, doi:10.1161/01.ATV.0000240248.55172.dd Abstract \| Full Text \| PDF Bone marrow-derived circulating endothelial progenitor cells (EPCs) may contribute to regeneration of infarcted myocardium and enhance neovascularization. Granulocyte colony-stimulating factor (G-CSF) is well-established to mobilize hematopoietic stem cells (HSCs) and might, thereby, also increase the pool of endogenously circulating EPC. Therefore, we investigated the effects of G-CSF administration on mobilization and functional activities of blood-derived EPC in patients with chronic ischemic heart disease (CIHD).
	Sca-1⁺ Progenitors Derived From Embryonic Stem Cells Differentiate Into Endothelial Cells Capable of Vascular Repair After Arterial Injury Qingzhong Xiao, Lingfang Zeng, Zhongyi Zhang, Andriana Margariti, Ziad A Ali, Keith M. Channon, Qingbo Xu, and Yanhua Hu Arterioscler Thromb Vasc Biol. 2006;26:2244-2251; published online before print August 10 2006, doi:10.1161/01.ATV.0000240251.50215.50 Abstract \| Full Text \| PDF \| Data Supplement We have successfully established a method for producing large numbers of endothelial cells (esECs) with high purity from embryonic stem cells and evaluated the therapeutic effect of esECs on re-endothelialization and neointima formation in a mouse model of arterial injury. We also demonstrate for the first time to our knowledge that HDAC3 is involved in VEGF-induced EC differentiation in Sca-1+ progenitor cells.
	Angiotensin II Type 1 Receptor–Mediated Inflammation Is Required for Choroidal Neovascularization Norihiro Nagai, Yuichi Oike, Kanako Izumi-Nagai, Takashi Urano, Yoshiaki Kubota, Kousuke Noda, Yoko Ozawa, Makoto Inoue, Kazuo Tsubota, Toshio Suda, and Susumu Ishida Arterioscler Thromb Vasc Biol. 2006;26:2252-2259; published online before print August 3 2006, doi:10.1161/01.ATV.0000240050.15321.fe Abstract \| Full Text \| PDF We analyzed the involvement of the renin-angiotensin system with the development of choroidal neovascularizaron (CNV), using human surgical samples and the murine model of laser-induced CNV and revealed that angiotensin II type 1 receptor-mediated inflammation, including macrophage infiltration and cytokine upregulation, plays a pivotal role in the development of CNV.
	High-Molecular-Weight Kininogen Fragments Stimulate the Secretion of Cytokines and Chemokines Through uPAR, Mac-1, and gC1qR in Monocytes Mohammad M. Khan, Harlan N. Bradford, Irma Isordia-Salas, Yuchuan Liu, Yi Wu, Ricardo G. Espinola, Berhane Ghebrehiwet, and Robert W. Colman Arterioscler Thromb Vasc Biol. 2006;26:2260-2266; published online before print August 10 2006, doi:10.1161/01.ATV.0000240290.70852.c0 Abstract \| Full Text \| PDF \| Data Supplement Cleavage of kininogen occurs in inflammation but its pathogenic mechanism is not clear. HKa releases inflammatory cytokines and chemokines from human monocytes. Receptors involved include uPAR, Mac-1, LFA-1, and gC1qR. Signaling pathways used are NFkB, p38, and JNK kinases. HKa is a target for therapy of inflammation.
	Beta-Adrenoceptor Blockade Markedly Attenuates Transgene Expression From Cytomegalovirus Promoters Within the Cardiovascular System Husein K. Salem, Parisa Ranjzad, Anita Driessen, Clare E. Appleby, Anthony M. Heagerty, and Paul A. Kingston Arterioscler Thromb Vasc Biol. 2006;26:2267-2274; published online before print August 3 2006, doi:10.1161/01.ATV.0000239445.67579.19 Abstract \| Full Text \| PDF \| Data Supplement The major immediate-early cytomegalovirus enhancer/promoter (MIECMV) is used extensively in studies of clinical cardiovascular gene transfer. Transgene expression from MIECMV within the vasculature is suppressed by ß-blockade. This interaction is highly pertinent to the interpretation of current studies and to the planning of future studies of therapeutic cardiovascular gene transfer.
