Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (26 [4])

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Volume 26, Issue 4; April 1, 2006

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

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	Editorials
	PAI-1 and TGF-ß: Unmasking the Real Driver of TGF-ß–Induced Vascular Pathology Douglas E. Vaughan Arterioscler Thromb Vasc Biol. 2006;26:679-680, doi:10.1161/01.ATV.0000209949.86606.c2 Extract \| Full Text \| PDF
	Cholesteryl Ester Transfer Protein Inhibition: Effect on Reverse Cholesterol Transport? Patrick C.N. Rensen and Louis M. Havekes Arterioscler Thromb Vasc Biol. 2006;26:681-684, doi:10.1161/01.ATV.0000214979.24518.95 Extract \| Full Text \| PDF
	Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries Rhian M. Touyz Arterioscler Thromb Vasc Biol. 2006;26:685-688, doi:10.1161/01.ATV.0000216428.90962.60 Extract \| Full Text \| PDF
	Brief Reviews
	Oxidative Stress and Vascular Disease: 2005 Duff Lecture Donald D. Heistad Arterioscler Thromb Vasc Biol. 2006;26:689-695; published online before print January 12 2006, doi:10.1161/01.ATV.0000203525.62147.28 Abstract \| Full Text \| PDF Oxidative stress plays a key role in the pathophysiology of atherosclerosis and several other major cardiovascular diseases. Antioxidant enzymes, including superoxide dismutases (SODs), protect against vasomoter dysfunction. An approach that we have used, based on gene transfer to examine the role of the heparin-binding domain of extracellular SOD, might be used to study many other proteins. Several important questions about oxidative stress and atherosclerosis are raised, and proposed as fruitful areas of research.
	ATVB In Focus: Nitric Oxide Redux Joseph Loscalzo Arterioscler Thromb Vasc Biol. 2006;26:696, doi:10.1161/01.ATV.0000209519.12258.74 Extract \| Full Text \| PDF
	Unraveling the Reactions of Nitric Oxide, Nitrite, and Hemoglobin in Physiology and Therapeutics Daniel B. Kim-Shapiro, Alan N. Schechter, and Mark T. Gladwin Arterioscler Thromb Vasc Biol. 2006;26:697-705; published online before print January 19 2006, doi:10.1161/01.ATV.0000204350.44226.9a Abstract \| Full Text \| PDF Several factors nitigate nitric oxide (NO) scavenging by red blood cell encapsulated hemoglobin (Hb). Recent data suggests that the nitrate amion is converted to NO by Hb under hyposia. The hypothesis is currently the subject of intense investigations in the areas of biochemistry, physiology, and therapatics.
	Cholesteryl Ester Transfer Protein (CETP) Inhibition Beyond Raising High-Density Lipoprotein Cholesterol Levels: Pathways by Which Modulation of CETP Activity May Alter Atherogenesis Anke H.E.M. Klerkx, Karim El Harchaoui, Wim A. van der Steeg, S. Matthijs Boekholdt, Erik S.G. Stroes, John J.P. Kastelein, and Jan Albert Kuivenhoven Arterioscler Thromb Vasc Biol. 2006;26:706-715; published online before print January 26 2006, doi:10.1161/01.ATV.0000205595.19612.c9 Abstract \| Full Text \| PDF The mechanism underlying the putative atheroprotective effect of CETP inhibition points not only toward beneficial effects through raising HDL-C levels. In addition, LDL-C and small dense LDL may decrease, consistent with the role of CETPs in reverse cholesterol transport. Furthermore, CETP inhibition may improve the antioxidant potential of HDL.
	Pericellular Proteases in Angiogenesis and Vasculogenesis Victor W.M. van Hinsbergh, Marten A. Engelse, and Paul H.A. Quax Arterioscler Thromb Vasc Biol. 2006;26:716-728; published online before print February 9 2006, doi:10.1161/01.ATV.0000209518.58252.17 Abstract \| Full Text \| PDF Pericellular proteases are involved in angiogenesis and vasculogenesis. They contribute to the degradation of the endothelial basal membrane, cell migration and invasion, and activation and liberation of angiogenic growth factors. They alter the properties of growth factors and cytokines by truncation, and generate protein fragments that have anti-angiogenic properties.
	Non-Exercise Activity Thermogenesis: The Crouching Tiger Hidden Dragon of Societal Weight Gain James A. Levine, Mark W. Vander Weg, James O. Hill, and Robert C. Klesges Arterioscler Thromb Vasc Biol. 2006;26:729-736; published online before print January 26 2006, doi:10.1161/01.ATV.0000205848.83210.73 Abstract \| Full Text \| PDF Non-exercise activity thermogenesis (NEAT) is the energy expenditure of all physical activities other than volitional sporting-like exercise. Because people of the same weight have markedly variable activity levels, it is not surprising that NEAT varies substantially between people by up to 2000 kcal per day. Evidence suggests that low NEAT may occur in obesity but in a very specific fashion. The obesity epidemic may reflect the emergence of a chair-enticing environment to which those with an innate tendency to sit, did so, and became obese. To reverse obesity, we need to develop individual strategies to promote standing and ambulating time by 2.5 hours per day and also re-engineer our work, school, and home environments to render active living the option of choice.
	Vascular Biology
	Transforming Growth Factor Beta 1 Induces Neointima Formation Through Plasminogen Activator Inhibitor-1–Dependent Pathways Goro Otsuka, Ramtin Agah, Andrew D. Frutkin, Thomas N. Wight, and David A. Dichek Arterioscler Thromb Vasc Biol. 2006;26:737-743; published online before print December 22 2005, doi:10.1161/01.ATV.0000201087.23877.e1 Abstract \| Full Text \| PDF \| Data Supplement We investigated mechanisms of TGF-ß1-induced intimal growth. TGF-ß1 induced neointimal formation through cell migration and matrix accumulation. Overexpression of TGF-ß1 in arteries of PAI-1-deficient mice revealed that PAI-1 is both a critical mediator of TGF-ß1-induced intimal growth and a key negative regulator of TGF-ß1 expression in the artery wall.
