Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (24 [11])

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Volume 24, Issue 11; November 1, 2004

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

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	Editorials
	Endothelial Progenitor Cells at Work: Not Mature Yet, but Already Stress-Resistant Lothar Rössig, Carmen Urbich, and Stefanie Dimmeler Arterioscler Thromb Vasc Biol. 2004;24:1977-1979, doi:10.1161/01.ATV.0000146815.54702.75. Full Text \| PDF
	Special Article
	Aspirin and Clopidogrel: Efficacy, Safety, and the Issue of Drug Resistance Marco Cattaneo Arterioscler Thromb Vasc Biol. 2004;24:1980-1987; published online before print September 23 2004, doi:10.1161/01.ATV.0000145980.39477.a9. Abstract \| Full Text \| PDF Aspirin and clopidogrel display good antithrombotic activity. For investigational purposes, aspirin and clopidogrel resistance should be evaluated in compliant patients by studying the effect of each drug on its specific target. They should not be looked for in the clinical setting yet, because definite demonstration of association with clinical events is lacking.
	Brief Reviews
	Reactive Oxygen Species: Players in the Platelet Game Florian Krötz, Hae-Young Sohn, and Ulrich Pohl Arterioscler Thromb Vasc Biol. 2004;24:1988-1996; published online before print September 16 2004, doi:10.1161/01.ATV.0000145574.90840.7d. Abstract \| Full Text \| PDF Platelets participate not only in thrombus formation but also in the regulation of vessel tone, the development of atherosclerosis, angiogenesis, and in neointima formation after vessel wall injury. It is not surprising, therefore, that the platelet activation cascade is tightly regulated. In addition to already well-defined platelet regulatory factors, such as nitric oxide (NO), prostacyclin (PGI2), and adenosine, reactive oxygen species (ROS) participate in the regulation of platelet activation. This review discusses the potential cellular and enzymatic sources of ROS in platelets, their molecular mechanisms of action in platelet activation, and summarizes in vitro and in vivo evidence for their physiological and potential therapeutic relevance.
	Chemokines: Key Regulators of Mononuclear Cell Recruitment in Atherosclerotic Vascular Disease Christian Weber, Andreas Schober, and Alma Zernecke Arterioscler Thromb Vasc Biol. 2004;24:1997-2008; published online before print August 19 2004, doi:10.1161/01.ATV.0000142812.03840.6f. Abstract \| Full Text \| PDF The complex role of chemokines in the recruitment of mononuclear cells to vascular lesions strongly suggests their specialization and cooperation in the atherosclerotic disease process. This review highlights recent insights into the function of chemokines in mediating distinct steps during the recruitment of monocytes and T cells to native atherosclerotic and neointimal lesions.
	Angiotensin II–Induced Insulin Resistance and Protein Tyrosine Phosphatases Mario B. Marrero, David Fulton, David Stepp, and David M. Stern Arterioscler Thromb Vasc Biol. 2004;24:2009-2013; published online before print July 22 2004, doi:10.1161/01.ATV.0000140059.04717.f3. Abstract \| Full Text \| PDF Although the importance of protein tyrosine phosphorylation by tyrosine kinases in mitogenic signaling is well-accepted, recent studies also suggest that tyrosine dephosphorylation by protein tyrosine phosphatases (PTPases) play an equally important role. In this review, we discuss the hypothesis that the protein tyrosine phosphatase (PTPase), PTP-1B, plays a central role in Ang II-induced insulin resistance by inhibiting activation of the insulin receptor.
	Id Family of Transcription Factors and Vascular Lesion Formation Scott Forrest and Coleen McNamara Arterioscler Thromb Vasc Biol. 2004;24:2014-2020; published online before print September 2 2004, doi:10.1161/01.ATV.0000143932.03151.ad. Abstract \| Full Text \| PDF The Id family of helix-loop-helix transcription factors has recently been implicated as regulators of growth and phenotypic modulation in VSMC and in the vascular response to injury. We summarize what is known about the functional role of Id proteins in controlling cellular growth and differentiation and vascular lesion formation.
