Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [2])

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Volume 25, Issue 2; February 1, 2005

Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Corrections

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	Editorials
	Exercise and the Prothrombotic State: A Paradox of Cardiovascular Prevention or an Enhanced Prothrombotic State? Graham Thrall and Gregory Y.H. Lip Arterioscler Thromb Vasc Biol. 2005;25:265-266, doi:10.1161/01.ATV.0000154579.11213.da. Full Text \| PDF
	Apolipoprotein E and Atherosclerosis: Beyond Lipid Effect Jean Davignon Arterioscler Thromb Vasc Biol. 2005;25:267-269, doi:10.1161/01.ATV.0000154570.50696.2c. Full Text \| PDF
	Are Circulating CD133⁺ Cells Biomarkers of Vascular Disease? Gina Schatteman Arterioscler Thromb Vasc Biol. 2005;25:270-271, doi:10.1161/01.ATV.0000154484.58485.24. Full Text \| PDF
	Brief Reviews
	ATVB In Focus: Redox Mechanisms in Blood Vessels Kathy K. Griendling Arterioscler Thromb Vasc Biol. 2005;25:272-273, doi:10.1161/01.ATV.0000153515.72375.3b. Full Text \| PDF
	Redox Mechanisms in Blood Vessels Cornelius F.H. Mueller, Karine Laude, J. Scott McNally, and David G. Harrison Arterioscler Thromb Vasc Biol. 2005;25:274-278; published online before print October 28 2004, doi:10.1161/01.ATV.0000149143.04821.eb. Abstract \| Full Text \| PDF Reactive oxygen species have been implicated in the pathogenesis of virtually every stage of vascular lesion formation, hypertension, and other vascular diseases. Upcoming series of articles in Arteriosclerosis, Thrombosis, and Vascular Biology help elucidate how reactive oxygen species are produced by vascular cells and their role in vascular homeostasis.
	Quantification of Isoprostanes as Indices of Oxidant Stress and the Risk of Atherosclerosis in Humans Jason D. Morrow Arterioscler Thromb Vasc Biol. 2005;25:279-286; published online before print December 9 2004, doi:10.1161/01.ATV.0000152605.64964.c0. Abstract \| Full Text \| PDF Enhanced oxidant stress occurring either locally in the vessel wall or systemically is implicated in the pathogenesis of atherosclerosis in humans. Nonetheless, evidence that oxidant stress is increased in vivo in association with this disease and that it can be quantified in living human beings has been lacking. Recently, the development of methods to quantify the F2-isoprostanes (IsoPs) has allowed a facile and accurate assessment of oxidant stress in vivo. The purpose of this brief review is to discuss the usefulness of quantifying IsoPs as an index of oxidative injury in association with atherosclerosis.
	Statins and Blood Coagulation Anetta Undas, Kathleen E. Brummel-Ziedins, and Kenneth G. Mann Arterioscler Thromb Vasc Biol. 2005;25:287-294; published online before print November 29 2004, doi:10.1161/01.ATV.0000151647.14923.ec. Abstract \| Full Text \| PDF The HMG-CoA reductase inhibitors (statins) have been shown to exhibit several vascular protective effects, including antithrombotic properties, that are not related to changes in lipid profile. Treatment with statins can lead to a significant downregulation of the blood coagulation cascade, most probably as a result of decreased tissue factor expression, which leads to reduced thrombin generation.
	Vascular Biology
	Block of Inward Rectifying K⁺ Channels (K_IR) Inhibits Bradykinin-Induced Vasodilatation in Human Forearm Resistance Vasculature R. Dwivedi, S. Saha, P.J. Chowienczyk, and J.M. Ritter Arterioscler Thromb Vasc Biol. 2005;25:e7-e9; published online before print December 9 2004, doi:10.1161/01.ATV.0000152610.40086.31. Abstract \| Full Text \| PDF The possible involvement of inward-rectifying K+ channels (KIR) in the action of bradykinin was investigated by administering drugs via the brachial artery in healthy men. Barium selectively inhibited the forearm blood flow response to bradykinin, indicating that a component of this response is mediated by KIR.