	Proangiogenic Effects of Protease-Activated Receptor 2 Are Tumor Necrosis Factor- ${alpha}$ and Consecutively Tie2 Dependent Tang Zhu, Florian Sennlaub, Martin Hervé Beauchamp, Li Fan, Jean Sebastian Joyal, Daniella Checchin, Satra Nim, Pierre Lachapelle, Mirna Sirinyan, Xin Hou, Michela Bossolasco, Georges-Etienne Rivard, Nikolaus Heveker, and Sylvain Chemtob Arterioscler Thromb Vasc Biol. 2006;26:744-750; published online before print January 26 2006, doi:10.1161/01.ATV.0000205591.88522.d4 Abstract \| Full Text \| PDF \| Data Supplement This article investigated PAR2 activation in retinal angiogenesis. TNF-{alpha} inhibitors (infliximab and etanercept) and the MEK inhibitor PD98059 prevented tie2 upregulation, endothelium proliferation, and retinal neovascularization induced by PAR2 activation. The PAR2 proangiogenic properties are involved in its proinflammatory effects and subsequent induction of tie2 via the MEK/ERK pathway.
	Granulocyte Colony-Stimulating Factor–Mobilized Circulating c-Kit+/Flk-1+ Progenitor Cells Regenerate Endothelium and Inhibit Neointimal Hyperplasia After Vascular Injury Michitaka Takamiya, Mitsuhiko Okigaki, Denan Jin, Shinji Takai, Yoshihisa Nozawa, Yasushi Adachi, Norifumi Urao, Kento Tateishi, Tetsuya Nomura, Kan Zen, Eishi Ashihara, Mizuo Miyazaki, Tetsuya Tatsumi, Tomosaburo Takahashi, and Hiroaki Matsubara Arterioscler Thromb Vasc Biol. 2006;26:751-757; published online before print January 26 2006, doi:10.1161/01.ATV.0000205607.98538.9a Abstract \| Full Text \| PDF \| Data Supplement Subcutaneous injection of G-CSF increases in re-endothelialization of the denuded vessels, followed by inhibition of neointimal formation. The G-CSF-induced endothelium exhibited normal acetylcholine-mediated vasodilatation in NO-dependent manner. Bone marrow (BM) replacement by GFP-overexpressing cells showed that G-CSF-mobilized Lin-/c-Kit+/Flk-1+ cells from BM contributes to endothelial regeneration.
	Differential Healing Activities of CD34⁺ and CD14⁺ Endothelial Cell Progenitors Ola Awad, Eduard I. Dedkov, Chunhua Jiao, Steven Bloomer, Robert J. Tomanek, and Gina C. Schatteman Arterioscler Thromb Vasc Biol. 2006;26:758-764; published online before print January 12 2006, doi:10.1161/01.ATV.0000203513.29227.6f Abstract \| Full Text \| PDF \| Data Supplement Human CD34+ and CD14+ blood-derived endothelial cell progenitors were injected into ischemic limbs of diabetic mice. CD14+ cell therapy accelerated healing, although not as much as CD34+ cell treatment. Nevertheless, CD14+ cells could provide a therapeutic option for diabetic patients, the function of whose CD34+ cells may be compromised.
	Endothelial NO Synthase Deficiency Promotes Smooth Muscle Progenitor Cells in Association With Upregulation of Stromal Cell-Derived Factor-1 ${alpha}$ in a Mouse Model of Carotid Artery Ligation Le-Ning Zhang, Dennis W. Wilson, Valdeci da Cunha, Mark E. Sullivan, Ronald Vergona, John C. Rutledge, and Yi-Xin Wang Arterioscler Thromb Vasc Biol. 2006;26:765-772; published online before print February 2 2006, doi:10.1161/01.ATV.0000207319.28254.8c Abstract \| Full Text \| PDF \| Data Supplement eNOS deficiency enhanced SMC-rich neointimal formation. SDF-1{alpha}-mediated recruitment of circulating SMC progenitor cells substantially contributed to the neointimal hyperplasia. Our results indicate that eNOS deficiency exacerbates expression of SDF-1{alpha}, which mediates the recruitment of SMC progenitor cells into the arterial wall. This contributes to vascular remodeling and SMC-rich neointimal formation.
	Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling Ludovic Waeckel, Jérôme Bignon, Jian-Miao Liu, Delphine Markovits, Téni G. Ebrahimian, José Vilar, Barend Mees, Olivier Blanc-Brude, Véronique Barateau, Sophie Le ricousse-Roussanne, Micheline Duriez, Gérard Tobelem, Joanna Wdzieczak-Bakala, Bernard I Lévy, and Jean-Sébastien Silvestre Arterioscler Thromb Vasc Biol. 2006;26:773-779; published online before print January 12 2006, doi:10.1161/01.ATV.0000203510.96492.14 Abstract \| Full Text \| PDF \| Data Supplement In this study, we investigated the putative proangiogenic activity and molecular pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lees-Pro (AcSDKP) in a model of surgically induced hind limb ischemia. AcSDKP stimulated MCP-1 mRNA and protein levels in cultured endothelial cells and ischemic tissue. Subsequently, AcSDKP-induced MCP-1 upregulation activated monocytes/macrophages infiltration to ischemic areas and promoted postischemic neovascularization.
	PKC ${delta}$ Is Necessary for Smad3 Expression and Transforming Growth Factor ß–Induced Fibronectin Synthesis in Vascular Smooth Muscle Cells Evan J. Ryer, R. Patrick Hom, Kenji Sakakibara, Keiichi I. Nakayama, Keiko Nakayama, Peter L. Faries, Bo Liu, and K. Craig Kent Arterioscler Thromb Vasc Biol. 2006;26:780-786; published online before print February 9 2006, doi:10.1161/01.ATV.0000209517.00220.cd Abstract \| Full Text \| PDF \| Data Supplement The mechanism by which TGFß regulates the synthesis of fibronectin remains inconclusive. Our data suggest that TGFß-activated PKC{delta} is critical to maintain Smad3 levels, which in turn are required for fibronectin expression. Thus, PKC{delta} may serve as a novel therapeutic target to prevent the fibroproliferative response after arterial injury.