	Vascular Biology
	Human Endothelial Progenitor Cells Tolerate Oxidative Stress Due to Intrinsically High Expression of Manganese Superoxide Dismutase Tongrong He, Timothy E. Peterson, Ekhson L. Holmuhamedov, Andre Terzic, Noel M. Caplice, Larry W. Oberley, and Zvonimir S. Katusic Arterioscler Thromb Vasc Biol. 2004;24:2021-2027; published online before print August 19 2004, doi:10.1161/01.ATV.0000142810.27849.8f. Abstract \| Full Text \| PDF \| Data Supplement We provide evidence that human endothelial progenitor cells (EPCs) are resistant to oxidative stress imposed by induced concentration of superoxide anions. Analysis of this phenomenon demonstrated that high intrinsic expression of manganese superoxide dismutase in EPCs is a critical mechanism underlying EPCs resistance to oxidative stress.
	Hypochlorous Acid Impairs Endothelium-Derived Nitric Oxide Bioactivity Through a Superoxide-Dependent Mechanism Roland Stocker, Annong Huang, Erin Jeranian, Jing Yun Hou, Tina T. Wu, Shane R. Thomas, and John F. Keaney, Jr Arterioscler Thromb Vasc Biol. 2004;24:2028-2033; published online before print August 26 2004, doi:10.1161/01.ATV.0000143388.20994.fa. Abstract \| Full Text \| PDF \| Data Supplement We found that hypochlorous acid (HOCl), the principal product of myleoperoxidase, produces impairment of endothelial NO bioactivity by reducing endothelial nitric oxide synthase dimer stability. This effect of HOCl was superoxide-dependent as it was inhibited by superoxide dismutase. Thus HOCl targets endothelial nitric oxide synthase in a superoxide-dependent manner.
	Hypercholesterolemia Impairs Transduction of Vasodilator Signals Derived From Ischemic Myocardium: Myocardium-Microvessel Cross-Talk Kouichi Sato, Tatsuya Komaru, Hiroki Shioiri, Satoru Takeda, Katsuaki Takahashi, Hiroshi Kanatsuka, Masaharu Nakayama, and Kunio Shirato Arterioscler Thromb Vasc Biol. 2004;24:2034-2039; published online before print August 26 2004, doi:10.1161/01.ATV.0000143387.58166.c0. Abstract \| Full Text \| PDF We evaluated the cross-talk between the coronary microvessels and the ischemic myocardium by using a novel bioassay method. We elucidated that hypercholesterolemia impairs the transduction of vasodilator signals derived from the ischemic myocardium in the coronary microvascular wall. The impaired cross-talk may underlie the susceptibility to ischemic insults.
	Hypoxia Increases LDL Oxidation and Expression of 15-Lipoxygenase-2 in Human Macrophages Ellen Knutsen Rydberg, Alexandra Krettek, Christina Ullström, Karin Ekström, Per-Arne Svensson, Lena M.S. Carlsson, Ann-Cathrine Jönsson-Rylander, Göran I. Hansson, William McPheat, Olov Wiklund, Bertil G. Ohlsson, and Lillemor Mattsson Hultén Arterioscler Thromb Vasc Biol. 2004;24:2040-2045; published online before print September 9 2004, doi:10.1161/01.ATV.0000144951.08072.0b. Abstract \| Full Text \| PDF \| Data Supplement Macrophage-mediated low-density lipoprotein oxidation and hypoxia are mechanisms involved in atherogenesis. Compared with normoxic macrophages, hypoxic-treated cells increased low-density lipoprotein oxidation and the protein expression as well as the activity of 15-lipoxygenase-2 (15-LOX-2). 15-LOX-2 was also identified in human carotid plaques. This suggests that 15-LOX-2 may be involved in atherogenesis.
	Monitoring the Cellular Effects of HMG-CoA Reductase Inhibitors In Vitro and Ex Vivo Iwona Cicha, Nicole Schneiderhan-Marra, Atilla Yilmaz, Christoph D. Garlichs, and Margarete Goppelt-Struebe Arterioscler Thromb Vasc Biol. 2004;24:2046-2050; published online before print September 23 2004, doi:10.1161/01.ATV.0000145943.19099.a3. Abstract \| Full Text \| PDF \| Data Supplement The purpose of this study was to directly monitor statin effects on Rho proteins. Using 2D electrophoresis, a significant shift toward nonisoprenylated RhoA was detected in fibroblasts and mononuclear cells treated with statins in vitro and in vivo. Thus, 2D electrophoresis is a sensitive method allowing monitoring the direct effects of statins.