	Repetitive Fluctuations in Blood Glucose Enhance Monocyte Adhesion to the Endothelium of Rat Thoracic Aorta Kosuke Azuma, Ryuzo Kawamori, Yukiko Toyofuku, Yoshiro Kitahara, Fumihiko Sato, Tomoaki Shimizu, Kyoko Miura, Tomoyuki Mine, Yasushi Tanaka, Masako Mitsumata, and Hirotaka Watada Arterioscler Thromb Vasc Biol. 2006;26:2275-2280; published online before print August 3 2006, doi:10.1161/01.ATV.0000239488.05069.03 Abstract \| Full Text \| PDF \| Data Supplement We investigated the distinct role of fluctuations in blood glucose on monocyte adhesion to aortic endothelial cells. Our data demonstrated that repetitive postprandial fluctuation in glucose concentration evokes monocyte adhesion to endothelial cells that was worse than that induced by stable hyperglycemia. Suppression of such fluctuations efficiently suppressed monocyte adhesion.
	Microcirculatory Hemodynamics and Endothelial Dysfunction in Systemic Lupus Erythematosus Stephen A. Wright, Fiona M. O’Prey, Derrick J. Rea, Rick D. Plumb, Andrew J. Gamble, William J. Leahey, Adrian B. Devine, R. Canice McGivern, Dennis G. Johnston, Michael B. Finch, Aubrey L. Bell, and Gary E. McVeigh Arterioscler Thromb Vasc Biol. 2006;26:2281-2287; published online before print July 27 2006, doi:10.1161/01.ATV.0000238351.82900.7f Abstract \| Full Text \| PDF \| Data Supplement Frequency domain analysis of pulsed Doppler velocity waveforms identifies altered forearm microvascular hemodynamics that contributes to impaired flow mediated dilation in systemic lupus erythematosus.
	Nuclear Receptors Nur77, Nurr1, and NOR-1 Expressed in Atherosclerotic Lesion Macrophages Reduce Lipid Loading and Inflammatory Responses Peter I. Bonta, Claudia M. van Tiel, Mariska Vos, Thijs W.H. Pols, Johannes V. van Thienen, Valérie Ferreira, E. Karin Arkenbout, Jurgen Seppen, C. Arnold Spek, Tom van der Poll, Hans Pannekoek, and Carlie J.M. de Vries Arterioscler Thromb Vasc Biol. 2006;26:2288; published online before print July 27 2006, doi:10.1161/01.ATV.0000238346.84458.5d Abstract \| Full Text \| PDF \| Data Supplement We demonstrate that the NR4A family of transcription factors, comprising Nur77, Nurr1, and NOR-1, is expressed in human atherosclerotic lesion macrophages and reduces inflammatory responses and lipid loading involving inhibition of macrophage differentiation. Consequently, these receptors reduce foam-cell formation and may prevent lesion macrophages from producing excessive chemokines and cytokines.
	Atherosclerosis and Lipoproteins
	Macrophage ABCG1 Deletion Disrupts Lipid Homeostasis in Alveolar Macrophages and Moderately Influences Atherosclerotic Lesion Development in LDL Receptor-Deficient Mice Ruud Out, Menno Hoekstra, Reeni B. Hildebrand, Janine K. Kruit, Illiana Meurs, Zhaosha Li, Folkert Kuipers, Theo J.C. Van Berkel, and Miranda Van Eck Arterioscler Thromb Vasc Biol. 2006;26:2295-2300; published online before print July 20 2006, doi:10.1161/01.ATV.0000237629.29842.4c Abstract \| Full Text \| PDF To assess the role of macrophage ABCG1 in atherosclerosis, we generated LDL receptor knockout mice that are selectively deficient in macrophage ABCG1 by using bone marrow transfer. Feeding the mice a high-cholesterol diet led to heavy lipid accumulation in macrophages of the lung, and moderately influenced atherosclerotic lesion development.
	Impaired Development of Atherosclerosis in Hyperlipidemic Ldlr^–/– and ApoE^–/– Mice Transplanted With Abcg1^–/– Bone Marrow Ángel Baldán, Liming Pei, Richard Lee, Paul Tarr, Rajendra K. Tangirala, Michael M. Weinstein, Joy Frank, Andrew C. Li, Peter Tontonoz, and Peter A. Edwards Arterioscler Thromb Vasc Biol. 2006;26:2301-2307; published online before print August 3 2006, doi:10.1161/01.ATV.0000240051.22944.dc Abstract \| Full Text \| PDF \| Data Supplement Transplantation of Abcg1-/- bone marrow into Ldlr-/- or ApoE-/- mice reduced atherosclerosis. The lesions of Ldlr-/- mice transplanted with Abcg1-/- cells also contained increased numbers of apoptotic cells. Further, Abcg1-/- macrophages are more susceptible to ox-LDL-induced apoptosis. These data suggest that loss of ABCG1 results in apoptosis and decreased atherosclerosis.