	Regulation of Vascular Endothelial Growth Factor Expression and Vascularization in the Myocardium by Insulin Receptor and PI3K/Akt Pathways in Insulin Resistance and Ischemia Zhiheng He, Darren M. Opland, Kerrie J. Way, Kohjiro Ueki, Natalya Bodyak, Peter M. Kang, Seigo Izumo, Rohit N. Kulkarni, Bo Wang, Ronglih Liao, C. Ronald Kahn, and George L. King Arterioscler Thromb Vasc Biol. 2006;26:787-793; published online before print February 9 2006, doi:10.1161/01.ATV.0000209500.15801.4e Abstract \| Full Text \| PDF \| Data Supplement We have shown that insulin stimulate the expression of VEGF in cardiomyocytes primarily via a PI3K/Akt2 activation-dependent pathway. Selective inhibition of this cascade results in the reduction of cardiomyocyte-derived VEGF expression and impaired vascularization at both basal and pathological conditions such as myocardial infarction.
	High Glucose Activates Nuclear Factor of Activated T Cells in Native Vascular Smooth Muscle Jenny Nilsson, Lisa M. Nilsson, Yung-Wu Chen, Jeffery D. Molkentin, David Erlinge, and Maria F. Gomez Arterioscler Thromb Vasc Biol. 2006;26:794-800; published online before print February 9 2006, doi:10.1161/01.ATV.0000209513.00765.13 Abstract \| Full Text \| PDF \| Data Supplement
	Urokinase Plasminogen Activator Stimulates Vascular Smooth Muscle Cell Proliferation Via Redox-Dependent Pathways Mikhail Menshikov, Olga Plekhanova, Hua Cai, Karel Chalupsky, Yelena Parfyonova, Pavel Bashtrikov, Vsevolod Tkachuk, and Bradford C. Berk Arterioscler Thromb Vasc Biol. 2006;26:801-807; published online before print February 2 2006, doi:10.1161/01.ATV.0000207277.27432.15 Abstract \| Full Text \| PDF \| Data Supplement uPA stimulates VSMC proliferation after vascular injury. uPA biphasically stimulated ROS production (which was partly inhibited by Nox1 or Nox4 siRNA) and increased expression of the oxidases Nox1 and Nox4. Transfection with uPA cDNA enhanced ROS production, suggesting that uPA-mediated autocrine ROS production contributes to vascular remodeling.
	PPAR ${gamma}$ Gene Transfer Sustains Apoptosis, Inhibits Vascular Smooth Muscle Cell Proliferation, and Reduces Neointima Formation After Balloon Injury in Rats Soo Lim, Cheng Ji Jin, Min Kim, Sung Soo Chung, Ho Seon Park, In Kyu Lee, Choon Taek Lee, Young Min Cho, Hong Kyu Lee, and Kyong Soo Park Arterioscler Thromb Vasc Biol. 2006;26:808-813; published online before print January 19 2006, doi:10.1161/01.ATV.0000204634.26163.a7 Abstract \| Full Text \| PDF \| Data Supplement There is debate as to whether protective effect of PPAR{gamma} ligands on atherosclerosis is dependant on the PPAR{gamma} gene itself or other pathway. We found that transfer of the PPAR{gamma} wild-type gene inhibited neointima formation after balloon injury, which indicates that PPAR{gamma} overexpression itself has a protective role against restenosis.
	Influence of Folate on Arterial Permeability and Stiffness in the Absence or Presence of Hyperhomocysteinemia J. David Symons, Ussama B. Zaid, Christian N. Athanassious, Adam E. Mullick, Steven R. Lentz, and John C. Rutledge Arterioscler Thromb Vasc Biol. 2006;26:814-818; published online before print January 19 2006, doi:10.1161/01.ATV.0000204408.01416.16 Abstract \| Full Text \| PDF We determined the influence of low-folate per se in the absence and presence of mild hyperhomocysteinemia (HHcy) on arterial permeability and stiffness. Arterial permeability was % greater (P<0.05) but vascular stiffening was unaltered by low folate per se. In the combined presence of low-folate and HHcy, vascular permeability ( %) and stiffness ( %) were greater (P<0.05).
	Vascular Responses to ${alpha}$ ₁-Adrenergic Receptors in Small Rat Mesenteric Arteries Depend on Mitochondrial Reactive Oxygen Species Li Hao, Tamiko Nishimura, Hua Wo, and Carlos Fernandez-Patron Arterioscler Thromb Vasc Biol. 2006;26:819-825; published online before print January 19 2006, doi:10.1161/01.ATV.0000204344.90301.7c Abstract \| Full Text \| PDF \| Data Supplement Agonists of G-protein-coupled receptors (eg, adrenoceptors and angiotensin receptors) signal, at least in part, through matrix metalloproteinases (such as matrix metalloproteinase [MMP]-7) that transactivate the epidermal growth factor receptor (EGFR). Focusing on adrenoceptors, we examined whether the MMP-dependent signaling pathway depends on reactive oxygen species (ROS). Production of mitochondrial ROS is a new event in the pathway by which vasoactive agonists that induce MMP transactivation of the EGFR modulate vascular tone. Moreover, our findings suggest a connection between agonist-induced activity of MMPs, the promotion of oxidative stress, enhanced vascular tone, and hypertrophy, which are all implicated in the development and progression of vascular disease.
	Angiotensin II Attenuates Endothelium-Dependent Responses in the Cerebral Microcirculation Through Nox-2–Derived Radicals Helene Girouard, Laibaik Park, Josef Anrather, Ping Zhou, and Costantino Iadecola Arterioscler Thromb Vasc Biol. 2006;26:826-832; published online before print January 26 2006, doi:10.1161/01.ATV.0000205849.22807.6e Abstract \| Full Text \| PDF \| Data Supplement We investigated the mechanism of the effect of angiotensin II on the increase in cerebral blood flow (CBF) produced by endothelium-dependent vasodilators. We found that the attenuation of endothelium-dependent responses induced by Ang II is mediated by free radicals produced by a NADPH oxidase containing nox-2 as the catalytic subunit.