	Statin Inhibition of Fc Receptor–Mediated Phagocytosis by Macrophages Is Modulated by Cell Activation and Cholesterol J.D. Loike, D.Y. Shabtai, R. Neuhut, S. Malitzky, E. Lu, J. Husemann, I.J. Goldberg, and S.C. Silverstein Arterioscler Thromb Vasc Biol. 2004;24:2051-2056; published online before print September 2 2004, doi:10.1161/01.ATV.0000143858.15909.29. Abstract \| Full Text \| PDF An inflammatory response to altered lipoproteins that accumulate in the arterial wall is a major component of pathogenesis of atherosclerosis. Statins reduce plasma levels of low-density lipoprotein and are effective treatments for atherosclerosis. It is hypothesized that they also modulate inflammation. The aim of this study was to examine whether lovastatin inhibits macrophage inflammatory processes and clarify its mechanism of action.
	Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts Noritaka Koga, Jun-ichi Suzuki, Hisanori Kosuge, Go Haraguchi, Yasuyuki Onai, Hideki Futamatsu, Yasuhiro Maejima, Ryo Gotoh, Hitoshi Saiki, Fumihiko Tsushima, Miyuki Azuma, and Mitsuaki Isobe Arterioscler Thromb Vasc Biol. 2004;24:2057-2062; published online before print September 16 2004, doi:10.1161/01.ATV.0000145015.23656.e4. Abstract \| Full Text \| PDF \| Data Supplement Programmed death 1 (PD-1) is involved in the negative regulation of immune responses. We evaluated the role of PD-ligand 1 (PD-L1) in graft arterial disease (GAD) of cardiac allografts. PD-L1 was expressed in smooth muscle cells of the thickened intima, and anti-PD-L1 monoclonal antibody enhanced the progression of GAD. In vitro, sensitized splenocytes increased smooth muscle cell proliferation, and anti-PD-L1 monoclonal antibody increased this proliferation. The PD-L1 pathway regulates GAD. Thus, control of this interaction is a promising strategy for suppression of GAD.
	E-Selectin Blockade Decreases Adventitial Inflammation and Attenuates Intimal Hyperplasia in Rat Carotid Arteries After Balloon Injury Ryo Gotoh, Jun-ichi Suzuki, Hisanori Kosuge, Tsunekazu Kakuta, Shinji Sakamoto, Masayuki Yoshida, and Mitsuaki Isobe Arterioscler Thromb Vasc Biol. 2004;24:2063-2068; published online before print September 23 2004, doi:10.1161/01.ATV.0000145942.31404.20. Abstract \| Full Text \| PDF E-selectin facilitates adherence of leukocytes at the site of inflammation. We studied the action of E-selectin in vascular injury with a rat model of carotid artery injury. The results suggested that E-selectin regulates adventitial inflammation through leukocyte adhesion and contributes to the process of intimal hyperplasia after balloon injury.
	Transcription Factor CHF1/Hey2 Regulates Neointimal Formation In Vivo and Vascular Smooth Muscle Proliferation and Migration In Vitro Yasuhiko Sakata, Fan Xiang, Zhiping Chen, Yoriko Kiriyama, Caramai N. Kamei, Daniel I. Simon, and Michael T. Chin Arterioscler Thromb Vasc Biol. 2004;24:2069-2074; published online before print September 2 2004, doi:10.1161/01.ATV.0000143936.77094.a4. Abstract \| Full Text \| PDF \| Data Supplement CHF1/Hey2-deficient mice show decreased neointima formation after vascular injury. VSMCs from these mice show decreased proliferation, migration, cytoskeletal rearrangement, activation of the small GTPase Rac1, and expression of the Rac guanine exchange factor (GEF), Sos1. CHF1/Hey2 is an important regulator of vascular remodeling and growth factor responsiveness in VSMCs.
	Carvedilol Inhibits Tumor Necrosis Factor- ${alpha}$ –Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells Jaw-Wen Chen, Feng-Yen Lin, Yung-Hsiang Chen, Tao-Cheng Wu, Yuh-Lien Chen, and Shing-Jong Lin Arterioscler Thromb Vasc Biol. 2004;24:2075-2081; published online before print September 16 2004, doi:10.1161/01.ATV.0000145016.69181.fa. Abstract \| Full Text \| PDF \| Data Supplement Carvedilol, a ß- and {alpha}-adrenoceptor antagonist, could prevent endothelial adhesiveness to human mononuclear cells by inhibiting intracellular reactive oxygen species production, redox-sensitive transcription pathways, and vascular cell adhesion molecule-1 and E-selectin expression in TNF-{alpha}-stimulated human aortic endothelial cells, suggesting its potential role in clinical atherosclerosis disease.