	Decreased Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice Transplanted With Abcg1^–/– Bone Marrow Mollie Ranalletta, Nan Wang, Seongah Han, Laurent Yvan-Charvet, Carrie Welch, and Alan R. Tall Arterioscler Thromb Vasc Biol. 2006;26:2308-2315; published online before print August 17 2006, doi:10.1161/01.ATV.0000242275.92915.43 Abstract \| Full Text \| PDF \| Data Supplement We examined the role of ABCG1 in atherosclerosis. Ldlr-/- mice transplanted with Abcg1-/- bone marrow showed decreased atherosclerosis after 11 weeks of Western diet, reflecting compensatory induction of Abca1 and apoE secretion by Abcg1-/- macrophages. These studies reveal an inverse relationship between Abcg1 expression and apoE accumulation and secretion in macrophages.
	FXR Deficiency Causes Reduced Atherosclerosis in Ldlr^–/– Mice Yanqiao Zhang, Xuping Wang, Charisse Vales, Florence Ying Lee, Hans Lee, Aldons J. Lusis, and Peter A. Edwards Arterioscler Thromb Vasc Biol. 2006;26:2316-2321; published online before print July 6 2006, doi:10.1161/01.ATV.0000235697.35431.05 Abstract \| Full Text \| PDF \| Data Supplement Based on the observation that Fxr-/- mice exhibit a proatherogenic lipoprotein profile, we investigated the role of FXR in the development of atherosclerosis. FXR deficiency in male, but not female, Ldlr-/- mice results in a reduction in the size of atherosclerotic lesions in the aorta. The reduction in atherosclerosis may result from a decrease in plasma low-density lipoprotein cholesterol, coupled with reduced expression of CD36 in macrophages of DKO mice.
	Fenofibrate Reduces Atherogenesis in ApoE3Leiden Mice: Evidence for Multiple Antiatherogenic Effects Besides Lowering Plasma Cholesterol T. Kooistra, L. Verschuren, J. de Vries-van der Weij, W. Koenig, K. Toet, H.M.G. Princen, and R. Kleemann Arterioscler Thromb Vasc Biol. 2006;26:2322-2330; published online before print July 27 2006, doi:10.1161/01.ATV.0000238348.05028.14 Abstract \| Full Text \| PDF \| Data Supplement It is becoming increasingly clear that factors other than cholesterol determine atherogenesis. Using ApoE3-Leiden mice, we demonstrate that fenofibrate, a PPAR{alpha}-agonist, reduces atherosclerosis beyond the effect attributable to lowering total plasma cholesterol per se via mechanisms that may involve reduced vascular and systemic inflammation and increased macrophage cholesterol efflux.
	MnSOD Deficiency Increases Endothelial Dysfunction in ApoE-Deficient Mice Masuo Ohashi, Marschall S. Runge, Frank M. Faraci, and Donald D. Heistad Arterioscler Thromb Vasc Biol. 2006;26:2331-2336; published online before print July 27 2006, doi:10.1161/01.ATV.0000238347.77590.c9 Abstract \| Full Text \| PDF \| Data Supplement The purpose of this study was to determine whether SOD2 provides protection against increased vascular superoxide and endothelial dysfunction in apoE-deficient mice. Superoxide was increased and relaxation to acetylcholine was impaired more in carotid artery of apoE-/-SOD2+/- mice than apoE-/-SOD2+/+ mice. These findings indicate that SOD2 protects against oxidative stress and endothelial dysfunction in atherosclerosis.
	GM-CSF Deficiency Reduces Macrophage PPAR- ${gamma}$ Expression and Aggravates Atherosclerosis in ApoE-Deficient Mice Michael Ditiatkovski, Ban-Hock Toh, and Alex Bobik Arterioscler Thromb Vasc Biol. 2006;26:2337-2344; published online before print July 27 2006, doi:10.1161/01.ATV.0000238357.60338.90 Abstract \| Full Text \| PDF \| Data Supplement We studied effect of GM-CSF deletion on atherosclerosis in apoE-/- mice. We observed increases in lesion size, macrophage accumulation, MCP-1, TNF-{alpha}, and VCAM-1; decreases in collagen content, PPAR-{gamma}, ABCA1, and cholesterol efflux from macrophages. GM-CSF promotes smaller stable atherosclerotic lesions by mechanisms dependant on PPAR-{gamma} and ABCA1.