	Increased Serum Cadmium and Strontium Levels in Young Smokers: Effects on Arterial Endothelial Cell Gene Transcription David Bernhard, Andrea Rossmann, Blair Henderson, Michaela Kind, Andreas Seubert, and Georg Wick Arterioscler Thromb Vasc Biol. 2006;26:833-838; published online before print January 26 2006, doi:10.1161/01.ATV.0000205616.70614.e5 Abstract \| Full Text \| PDF \| Data Supplement Cigarette smoking interferes with metal homeostasis of the human body. In this study, we show that serum cadmium and strontium levels are significantly increased in smokers compared with nonsmokers. Further, we analyze the effects of these metals on primary arterial endothelial cell transcription using microarray technology and real-time polymerase chain reaction.
	Cardiac and Vascular Hypertrophy in Fabry Disease: Evidence for a New Mechanism Independent of Blood Pressure and Glycosphingolipid Deposition Frédéric Barbey, Noureddine Brakch, Ales Linhart, Nathalie Rosenblatt-Velin, Xavier Jeanrenaud, Salah Qanadli, Beat Steinmann, Michel Burnier, Tomas Palecek, Jan Bultas, and Daniel Hayoz Arterioscler Thromb Vasc Biol. 2006;26:839-844; published online before print February 9 2006, doi:10.1161/01.ATV.0000209649.60409.38 Abstract \| Full Text \| PDF The study examined and confirmed the correlation between 2 cardiovascular findings in Fabry disease, LVH and CCA IMT. Further in vitro investigation confirmed the presence of a circulating growth-promoting factor that may be at least partially responsible for these clinical findings.
	Effect of Rosiglitazone Treatment on Plaque Inflammation and Collagen Content in Nondiabetic Patients: Data From a Randomized Placebo-Controlled Trial Franz Meisner, Daniel Walcher, Florence Gizard, Xaver Kapfer, Roman Huber, Anja Noak, Ludger Sunder-Plassmann, Helga Bach, Cornelia Haug, Max Bachem, Tatjana Stojakovic, Winfried März, Vinzenz Hombach, Wolfgang Koenig, Bart Staels, and Nikolaus Marx Arterioscler Thromb Vasc Biol. 2006;26:845-850; published online before print January 12 2006, doi:10.1161/01.ATV.0000203511.66681.7f Abstract \| Full Text \| PDF \| Data Supplement The present randomized, placebo-controlled, single-blind trial demonstrates in nondiabetic patients scheduled for carotid endarterectomy that 4 weeks of treatment with rosiglitazone significantly reduces vascular inflammation, leading to a more stable type of arteriosclerotic lesion.
	Atherosclerosis and Lipoproteins
	Destabilizing Role of Cathepsin S in Murine Atherosclerotic Plaques Kenneth J. Rodgers, Deborah J. Watkins, Alastair L. Miller, Peter Y. Chan, Sharada Karanam, William H. Brissette, Clive J. Long, and Christopher L. Jackson Arterioscler Thromb Vasc Biol. 2006;26:851-856; published online before print January 12 2006, doi:10.1161/01.ATV.0000203526.75772.4b Abstract \| Full Text \| PDF \| Data Supplement Apolipoprotein E knockout mice fed a high-fat diet rapidly develop unstable plaques in the brachiocephalic artery. Making these mice additionally null to the cysteine proteinase cathepsin S resulted in a significant reduction in plaque size and an independent reduction in the incidence of plaque rupture. Human atherosclerotic plaques contain active cysteine proteinases as detected with a novel active site-directed probe. These data support the idea that cathepsin S is a mediator of plaque destabilization and rupture.
	Enhanced T-Cell Expression of RANK Ligand in Acute Coronary Syndrome: Possible Role in Plaque Destabilization Wiggo J. Sandberg, Arne Yndestad, Erik Øie, Camilla Smith, Thor Ueland, Olga Ovchinnikova, Anna-Karin L. Robertson, Fredrik Müller, Anne G. Semb, Hanne Scholz, Arne K. Andreassen, Lars Gullestad, Jan Kristian Damås, Stig S. Frøland, Göran K. Hansson, Bente Halvorsen, and Pål Aukrust Arterioscler Thromb Vasc Biol. 2006;26:857-863; published online before print January 19 2006, doi:10.1161/01.ATV.0000204334.48195.6a Abstract \| Full Text \| PDF \| Data Supplement We show enhanced expression of osteoprotegerin (OPG), RANK, and RANK ligand (RANKL) in clinical and experimental atherosclerosis with enhanced T-cell expression of RANKL as an important feature of unstable disease, further supporting a role for the OPG/RANKL/RANK axis in atherogenesis and plaque destabilization.
	Adoptive Transfer of CD4⁺ T Cells Reactive to Modified Low-Density Lipoprotein Aggravates Atherosclerosis Xinghua Zhou, Anna-Karin L. Robertson, Charlotta Hjerpe, and Göran K. Hansson Arterioscler Thromb Vasc Biol. 2006;26:864-870; published online before print February 2 2006, doi:10.1161/01.ATV.0000206122.61591.ff Abstract \| Full Text \| PDF \| Data Supplement To test whether atherogenesis depends on specific disease-associated antigens, we transferred CD4+ T-cells from immunized donors into apoE-/- scid/scid mice. Mice receiving T cells from oxLDL-immunized mice had accelerated lesion progression compared with those receiving naive or KLH-primed T cells. These findings demonstrate that T-cell response to oxLDL is critical in atherogenesis.