	Nitric Oxide–Releasing Aspirin Derivative, NCX 4016, Promotes Reparative Angiogenesis and Prevents Apoptosis and Oxidative Stress in a Mouse Model of Peripheral Ischemia Costanza Emanueli, Sophie Van Linthout, Maria Bonaria Salis, Angela Monopoli, Piero Del Soldato, Ennio Ongini, and Paolo Madeddu Arterioscler Thromb Vasc Biol. 2004;24:2082-2087; published online before print September 2 2004, doi:10.1161/01.ATV.0000144030.39087.3b. Abstract \| Full Text \| PDF We evaluated whether aspirin coupled to an NO-releasing moiety (NCX 4016) exerts vascular protection. Mice given regular chow, NCX 4016, or aspirin underwent operative limb ischemia. Compared with controls, NCX 4016 improved hemodynamic recovery, stimulated angiogenesis, reduced apoptosis and oxidative stress, and increased nitrite levels in circulation and ischemic muscles. This new drug could alleviate the consequences of arterial occlusion.
	Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells Michael B. Dancu, Danielle E. Berardi, John P. Vanden Heuvel, and John M. Tarbell Arterioscler Thromb Vasc Biol. 2004;24:2088-2094; published online before print September 2 2004, doi:10.1161/01.ATV.0000143855.85343.0e. Abstract \| Full Text \| PDF \| Data Supplement Asynchronous hemodynamic circumferential strain and wall shear stress occur in pathologic regions. Vasoactive gene expression of eNOS, ET-1, and COX-2 in endothelial cells exhibited a pathologic profile during asynchronous (SPA=-180{degrees}) hemodynamics. Asynchronous mechanical force patterns (SPA=-180{degrees}) can elicit proatherogenic responses in endothelial cells, indicating a novel mechanism that induces cardiovascular pathology.
	Altered PDGF-BB–Induced p38 MAP Kinase Activation in Diabetic Vascular Smooth Muscle Cells: Roles of Protein Kinase C- ${delta}$ Hiroshi Yamaguchi, Masahiko Igarashi, Akihiko Hirata, Naoko Sugae, Hiromi Tsuchiya, Yumi Jimbu, Makoto Tominaga, and Takeo Kato Arterioscler Thromb Vasc Biol. 2004;24:2095-2101; published online before print September 2 2004, doi:10.1161/01.ATV.0000144009.35400.65. Abstract \| Full Text \| PDF \| Data Supplement We investigated the regulation of p38 MAP kinase (MAPK) by platelet-derived growth factor (PDGF)-BB in diabetic rat vascular smooth muscle cells. PDGF-BB phosphorylated p38 via protein kinase C-{delta} and the subsequent MAPK kinase (MKK) 3/6, leading to cell growth regulation and the progression of a chronic inflammatory process in diabetes.
	Sonic Hedgehog Induces Arteriogenesis in Diabetic Vasa Nervorum and Restores Function in Diabetic Neuropathy Kengo F. Kusano, Karen L. Allendoerfer, William Munger, Roberto Pola, Marta Bosch-Marce, Rudolf Kirchmair, Young-sup Yoon, Cynthia Curry, Marcy Silver, Marianne Kearney, Takayuki Asahara, and Douglas W. Losordo Arterioscler Thromb Vasc Biol. 2004;24:2102-2107; published online before print September 9 2004, doi:10.1161/01.ATV.0000144813.44650.75. Abstract \| Full Text \| PDF \| Data Supplement We administered Sonic Hedgehog (SHh) in a rat model of diabetic neuropathy (DN) and found that it replenishes the depleted vasa nervora that are depleted by diabetes and restores nerve function. Notably, the neurovasculature induced by SHh is composed of significantly greater numbers of arterioles than in VEGF-treated rats.
	ß3-Integrin Regulates Vascular Endothelial Growth Factor-A–Dependent Permeability Stephen D. Robinson, Louise E. Reynolds, Lorenza Wyder, Daniel J. Hicklin, and Kairbaan M. Hodivala-Dilke Arterioscler Thromb Vasc Biol. 2004;24:2108-2114; published online before print September 2 2004, doi:10.1161/01.ATV.0000143857.27408.de. Abstract \| Full Text \| PDF \| Data Supplement Blood vessels in ß3-integrin-deficient mice are histologically normal and functionally intact. However, they express elevated levels of Flk-1 and are more sensitive than wild-type blood vessels to VEGF-A-induced permeability, but not to permeability induced by acute inflammatory agents.
	Atherosclerosis and Lipoproteins