	Serum Levels of Mannose-Binding Lectin and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women Tymen T. Keller, Sander I. van Leuven, Marijn C. Meuwese, Nicholas J. Wareham, Robert Luben, Erik S. Stroes, C. Erik Hack, Marcel Levi, Kay-Tee Khaw, and S. Matthijs Boekholdt Arterioscler Thromb Vasc Biol. 2006;26:2345-2350; published online before print August 10 2006, doi:10.1161/01.ATV.0000240517.69201.77 Abstract \| Full Text \| PDF The purpose of this study was to determine the association between serum levels of mannose-binding lectin (MBL) and the risk of future coronary artery disease (CAD) in apparently healthy men and women. Elevated levels of MBL are associated with an increased risk of future CAD in apparently healthy men but not in women. The sex difference merits further exploration.
	Quantitation and Localization of Matrix Metalloproteinases and Their Inhibitors in Human Carotid Endarterectomy Tissues Salman Choudhary, Catherine L. Higgins, Iou Yih Chen, Michael Reardon, Gerald Lawrie, G. Wesley Vick, III, Christof Karmonik, David P. Via, and Joel D. Morrisett Arterioscler Thromb Vasc Biol. 2006;26:2351-2358; published online before print August 3 2006, doi:10.1161/01.ATV.0000239461.87113.0b Abstract \| Full Text \| PDF \| Data Supplement Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) play a central role in arterial wall remodeling. Their spatial distribution in carotid atherosclerotic lesions is highly heterogeneous, reflecting lesion location, size, and composition. This study provides the first semiquantitative maps of differential distribution of MMPs and TIMPs over atherosclerotic plaques.
	Direct and Indirect Effects of Alloantibodies Link Neointimal and Medial Remodeling in Graft Arteriosclerosis Olivier Thaunat, Liliane Louedec, Jianping Dai, Florence Bellier, Emilie Groyer, Sandrine Delignat, Anh-Thu Gaston, Giuseppina Caligiuri, Etienne Joly, Didier Plissonnier, Jean-Baptiste Michel, and Antonino Nicoletti Arterioscler Thromb Vasc Biol. 2006;26:2359-2365; published online before print August 17 2006, doi:10.1161/01.ATV.0000241980.09816.ac Abstract \| Full Text \| PDF \| Data Supplement A rat model of graft arteriosclerosis was used to show that binding of alloantibodies on SMCs of medial donor sequentially triggers (1) the production of growth factors responsible for the proliferation of recipient SMCs in the neointima and (2) the apoptosis of donor SMCs in the media.
	In Vivo Characterization and Quantification of Atherosclerotic Carotid Plaque Components With Multidetector Computed Tomography and Histopathological Correlation Thomas T. de Weert, Mohamed Ouhlous, Erik Meijering, Pieter E. Zondervan, Johanna M. Hendriks, Marc R.H.M. van Sambeek, Diederik W.J. Dippel, and Aad van der Lugt Arterioscler Thromb Vasc Biol. 2006;26:2366-2372; published online before print August 10 2006, doi:10.1161/01.ATV.0000240518.90124.57 Abstract \| Full Text \| PDF \| Data Supplement The present study shows that multidetector computed tomography (MDCT) can quantify plaque and plaque component areas in good correlation with histology. However, lipid core can only be adequately quantified in mildly calcified plaques. MDCT based plaque quantification may evolve into an important feature in risk assessment of patients with carotid atherosclerosis.
	Intrauterine, Environmental, and Genetic Influences in the Relationship Between Birth Weight and Lipids in a Female Twin Cohort Paula M.L. Skidmore, Aedin Cassidy, Ramasamyiyer Swaminathan, Mario Falchi, Tim D. Spector, and Alex J. MacGregor Arterioscler Thromb Vasc Biol. 2006;26:2373-2379; published online before print July 27 2006, doi:10.1161/01.ATV.0000238354.39875.75 Abstract \| Full Text \| PDF In a cohort of 2900 female twins, we found that birth weight was inversely significantly related to total and LDL cholesterol, between twin pairs only and not within pairs. These findings indicate that the relationships between birth weight and lipids are mediated through shared influences on the maternal environment.