	Comparison of Circulating Adiponectin and Proinflammatory Markers Regarding Their Association With Metabolic Syndrome in Japanese Men Kunihiro Matsushita, Hiroshi Yatsuya, Koji Tamakoshi, Keiko Wada, Rei Otsuka, Seiko Takefuji, Kaichiro Sugiura, Takahisa Kondo, Toyoaki Murohara, and Hideaki Toyoshima Arterioscler Thromb Vasc Biol. 2006;26:871-876; published online before print February 2 2006, doi:10.1161/01.ATV.0000208363.85388.8f Abstract \| Full Text \| PDF We compared serum TNF-{alpha}, IL-6, CRP, and adiponectin levels regarding associations with MetS using 624 Japanese men. Adiponectin was most strongly associated with MetS in regard both to individual components and their clustering, suggesting that decreased serum adiponectin might be fundamentally involved in the development of MetS.
	Persistent High Levels of Plasma Oxidized Low-Density Lipoprotein After Acute Myocardial Infarction Predict Stent Restenosis Takahiko Naruko, Makiko Ueda, Shoichi Ehara, Akira Itoh, Kazuo Haze, Nobuyuki Shirai, Yoshihiro Ikura, Masahiko Ohsawa, Hiroyuki Itabe, Yoshiki Kobayashi, Hiroyuki Yamagishi, Minoru Yoshiyama, Junichi Yoshikawa, and Anton E. Becker Arterioscler Thromb Vasc Biol. 2006;26:877-883; published online before print February 9 2006, doi:10.1161/01.ATV.0000209886.31510.7f Abstract \| Full Text \| PDF We investigated prospectively 102 patients with acute myocardial infarction (AMI) after stenting to evaluate whether plasma oxidized low-density lipoprotein (ox-LDL) levels could predict outcome. This study demonstrates that an increased levels of plasma ox-LDL at discharge is an independent predictor of stent restenosis in AMI patients (ß=0.645;P<0.0001).
	Effect of Inhibiting Cholesteryl Ester Transfer Protein on the Kinetics of High-Density Lipoprotein Cholesteryl Ester Transport in Plasma: In Vivo Studies in Rabbits P. Kee, D. Caiazza, K.-A. Rye, P.H.R. Barrett, L.A. Morehouse, and P.J. Barter Arterioscler Thromb Vasc Biol. 2006;26:884-890; published online before print December 22 2005, doi:10.1161/01.ATV.0000201064.89581.35 Abstract \| Full Text \| PDF An 80% to 90% inhibition of plasma CETP activity in rabbits doubled the concentration of HDL CE by blocking its transfer to the VLDL/LDL fraction. However, this did not compromise the removal of HDL CE from plasma.
	Lipoprotein Lipase Bound to Apolipoprotein B Lipoproteins Accelerates Clearance of Postprandial Lipoproteins in Humans Chunyu Zheng, Susan J. Murdoch, John D. Brunzell, and Frank M. Sacks Arterioscler Thromb Vasc Biol. 2006;26:891-896; published online before print January 12 2006, doi:10.1161/01.ATV.0000203512.01007.3d Abstract \| Full Text \| PDF \| Data Supplement We studied the role of lipoprotein lipase (LpL) in the metabolism of plasma apoB lipoproteins. Postprandially, apoB lipoproteins with LpL had significantly greater increases and faster rates of clearance. The results suggest plasma LpL may act like an apolipoprotein and enhance the clearance from plasma of apoB lipoproteins.
	Decreased High-Density Lipoprotein (HDL) Particle Size, Preß-, and Large HDL Subspecies Concentration in Finnish Low-HDL Families: Relationship With Intima-Media Thickness Hiroshi Watanabe, Sanni Söderlund, Aino Soro-Paavonen, Anne Hiukka, Eeva Leinonen, Corradina Alagona, Riitta Salonen, Tomi-Pekka Tuomainen, Christian Ehnholm, Matti Jauhiainen, and Marja-Riitta Taskinen Arterioscler Thromb Vasc Biol. 2006;26:897-902; published online before print February 9 2006, doi:10.1161/01.ATV.0000209577.04246.c0 Abstract \| Full Text \| PDF \| Data Supplement The precise antiatherogenic mechanisms of high-density lipoprotein (HDL) subspecies are not thoroughly elucidated. HDL particle size and levels of HDL2b, HDL2a, and preß-HDL were decreased, and intima-media thickness (IMT) was increased in Finnish subjects with familial low HDL. Age, HDL2b, systolic blood pressure, and preß-HDL were significant independent determinants of IMT.
	A Possible Association Between Coronary Plaque Instability and Complex Plaques in Abdominal Aorta Yukihiko Momiyama, Ryuichi Kato, Zahi A. Fayad, Nobukiyo Tanaka, Hiroaki Taniguchi, Reiko Ohmori, Teruyoshi Kihara, Akira Kameyama, Koji Miyazaki, Kazuo Kimura, Koh Arakawa, Masatoshi Kusuhara, Masayoshi Nagata, Haruo Nakamura, and Fumitaka Ohsuzu Arterioscler Thromb Vasc Biol. 2006;26:903-909; published online before print January 19 2006, doi:10.1161/01.ATV.0000204637.00865.87 Abstract \| Full Text \| PDF To elucidate the association between coronary and aortic plaque instability, aortic MRI was performed in 146 patients undergoing coronary angiography. Complex plaques in abdominal aorta were associated with myocardial infarction and complex coronary lesions, suggesting a link between coronary and aortic plaque instability.
	Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E^–/– Mice Reiko Matsui, Shanqin Xu, Karlene A. Maitland, Roberto Mastroianni, Jane A. Leopold, Diane E. Handy, Joseph Loscalzo, and Richard A. Cohen Arterioscler Thromb Vasc Biol. 2006;26:910-916; published online before print January 26 2006, doi:10.1161/01.ATV.0000205850.49390.3b Abstract \| Full Text \| PDF \| Data Supplement Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway that is a major source of cellular NADPH. The purpose of this study was to examine whether G6PD deficiency affects vascular oxidants and atherosclerosis in high-fat fed apolipoprotein (apo) E-/- mice. Lower NADPH production in G6PD deficiency may result in lower NADPH oxidase-derived superoxide anion, and thus lower aortic lesion growth. The association of higher blood pressure with lower serum cholesterol levels in this mouse model is indicative of the complex effects that G6PD deficiency may have on vascular disease.