	Bone Marrow–Derived Monocyte Chemoattractant Protein-1 Receptor CCR2 Is Critical in Angiotensin II–Induced Acceleration of Atherosclerosis and Aneurysm Formation in Hypercholesterolemic Mice Minako Ishibashi, Kensuke Egashira, Qingwei Zhao, Ken-ichi Hiasa, Kisho Ohtani, Yoshiko Ihara, Israel F. Charo, Shinobu Kura, Teruhisa Tsuzuki, Akira Takeshita, and Kenji Sunagawa Arterioscler Thromb Vasc Biol. 2004;24:e174-e178; published online before print August 26 2004, doi:10.1161/01.ATV.0000143384.69170.2d. Abstract \| Full Text \| PDF We determined the role of leukocyte-derived CCR2 (the receptor for monocyte chemoattractant protein-1) in the angiotensin II (Ang II)-induced acceleration of atherosclerotic process. We show that Ang II-induced atherosclerotic process was blunted in hypercholesterolemic apoE-/- mice with deficiency of leukocyte-derived CCR2. These data suggest that leukocyte-derived CCR2 is critical in Ang II-induced atherosclerosis.
	Gender Differences in Experimental Aortic Aneurysm Formation Gorav Ailawadi, Jonathan L. Eliason, Karen J. Roelofs, Indranil Sinha, Kevin K. Hannawa, Eric P. Kaldjian, Guanyi Lu, Peter K. Henke, James C. Stanley, Stephen J. Weiss, Robert W. Thompson, and Gilbert R. Upchurch, Jr Arterioscler Thromb Vasc Biol. 2004;24:2116-2122; published online before print August 26 2004, doi:10.1161/01.ATV.0000143386.26399.84. Abstract \| Full Text \| PDF Male rats demonstrated larger aortic dilatation than females after elastase exposure. Next, female rat aortas transplanted into males after elastase exposure lost aneurysm resistance. Finally, estradiol inhibited experimental aneurysm formation. Aneurysms correlated with increased macrophage and MMP-9 infiltration. Gender-related differences in aneurysms may be estrogen-mediated via reductions in macrophage MMP-9.
	Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity Susan M. Lessner, Deborah E. Martinson, and Zorina S. Galis Arterioscler Thromb Vasc Biol. 2004;24:2123-2129; published online before print August 12 2004, doi:10.1161/01.ATV.0000141840.27300.fd. Abstract \| Full Text \| PDF \| Data Supplement MMP-9 deficiency impairs the compensatory outward remodeling during carotid lesion development in an apoE-/- mouse model of atherosclerosis without significantly altering neointimal macrophage accumulation. Arterial expansion becomes relatively insensitive to lesion macrophage content in the absence of MMP-9.
	Enzymatic Modification of Low-Density Lipoprotein in the Arterial Wall: A New Role for Plasmin and Matrix Metalloproteinases in Atherogenesis Michael Torzewski, Prapat Suriyaphol, Kerstin Paprotka, Lena Spath, Viola Ochsenhirt, Andrea Schmitt, Shan-Rui Han, Matthias Husmann, Verena B. Gerl, Sucharit Bhakdi, and Karl J. Lackner Arterioscler Thromb Vasc Biol. 2004;24:2130-2136; published online before print September 2 2004, doi:10.1161/01.ATV.0000144016.85221.66. Abstract \| Full Text \| PDF \| Data Supplement Plasmin and matrix metalloproteinases are present in early human atherosclerotic lesions. Both can synergize with cholesterylesterase to transform low-density lipoprotein into a molecule that binds C-reactive protein, activates complement, and induces macrophage foam cell formation. These processes may serve to remove stranded low-density lipoprotein from tissues, but excessive immune activation could trigger atherogenesis.
	Inhibition of Tumor Necrosis Factor- ${alpha}$ Reduces Atherosclerosis in Apolipoprotein E Knockout Mice Lena Brånén, Lars Hovgaard, Mihaela Nitulescu, Eva Bengtsson, Jan Nilsson, and Stefan Jovinge Arterioscler Thromb Vasc Biol. 2004;24:2137-2142; published online before print September 2 2004, doi:10.1161/01.ATV.0000143933.20616.1b. Abstract \| Full Text \| PDF \| Data Supplement Atherosclerosis is an inflammatory disease. We have shown that deficiency in TNF-{alpha} reduces atherosclerosis. This implies that TNF antagonizers are interesting candidates for testing in clinical studies of atherosclerosis prevention.
	Angiotensin II Amplifies Macrophage-Driven Atherosclerosis Ayabe Nobuhiko, Eisuke Suganuma, Vladimir R. Babaev, Agnes Fogo, Larry L. Swift, MacRae F. Linton, Sergio Fazio, Iekuni Ichikawa, and Valentina Kon Arterioscler Thromb Vasc Biol. 2004;24:2143-2148; published online before print September 16 2004, doi:10.1161/01.ATV.0000145607.03879.e0. Abstract \| Full Text \| PDF Wild-type mice reconstituted with bone marrow from apolipoprotein E-deficient mice (apoE-/--> apoE+/+) exposed to angiotensin II (AII) had 3-times greater atherosclerosis than mice reconstituted with wild-type marrow (apoE+/+-> apoE+/+). AII increased macrophage-positive areas and elastin fragmentation in both groups. AII promotes macrophage migration to initiate atherosclerosis and elastin breaks that expands atherosclerosis.