	Individual Measurement and Significance of Carotid Intima, Media, and Intima–Media Thickness by B-Mode Ultrasonographic Image Processing Jang-Ho Bae, Wuon-Shik Kim, Charanjit S. Rihal, and Amir Lerman Arterioscler Thromb Vasc Biol. 2006;26:2380-2385; published online before print August 10 2006, doi:10.1161/01.ATV.0000240420.36229.f9 Abstract \| Full Text \| PDF We assessed the individual clinical significance of carotid intima, media, and intima-media thickness by separate measurements using B-mode ultrasonographic image processing. This study suggests a differential response of the vasculature to systemic risk factors and that the individual measurement of carotid artery wall will be useful in future clinical studies.
	Close Approximation of Two Platelet Factor 4 Tetramers by Charge Neutralization Forms the Antigens Recognized by HIT Antibodies Andreas Greinacher, Manesh Gopinadhan, Jens-Uwe Günther, Mahmoud A. Omer-Adam, Ulrike Strobel, Theodore E. Warkentin, Georg Papastavrou, Werner Weitschies, and Christiane A. Helm Arterioscler Thromb Vasc Biol. 2006;26:2386-2393; published online before print July 27 2006, doi:10.1161/01.ATV.0000238350.89477.88 Abstract \| Full Text \| PDF \| Data Supplement By atomic force microscopy we show that positively charged platelet factor 4 (PF4) forms clusters with polyanions (UFH>LMWH>>fondaparinux) in which PF4 tetramers lose their intermolecular distance. This generates the binding site for heparin-induced thrombocytopenia antibodies. All 3 polyanions induce the antigen but in very different quantities (UFH>LMWH>>fondaparinux).
	Thrombosis
	Staphylococcus aureus Adhesion via Spa, ClfA, and SdrCDE to Immobilized Platelets Demonstrates Shear-Dependent Behavior Niraj Procopio Evagrio George, Qi Wei, Pyong Kyun Shin, Konstantinos Konstantopoulos, and Julia M. Ross Arterioscler Thromb Vasc Biol. 2006;26:2394-2400; published online before print July 20 2006, doi:10.1161/01.ATV.0000237606.90253.94 Abstract \| Full Text \| PDF Addition of plasma proteins potentiates S. aureus-platelet interactions at all shear rates examined. While fibrinogen plays a significant role in all shear regimes, VWF mediation becomes increasingly important as wall shear rate increases. Fibrinogen binding is dependent on bacterial adhesins ClfA and SdrCDE whereas Spa is the dominant receptor for VWF.
	Induction of Monocytic Tissue Factor Expression After Rewarming From Hypothermia In Vivo Is Counteracted by Heat Shock in c-Jun–Dependent Manner Elena M. Egorina, Mikhail A. Sovershaev, Timofei V. Kondratiev, Jan O. Olsen, Torkjel Tveita, and Bjarne Østerud Arterioscler Thromb Vasc Biol. 2006;26:2401-2406; published online before print August 10 2006, doi:10.1161/01.ATV.0000240519.46754.9c Abstract \| Full Text \| PDF In this study we report post-rewarming c-Jun-dependent induction and surface redistribution of active tissue factor antigen in rat mononuclear cells using in vivo model. This induction was counteracted by heat shock pretreatment via upregulation of heat shock protein 70 and suppression of c-Jun activation.
	Hepatocyte Growth Factor Regulates E Box–Dependent Plasminogen Activator Inhibitor Type 1 Gene Expression in HepG2 Liver Cells Shogo Imagawa, Satoshi Fujii, Jie Dong, Tomoo Furumoto, Takeaki Kaneko, Tarikuz Zaman, Yuki Satoh, Hiroyuki Tsutsui, and Burton E Sobel Arterioscler Thromb Vasc Biol. 2006;26:2407-2413; published online before print August 10 2006, doi:10.1161/01.ATV.0000240318.61359.e3 Abstract \| Full Text \| PDF Hepatocyte growth factor increased PAI-1 mRNA expression and protein in highly differentiated human liver-derived HepG2 cells, and increased hepatic PAI-1 mRNA expression in vivo in mice. The increases were mediated by E box of the PAI-1 promoter. Targeting HGF pathway may modulate the thrombotic risk in high-risk patients.
	Letters to the Editor
	Mycophenolic Acid Is a Potent Inhibitor of Angiogenesis Xinrong Wu, Hanbing Zhong, Jianbo Song, Robert Damoiseaux, Zhen Yang, and Shuo Lin Arterioscler Thromb Vasc Biol. 2006;26:2414-2416, doi:10.1161/01.ATV.0000238361.07225.fc Full Text \| PDF \| Data Supplement