	Eplerenone With Valsartan Effectively Reduces Atherosclerotic Lesion by Attenuation of Oxidative Stress and Inflammation Jun Suzuki, Masaru Iwai, Masaki Mogi, Akira Oshita, Toyofumi Yoshii, Jitsuo Higaki, and Masatsugu Horiuchi Arterioscler Thromb Vasc Biol. 2006;26:917-921; published online before print January 19 2006, doi:10.1161/01.ATV.0000204635.75748.0f Abstract \| Full Text \| PDF \| Data Supplement Eplerenone (1.67 g/kg in 1.25% high-cholesterol diet) inhibited the increase in atherosclerotic lesion formation, oxidative stress, and inflammation in male apolipoprotein E-deficient mice treated with a high-cholesterol diet. Eplerenone also enhanced the inhibitory action of an AT1 receptor blocker, valsartan, suggesting the beneficial effect of combination therapy for atherosclerosis.
	Peroxisome Proliferator-Activated Receptor- ${alpha}$ , ${gamma}$ -Agonist Improves Insulin Sensitivity and Prevents Loss of Left Ventricular Function in Obese Dyslipidemic Mice Wim Verreth, Javier Ganame, Ann Mertens, Hilde Bernar, Marie-Christine Herregods, and Paul Holvoet Arterioscler Thromb Vasc Biol. 2006;26:922-928; published online before print February 2 2006, doi:10.1161/01.ATV.0000207318.42066.bb Abstract \| Full Text \| PDF \| Data Supplement We investigated the effect of a dual PPAR{alpha},{gamma}-agonist on atherosclerosis and cardiac function in mice with combined leptin and LDL receptor deficiency (DKO). In these mice, obesity, diabetes, and hyperlipidemia are associated with accelerated atherosclerosis and loss of cardiac function. The agonist lowered free fatty acids and increased glucose tolerance and insulin sensitivity. It had no effect on plasma cholesterol and triglycerides. It prevented the loss of cardiac function but had no effect on atherosclerosis in DKO mice.
	Macrophage ATP-Binding Cassette Transporter A1 Overexpression Inhibits Atherosclerotic Lesion Progression in Low-Density Lipoprotein Receptor Knockout Mice Miranda Van Eck, Roshni R. Singaraja, Dan Ye, Reeni B. Hildebrand, Erick R. James, Michael R. Hayden, and Theo J.C. Van Berkel Arterioscler Thromb Vasc Biol. 2006;26:929-934; published online before print February 2 2006, doi:10.1161/01.ATV.0000208364.22732.16 Abstract \| Full Text \| PDF ATP-binding cassette transporter 1 (ABCA1) is a key regulator of cellular cholesterol and phospholipid transport. To investigate the therapeutic benefit of upregulation of macrophage ABCA1, chimeras were created that specifically overexpress ABCA1 in macrophages by bone marrow transplantation. The studies show that ABCA1 upregulation in macrophages inhibited the progression of atherosclerotic lesions.
	Effect of Modified C-Reactive Protein on Complement Activation: A Possible Complement Regulatory Role of Modified or Monomeric C-Reactive Protein in Atherosclerotic Lesions Shang-Rong Ji, Yi Wu, Lawrence A. Potempa, Yu-Heng Liang, and Jing Zhao Arterioscler Thromb Vasc Biol. 2006;26:935-941; published online before print February 2 2006, doi:10.1161/01.ATV.0000206211.21895.73 Abstract \| Full Text \| PDF \| Data Supplement The current work studied interaction of mCRP with complement. Our data showed that mCRP can both inhibit and activate the classical complement pathway by binding C1q, depending on whether it is in fluid phase or surface bound.
	Thrombosis
	Thrombomodulin Gene Polymorphisms and Haplotypes and the Risk of Cardiovascular Events: A Prospective Follow-Up Study K. Auro, K. Komulainen, M. Alanne, K. Silander, L. Peltonen, M. Perola, and V. Salomaa Arterioscler Thromb Vasc Biol. 2006;26:942-947; published online before print February 2 2006, doi:10.1161/01.ATV.0000208365.45200.41 Abstract \| Full Text \| PDF \| Data Supplement Thrombomodulin, a natural anticoagulant and a biological marker for endothelial activation and damage, has been suggested to contribute to the pathogenesis of cardiovascular diseases. In a prospective follow-up study combining 2 large, independent Finnish cohorts, common allelic variants of the thrombomodulin gene did not show consistent association with the risk of cardiovascular events.
	Plasminogen Activator Inhibitor-1 Gene: Selection of Tagging Single Nucleotide Polymorphisms and Association With Coronary Heart Disease Shaoyong Su, Shufeng Chen, Jiangong Zhao, Jianfeng Huang, Xiaoling Wang, Runsheng Chen, and Dongfeng Gu Arterioscler Thromb Vasc Biol. 2006;26:948-954; published online before print January 19 2006, doi:10.1161/01.ATV.0000204731.17646.f2 Abstract \| Full Text \| PDF \| Data Supplement We examined the association of 5 tagging SNPs of PAI-1 gene with coronary heart disease (CHD) in 816 patients and 937 controls. A significant interaction between PAI-1 gene and smoking status was identified, with rs2227631 A allele and rs1799889 4G allele increasing the risk of CHD among nonsmokers in Chinese.
	Letters to the Editor
	Optimal Treatments for the Metabolic Syndrome Dario Giugliano and Katherine Esposito Arterioscler Thromb Vasc Biol. 2006;26:e30, doi:10.1161/01.ATV.0000207278.11455.8b Extract \| Full Text \| PDF
	Oxidized LDL and the Metabolic Syndrome Paul Holvoet, Tamara B. Harris, Russell P. Tracy, and Stephen B. Kritchevsky Arterioscler Thromb Vasc Biol. 2006;26:e31, doi:10.1161/01.ATV.0000210271.36395.43 Extract \| Full Text \| PDF
	In Response: Per Sjogren, Anders Hamsten, Mai-Lis Hellenius, and Rachel M. Fisher Arterioscler Thromb Vasc Biol. 2006;26:e31-e32, doi:10.1161/01.ATV.0000210272.82833.a0 Extract \| Full Text \| PDF
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2006;26:e33, doi:10.1161/01.ATV.0000216790.05084.4c Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 26, Issue 4; April 1, 2006