	Differential Gene Expression of Blood-Derived Cell Lines in Familial Combined Hyperlipidemia Fulvio Morello, Tjerk W.A. de Bruin, Jerome I. Rotter, Richard E. Pratt, Carla J.H. van der Kallen, Gary A. Hladik, Victor J. Dzau, Choong-Chin Liew, and Yii-Der I. Chen Arterioscler Thromb Vasc Biol. 2004;24:2149-2154; published online before print September 23 2004, doi:10.1161/01.ATV.0000145978.70872.63. Abstract \| Full Text \| PDF \| Data Supplement We studied the transcriptional profile of FCHL-derived lymphoblast cell lines using microarrays. Of note was the differential expression of EGR-1, several lipid metabolism-related genes, and many novel genes.
	Cyclosporin A Traps ABCA1 at the Plasma Membrane and Inhibits ABCA1-Mediated Lipid Efflux to Apolipoprotein A-I Wilfried Le Goff, Dao-Quan Peng, Megan Settle, Gregory Brubaker, Richard E. Morton, and Jonathan D. Smith Arterioscler Thromb Vasc Biol. 2004;24:2155-2161; published online before print September 9 2004, doi:10.1161/01.ATV.0000144811.94581.52. Abstract \| Full Text \| PDF Cyclosporin A inhibited ABCA1-mediated lipid efflux to apoAI. This inhibition was associated with increased plasma membrane ABCA1, which was defective in its ability to take-up exogenous apoAI. Administration of cyclosporin A to mice led to a 33% decrease in plasma HDL, supporting the physiological relevance of these findings.
	Arterial Permeability and Efflux of Apolipoprotein B–Containing Lipoproteins Assessed by In Situ Perfusion and Three-Dimensional Quantitative Confocal Microscopy Spencer D. Proctor, Donna F. Vine, and John C.L. Mamo Arterioscler Thromb Vasc Biol. 2004;24:2162-2167; published online before print September 2 2004, doi:10.1161/01.ATV.0000143859.75035.5a. Abstract \| Full Text \| PDF \| Data Supplement Results indicate that although LDL particles have a higher rate of arterial delivery, they efflux more readily from vessels compared with the larger chylomicron remnants. Findings highlight that lipoproteins permeate through arterial tissue differently and may be dependent on the phenotype and potential interactions with extracellular matrix components.
	Genetic Influence on Inflammation Variables in the Elderly Moniek P.M. de Maat, Else Marie Bladbjerg, Jacob von Bornemann Hjelmborg, Lise Bathum, Jørgen Jespersen, and Kaare Christensen Arterioscler Thromb Vasc Biol. 2004;24:2168-2173; published online before print September 2 2004, doi:10.1161/01.ATV.0000143856.01669.e7. Abstract \| Full Text \| PDF Inflammation variables have been identified as risk factors for cardiovascular disease. The heritability of inflammation variables at older ages was considered in a twin study on 129 monozygotic and 153 dizygotic same-sex twin pairs aged 73 to 94 years. Genetic factors accounted for 20% to 55% of the variation in levels of the inflammation variables studied.
	Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide Pirkko J. Pussinen, Tiina Vilkuna-Rautiainen, Georg Alfthan, Timo Palosuo, Matti Jauhiainen, Jouko Sundvall, Marja Vesanen, Kimmo Mattila, and Sirkka Asikainen Arterioscler Thromb Vasc Biol. 2004;24:2174-2180; published online before print September 23 2004, doi:10.1161/01.ATV.0000145979.82184.9f. Abstract \| Full Text \| PDF The effect of periodontal treatment on proatherogenic properties of LDL and, thus, macrophage activation was investigated. LDL was isolated and LDL-associated proatherogenic parameters were determined from 30 systemically healthy patients with periodontitis. Our results suggest that the infected/inflamed area in periodontitis is associated with macrophage activation via increased serum LPS.
	High-Density Lipoprotein Subpopulation Profile and Coronary Heart Disease Prevalence in Male Participants of the Framingham Offspring Study Bela F. Asztalos, L. Adrienne Cupples, Serkalem Demissie, Katalin V. Horvath, Caitlin E. Cox, Marcelo C. Batista, and Ernst J. Schaefer Arterioscler Thromb Vasc Biol. 2004;24:2181-2187; published online before print September 23 2004, doi:10.1161/01.ATV.0000146325.93749.a8. Abstract \| Full Text \| PDF Specific HDL subpopulations were positively correlated whereas others were inversely correlated with coronary heart disease (CHD) prevalence in male subjects in the Framingham Offspring Study, indicating that the various HDL particles might have different roles in the cause of CHD. Moreover, specific HDL particles had stronger association with CHD prevalence than either HDL cholesterol or LDL cholesterol levels.