Spotlight

TOC Spotlight File

Volume 26, Issue 10; October 1, 2006

Editorials

Is Two out of Three Enough for ABCG1?

Epidemiology Complements Immunology in the Heart

Perplexity of Plaque Proteinases

A Role for Plasminogen Activator Inhibitor-1 in Obesity: From Pie to PAI?

Summary of American Heart Association Diet and Lifestyle Recommendations Revision 2006

Brief Reviews

Selective Agonists of Estrogen Receptor Isoforms: New Perspectives for Cardiovascular Disease

PAI-1 and the Metabolic Syndrome: Links, Causes, and Consequences

Vascular Biology

Blockade of Angiotensin II Receptors Reduces the Expression of Receptors for Advanced Glycation End Products in Human Endothelial Cells

Blockade of Angiotensin II Receptors Reduces the Expression of Receptors for Advanced Glycation End Products in Human Endothelial Cells

Modulation of Adipose Tissue Development by Pharmacological Inhibition of PAI-1

Oxidized Phospholipids Alter Vascular Connexin Expression, Phosphorylation, and Heterocellular Communication

Atypical GPI-Anchored T-Cadherin Stimulates Angiogenesis In Vitro and In Vivo

l-Caldesmon Regulates Proliferation and Migration of Vascular Smooth Muscle Cells and Inhibits Neointimal Formation After Angioplasty

Effects of Granulocyte Colony Stimulating Factor on Functional Activities of Endothelial Progenitor Cells in Patients With Chronic Ischemic Heart Disease

Sca-1+ Progenitors Derived From Embryonic Stem Cells Differentiate Into Endothelial Cells Capable of Vascular Repair After Arterial Injury