Editorials

PAI-1 and TGF-ß: Unmasking the Real Driver of TGF-ß–Induced Vascular Pathology

Cholesteryl Ester Transfer Protein Inhibition: Effect on Reverse Cholesterol Transport?

Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries

Brief Reviews

Oxidative Stress and Vascular Disease: 2005 Duff Lecture

ATVB In Focus: Nitric Oxide Redux

Unraveling the Reactions of Nitric Oxide, Nitrite, and Hemoglobin in Physiology and Therapeutics

Cholesteryl Ester Transfer Protein (CETP) Inhibition Beyond Raising High-Density Lipoprotein Cholesterol Levels: Pathways by Which Modulation of CETP Activity May Alter Atherogenesis

Pericellular Proteases in Angiogenesis and Vasculogenesis

Non-Exercise Activity Thermogenesis: The Crouching Tiger Hidden Dragon of Societal Weight Gain

Vascular Biology

Transforming Growth Factor Beta 1 Induces Neointima Formation Through Plasminogen Activator Inhibitor-1–Dependent Pathways

Proangiogenic Effects of Protease-Activated Receptor 2 Are Tumor Necrosis Factor- and Consecutively Tie2 Dependent

Granulocyte Colony-Stimulating Factor–Mobilized Circulating c-Kit+/Flk-1+ Progenitor Cells Regenerate Endothelium and Inhibit Neointimal Hyperplasia After Vascular Injury

Differential Healing Activities of CD34+ and CD14+ Endothelial Cell Progenitors

Endothelial NO Synthase Deficiency Promotes Smooth Muscle Progenitor Cells in Association With Upregulation of Stromal Cell-Derived Factor-1 in a Mouse Model of Carotid Artery Ligation

Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling

PKC Is Necessary for Smad3 Expression and Transforming Growth Factor ß–Induced Fibronectin Synthesis in Vascular Smooth Muscle Cells