	ATP-Binding Cassette Transporter G8 Gene As a Determinant of Apolipoprotein B-100 Kinetics in Overweight Men D.C. Chan, G.F. Watts, P.H.R. Barrett, A.J. Whitfield, and F.M. van Bockxmeer Arterioscler Thromb Vasc Biol. 2004;24:2188-2191; published online before print August 26 2004, doi:10.1161/01.ATV.0000143532.93729.d6. Abstract \| Full Text \| PDF This study demonstrates that subjects carrying the ABCG8 400K allele had lower production rate of VLDL-apoB and higher VLDL to LDL-apoB conversion. The production rate and fractional catabolic rate of LDL-apoB were also higher with 400K allele. During multiple regression analysis, ABCG8 genotype was an independent determinant of VLDL-apoB production rate.
	Common Promoter C516T Polymorphism in the ApoB Gene Is an Independent Predictor of Carotid Atherosclerotic Disease in Subjects Presenting a Broad Range of Plasma Cholesterol Levels Andrei C. Sposito, Sophie Gonbert, Gerard Turpin, M. John Chapman, and Joëlle Thillet Arterioscler Thromb Vasc Biol. 2004;24:2192-2195; published online before print September 9 2004, doi:10.1161/01.ATV.0000144810.10164.50. Abstract \| Full Text \| PDF The common -516C/T polymorphism in the apolipoprotein B (apoB) gene increases the transcription rate of apoB, resulting in elevated circulating levels of low-density lipoprotein. A C to T change at position -516 in the apoB gene is independently associated with the presence of carotid atherosclerotic disease. Identification of this polymorphism may contribute to estimation of global cardiovascular risk.
	Thrombosis
	Inhibition of Endogenous Leptin Protects Mice From Arterial and Venous Thrombosis Stavros Konstantinides, Katrin Schäfer, Jaap G. Neels, Claudia Dellas, and David J. Loskutoff Arterioscler Thromb Vasc Biol. 2004;24:2196-2201; published online before print September 30 2004, doi:10.1161/01.ATV.0000146531.79402.9a. Abstract \| Full Text \| PDF Human obesity is associated with an increased risk for thrombosis and with elevated leptin. We show that inhibiting circulating leptin protects wild-type mice from arterial and venous thrombosis in vivo. Leptin inhibition may represent a new strategy for reducing the risk of cardiovascular disease in obese hyperleptinemic individuals.
	Letters to the Editor
	The Antiinflammatory Effects of Purple Grape Juice Consumption in Subjects with Stable Coronary Artery Disease Anne R. Albers, Sonia Varghese, Olga Vitseva, Joseph A. Vita, and Jane E. Freedman Arterioscler Thromb Vasc Biol. 2004;24:e179-e180, doi:10.1161/01.ATV.0000143479.97844.af. Full Text \| PDF
	Measurement of Platelet Collagen Receptor Density in Human Subjects Frederick F. Samaha, Christopher Hibbard, Jay Sacks, Hong Chen, Michael A. Varello, Thomas George, and Mark L. Kahn Arterioscler Thromb Vasc Biol. 2004;24:e181-e182, doi:10.1161/01.ATV.0000144809.49724.71. Full Text \| PDF
	Gender Dependent Association of Thrombospondin-4 A387P Polymorphism With Myocardial Infarction Jianxun Cui, Edward Randell, James Renouf, Guang Sun, Fei-Yu Han, Banfield Younghusband, and Ya-Gang Xie Arterioscler Thromb Vasc Biol. 2004;24:e183-e184, doi:10.1161/01.ATV.0000147304.67100.ee. Full Text \| PDF
	Mouse Models of Vein Grafts Qingbo Xu, Masataka Sata, and Ryozo Nagai Arterioscler Thromb Vasc Biol. 2004;24:e185-e187, doi:10.1161/01.ATV.0000142809.94325.af. Full Text \| PDF
	Noninvasive Phenotypes of Atherosclerosis J. David Spence, Robert A. Hegele, Teri Manolio, Eric Boerwinkle, Christopher O’Donnell, and Alexander F. Wilson Arterioscler Thromb Vasc Biol. 2004;24:e188-e189, doi:10.1161/01.ATV.0000146160.22637.33. Full Text \| PDF
	Estrogens, Progestins, and Atherosclerosis Michael R. Adams, J. Koudy Williams, Jay R. Kaplan, Kwang Kon Koh, and Ichiro Sakuma Arterioscler Thromb Vasc Biol. 2004;24:e190-e191, doi:10.1161/01.ATV.0000146176.62463.87. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 24, Issue 11; November 1, 2004