Angiotensin II Type 1 Receptor–Mediated Inflammation Is Required for Choroidal Neovascularization

High-Molecular-Weight Kininogen Fragments Stimulate the Secretion of Cytokines and Chemokines Through uPAR, Mac-1, and gC1qR in Monocytes

Beta-Adrenoceptor Blockade Markedly Attenuates Transgene Expression From Cytomegalovirus Promoters Within the Cardiovascular System

Repetitive Fluctuations in Blood Glucose Enhance Monocyte Adhesion to the Endothelium of Rat Thoracic Aorta

Microcirculatory Hemodynamics and Endothelial Dysfunction in Systemic Lupus Erythematosus

Nuclear Receptors Nur77, Nurr1, and NOR-1 Expressed in Atherosclerotic Lesion Macrophages Reduce Lipid Loading and Inflammatory Responses

Atherosclerosis and Lipoproteins

Macrophage ABCG1 Deletion Disrupts Lipid Homeostasis in Alveolar Macrophages and Moderately Influences Atherosclerotic Lesion Development in LDL Receptor-Deficient Mice

Impaired Development of Atherosclerosis in Hyperlipidemic Ldlr–/– and ApoE–/– Mice Transplanted With Abcg1–/– Bone Marrow

Decreased Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice Transplanted With Abcg1–/– Bone Marrow

FXR Deficiency Causes Reduced Atherosclerosis in Ldlr–/– Mice

Fenofibrate Reduces Atherogenesis in ApoE*3Leiden Mice: Evidence for Multiple Antiatherogenic Effects Besides Lowering Plasma Cholesterol

MnSOD Deficiency Increases Endothelial Dysfunction in ApoE-Deficient Mice

GM-CSF Deficiency Reduces Macrophage PPAR- Expression and Aggravates Atherosclerosis in ApoE-Deficient Mice

Serum Levels of Mannose-Binding Lectin and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women

Quantitation and Localization of Matrix Metalloproteinases and Their Inhibitors in Human Carotid Endarterectomy Tissues

Direct and Indirect Effects of Alloantibodies Link Neointimal and Medial Remodeling in Graft Arteriosclerosis

In Vivo Characterization and Quantification of Atherosclerotic Carotid Plaque Components With Multidetector Computed Tomography and Histopathological Correlation

Intrauterine, Environmental, and Genetic Influences in the Relationship Between Birth Weight and Lipids in a Female Twin Cohort

Individual Measurement and Significance of Carotid Intima, Media, and Intima–Media Thickness by B-Mode Ultrasonographic Image Processing

Close Approximation of Two Platelet Factor 4 Tetramers by Charge Neutralization Forms the Antigens Recognized by HIT Antibodies

Thrombosis

Staphylococcus aureus Adhesion via Spa, ClfA, and SdrCDE to Immobilized Platelets Demonstrates Shear-Dependent Behavior

Induction of Monocytic Tissue Factor Expression After Rewarming From Hypothermia In Vivo Is Counteracted by Heat Shock in c-Jun–Dependent Manner

Hepatocyte Growth Factor Regulates E Box–Dependent Plasminogen Activator Inhibitor Type 1 Gene Expression in HepG2 Liver Cells

Letters to the Editor

Mycophenolic Acid Is a Potent Inhibitor of Angiogenesis

Spotlight

Sca-1⁺ Progenitors Derived From Embryonic Stem Cells Differentiate Into Endothelial Cells Capable of Vascular Repair After Arterial Injury

Impaired Development of Atherosclerosis in Hyperlipidemic Ldlr^–/– and ApoE^–/– Mice Transplanted With Abcg1^–/– Bone Marrow

Decreased Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice Transplanted With Abcg1^–/– Bone Marrow

FXR Deficiency Causes Reduced Atherosclerosis in Ldlr^–/– Mice

GM-CSF Deficiency Reduces Macrophage PPAR- ${gamma}$ Expression and Aggravates Atherosclerosis in ApoE-Deficient Mice