Regulation of Vascular Endothelial Growth Factor Expression and Vascularization in the Myocardium by Insulin Receptor and PI3K/Akt Pathways in Insulin Resistance and Ischemia

High Glucose Activates Nuclear Factor of Activated T Cells in Native Vascular Smooth Muscle

Urokinase Plasminogen Activator Stimulates Vascular Smooth Muscle Cell Proliferation Via Redox-Dependent Pathways

PPAR Gene Transfer Sustains Apoptosis, Inhibits Vascular Smooth Muscle Cell Proliferation, and Reduces Neointima Formation After Balloon Injury in Rats

Influence of Folate on Arterial Permeability and Stiffness in the Absence or Presence of Hyperhomocysteinemia

Vascular Responses to 1-Adrenergic Receptors in Small Rat Mesenteric Arteries Depend on Mitochondrial Reactive Oxygen Species

Angiotensin II Attenuates Endothelium-Dependent Responses in the Cerebral Microcirculation Through Nox-2–Derived Radicals

Increased Serum Cadmium and Strontium Levels in Young Smokers: Effects on Arterial Endothelial Cell Gene Transcription

Cardiac and Vascular Hypertrophy in Fabry Disease: Evidence for a New Mechanism Independent of Blood Pressure and Glycosphingolipid Deposition

Effect of Rosiglitazone Treatment on Plaque Inflammation and Collagen Content in Nondiabetic Patients: Data From a Randomized Placebo-Controlled Trial

Atherosclerosis and Lipoproteins

Destabilizing Role of Cathepsin S in Murine Atherosclerotic Plaques

Enhanced T-Cell Expression of RANK Ligand in Acute Coronary Syndrome: Possible Role in Plaque Destabilization

Adoptive Transfer of CD4+ T Cells Reactive to Modified Low-Density Lipoprotein Aggravates Atherosclerosis

Comparison of Circulating Adiponectin and Proinflammatory Markers Regarding Their Association With Metabolic Syndrome in Japanese Men

Persistent High Levels of Plasma Oxidized Low-Density Lipoprotein After Acute Myocardial Infarction Predict Stent Restenosis

Effect of Inhibiting Cholesteryl Ester Transfer Protein on the Kinetics of High-Density Lipoprotein Cholesteryl Ester Transport in Plasma: In Vivo Studies in Rabbits

Lipoprotein Lipase Bound to Apolipoprotein B Lipoproteins Accelerates Clearance of Postprandial Lipoproteins in Humans

Decreased High-Density Lipoprotein (HDL) Particle Size, Preß-, and Large HDL Subspecies Concentration in Finnish Low-HDL Families: Relationship With Intima-Media Thickness

A Possible Association Between Coronary Plaque Instability and Complex Plaques in Abdominal Aorta

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E–/– Mice

Eplerenone With Valsartan Effectively Reduces Atherosclerotic Lesion by Attenuation of Oxidative Stress and Inflammation

Peroxisome Proliferator-Activated Receptor-,-Agonist Improves Insulin Sensitivity and Prevents Loss of Left Ventricular Function in Obese Dyslipidemic Mice

Macrophage ATP-Binding Cassette Transporter A1 Overexpression Inhibits Atherosclerotic Lesion Progression in Low-Density Lipoprotein Receptor Knockout Mice

Effect of Modified C-Reactive Protein on Complement Activation: A Possible Complement Regulatory Role of Modified or Monomeric C-Reactive Protein in Atherosclerotic Lesions

Thrombosis

Thrombomodulin Gene Polymorphisms and Haplotypes and the Risk of Cardiovascular Events: A Prospective Follow-Up Study

Plasminogen Activator Inhibitor-1 Gene: Selection of Tagging Single Nucleotide Polymorphisms and Association With Coronary Heart Disease

Letters to the Editor

Optimal Treatments for the Metabolic Syndrome

Oxidized LDL and the Metabolic Syndrome

In Response:

Corrections

Correction

Spotlight

Proangiogenic Effects of Protease-Activated Receptor 2 Are Tumor Necrosis Factor- ${alpha}$ and Consecutively Tie2 Dependent

Differential Healing Activities of CD34⁺ and CD14⁺ Endothelial Cell Progenitors

Endothelial NO Synthase Deficiency Promotes Smooth Muscle Progenitor Cells in Association With Upregulation of Stromal Cell-Derived Factor-1 ${alpha}$ in a Mouse Model of Carotid Artery Ligation

PKC ${delta}$ Is Necessary for Smad3 Expression and Transforming Growth Factor ß–Induced Fibronectin Synthesis in Vascular Smooth Muscle Cells

PPAR ${gamma}$ Gene Transfer Sustains Apoptosis, Inhibits Vascular Smooth Muscle Cell Proliferation, and Reduces Neointima Formation After Balloon Injury in Rats

Vascular Responses to ${alpha}$ ₁-Adrenergic Receptors in Small Rat Mesenteric Arteries Depend on Mitochondrial Reactive Oxygen Species

Adoptive Transfer of CD4⁺ T Cells Reactive to Modified Low-Density Lipoprotein Aggravates Atherosclerosis

Glucose-6-Phosphate Dehydrogenase Deficiency Decreases Vascular Superoxide and Atherosclerotic Lesions in Apolipoprotein E^–/– Mice

Peroxisome Proliferator-Activated Receptor- ${alpha}$ , ${gamma}$ -Agonist Improves Insulin Sensitivity and Prevents Loss of Left Ventricular Function in Obese Dyslipidemic Mice