Editorials

Endothelial Progenitor Cells at Work: Not Mature Yet, but Already Stress-Resistant

Special Article

Aspirin and Clopidogrel: Efficacy, Safety, and the Issue of Drug Resistance

Brief Reviews

Reactive Oxygen Species: Players in the Platelet Game

Chemokines: Key Regulators of Mononuclear Cell Recruitment in Atherosclerotic Vascular Disease

Angiotensin II–Induced Insulin Resistance and Protein Tyrosine Phosphatases

Id Family of Transcription Factors and Vascular Lesion Formation

Vascular Biology

Human Endothelial Progenitor Cells Tolerate Oxidative Stress Due to Intrinsically High Expression of Manganese Superoxide Dismutase

Hypochlorous Acid Impairs Endothelium-Derived Nitric Oxide Bioactivity Through a Superoxide-Dependent Mechanism

Hypercholesterolemia Impairs Transduction of Vasodilator Signals Derived From Ischemic Myocardium: Myocardium-Microvessel Cross-Talk

Hypoxia Increases LDL Oxidation and Expression of 15-Lipoxygenase-2 in Human Macrophages

Monitoring the Cellular Effects of HMG-CoA Reductase Inhibitors In Vitro and Ex Vivo

Statin Inhibition of Fc Receptor–Mediated Phagocytosis by Macrophages Is Modulated by Cell Activation and Cholesterol

Blockade of the Interaction Between PD-1 and PD-L1 Accelerates Graft Arterial Disease in Cardiac Allografts

E-Selectin Blockade Decreases Adventitial Inflammation and Attenuates Intimal Hyperplasia in Rat Carotid Arteries After Balloon Injury

Transcription Factor CHF1/Hey2 Regulates Neointimal Formation In Vivo and Vascular Smooth Muscle Proliferation and Migration In Vitro

Carvedilol Inhibits Tumor Necrosis Factor-–Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells

Nitric Oxide–Releasing Aspirin Derivative, NCX 4016, Promotes Reparative Angiogenesis and Prevents Apoptosis and Oxidative Stress in a Mouse Model of Peripheral Ischemia

Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells

Altered PDGF-BB–Induced p38 MAP Kinase Activation in Diabetic Vascular Smooth Muscle Cells: Roles of Protein Kinase C-

Sonic Hedgehog Induces Arteriogenesis in Diabetic Vasa Nervorum and Restores Function in Diabetic Neuropathy

ß3-Integrin Regulates Vascular Endothelial Growth Factor-A–Dependent Permeability

Atherosclerosis and Lipoproteins

Bone Marrow–Derived Monocyte Chemoattractant Protein-1 Receptor CCR2 Is Critical in Angiotensin II–Induced Acceleration of Atherosclerosis and Aneurysm Formation in Hypercholesterolemic Mice

Gender Differences in Experimental Aortic Aneurysm Formation

Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity

Enzymatic Modification of Low-Density Lipoprotein in the Arterial Wall: A New Role for Plasmin and Matrix Metalloproteinases in Atherogenesis

Inhibition of Tumor Necrosis Factor- Reduces Atherosclerosis in Apolipoprotein E Knockout Mice

Angiotensin II Amplifies Macrophage-Driven Atherosclerosis

Differential Gene Expression of Blood-Derived Cell Lines in Familial Combined Hyperlipidemia

Cyclosporin A Traps ABCA1 at the Plasma Membrane and Inhibits ABCA1-Mediated Lipid Efflux to Apolipoprotein A-I

Arterial Permeability and Efflux of Apolipoprotein B–Containing Lipoproteins Assessed by In Situ Perfusion and Three-Dimensional Quantitative Confocal Microscopy

Genetic Influence on Inflammation Variables in the Elderly

Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide

High-Density Lipoprotein Subpopulation Profile and Coronary Heart Disease Prevalence in Male Participants of the Framingham Offspring Study

ATP-Binding Cassette Transporter G8 Gene As a Determinant of Apolipoprotein B-100 Kinetics in Overweight Men

Common Promoter C516T Polymorphism in the ApoB Gene Is an Independent Predictor of Carotid Atherosclerotic Disease in Subjects Presenting a Broad Range of Plasma Cholesterol Levels

Thrombosis

Inhibition of Endogenous Leptin Protects Mice From Arterial and Venous Thrombosis

Letters to the Editor

The Antiinflammatory Effects of Purple Grape Juice Consumption in Subjects with Stable Coronary Artery Disease

Measurement of Platelet Collagen Receptor Density in Human Subjects

Gender Dependent Association of Thrombospondin-4 A387P Polymorphism With Myocardial Infarction

Mouse Models of Vein Grafts

Noninvasive Phenotypes of Atherosclerosis

Estrogens, Progestins, and Atherosclerosis

Spotlight

Carvedilol Inhibits Tumor Necrosis Factor- ${alpha}$ –Induced Endothelial Transcription Factor Activation, Adhesion Molecule Expression, and Adhesiveness to Human Mononuclear Cells

Altered PDGF-BB–Induced p38 MAP Kinase Activation in Diabetic Vascular Smooth Muscle Cells: Roles of Protein Kinase C- ${delta}$

Inhibition of Tumor Necrosis Factor- ${alpha}$ Reduces Atherosclerosis in Apolipoprotein E Knockout Mice