	Granulocyte Colony-Stimulating Factor Mobilizes Functional Endothelial Progenitor Cells in Patients With Coronary Artery Disease Tiffany M. Powell, Jonathan D. Paul, Jonathan M. Hill, Michael Thompson, Moshe Benjamin, Maria Rodrigo, J. Philip McCoy, Elizabeth J. Read, Hanh M. Khuu, Susan F. Leitman, Toren Finkel, and Richard O. Cannon, III Arterioscler Thromb Vasc Biol. 2005;25:296-301; published online before print November 29 2004, doi:10.1161/01.ATV.0000151690.43777.e4. Abstract \| Full Text \| PDF Endothelial progenitor cells (EPCs) are reduced in coronary artery disease. Granulocyte colony-stimulating factor (CSF) administered to patients increased: (1) CD133+/VEGFR-2+ cells consistent with EPC phenotype; (2) CD133+ cells coexpressing the chemokine receptor CXCR4, important for homing of EPCs to ischemic tissue; and (3) endothelial cell-forming clusters in culture. Whether EPCs mobilized into the circulation will be useful for the purpose of initiating vascular growth and myocyte repair in coronary artery disease patients must be tested in clinical trials.
	Mouse Strain–Specific Differences in Vascular Wall Gene Expression and Their Relationship to Vascular Disease Raymond Tabibiazar, Roger A. Wagner, Joshua M. Spin, Euan A. Ashley, Balasubramanian Narasimhan, Edward M. Rubin, Bradley Efron, Phil S. Tsao, Robert Tibshirani, and Thomas Quertermous Arterioscler Thromb Vasc Biol. 2005;25:302-308; published online before print November 18 2004, doi:10.1161/01.ATV.0000151372.86863.a5. Abstract \| Full Text \| PDF \| Data Supplement To gain insights into the molecular pathways that are differentially activated in strains of mice with varied susceptibility to atherosclerosis, we performed comprehensive transcriptional profiling of their vascular wall. Genes identified through these studies expand the repertoire of factors in disease-related signaling pathways and identify novel candidate genes in atherosclerosis.
	GATA-6 Regulates Genes Promoting Synthetic Functions in Vascular Smooth Muscle Cells John J. Lepore, Thomas P. Cappola, Patricia A. Mericko, Edward E. Morrisey, and Michael S. Parmacek Arterioscler Thromb Vasc Biol. 2005;25:309-314; published online before print December 9 2004, doi:10.1161/01.ATV.0000152725.76020.3c. Abstract \| Full Text \| PDF \| Data Supplement An unbiased microarray screen of genes regulated by GATA-6 in VSMCs identified multiple genes involved in cell-cell signaling and cell-matrix interactions. The endothelin-1 and the AT1a receptor genes were shown to be direct GATA-6 target genes. These data suggest that GATA-6 plays a role in promoting synthetic functions in VSMCs.
	Prostaglandin E Synthases in Zebrafish Barbara Pini, Tilo Grosser, John A. Lawson, Tom S. Price, Michael A. Pack, and Garret A. FitzGerald Arterioscler Thromb Vasc Biol. 2005;25:315-320; published online before print December 2 2004, doi:10.1161/01.ATV.0000152355.97808.10. Abstract \| Full Text \| PDF \| Data Supplement Mircosomal prostaglandin E synthase (mPGES)-1, located downstream of COX-2, may represent a novel antiinflammatory drug target. Zebrafish cytosolic (c) PGES-1 and COX-1 were coordinately expressed; mPGES-1 and COX-2 were expressed particularly in the vasculature. Zebrafish may afford a high throughput system for detection of novel PGES inhibitors.
	Cytochrome P4502C9-Derived Epoxyeicosatrienoic Acids Induce the Expression of Cyclooxygenase-2 in Endothelial Cells U. Ruth Michaelis, John R. Falck, Ronald Schmidt, Rudi Busse, and Ingrid Fleming Arterioscler Thromb Vasc Biol. 2005;25:321-326; published online before print November 29 2004, doi:10.1161/01.ATV.0000151648.58516.eb. Abstract \| Full Text \| PDF \| Data Supplement Overexpression of cytochrome P450 (CYP) 2C9 in endothelial cells increased cAMP levels, stimulated the cAMP-response element-binding protein, and enhanced cyclooxygenase-2 (COX-2) promoter activity, protein expression, and prostacyclin production. CYP2C9 overexpression stimulated endothelial tube formation, which was attenuated by the COX-2 inhibitor celecoxib. Thus, COX-2 contributes to CYP2C9-induced angiogenesis.
	Fluvastatin Prevents Vascular Hyperplasia by Inhibiting Phenotype Modulation and Proliferation Through Extracellular Signal-Regulated Kinase 1 and 2 and p38 Mitogen-Activated Protein Kinase Inactivation in Organ-Cultured Artery Kenichi Sakamoto, Takahisa Murata, Hiroko Chuma, Masatoshi Hori, and Hiroshi Ozaki Arterioscler Thromb Vasc Biol. 2005;25:327-333; published online before print December 9 2004, doi:10.1161/01.ATV.0000152611.50953.e2. Abstract \| Full Text \| PDF We examined the inhibitory mechanisms of fluvastatin on FBS-induced vascular hypertrophy assessed by organ-cultured artery. Results suggest that fluvastatin inhibits vascular smooth muscle phenotype modulation and proliferation by inhibiting the ERK1/2 and p38MAPK activities through depletion of mevalonate in smooth muscle cells, resulting in inhibiting vascular hyperplastic changes.
	Superoxide Dismutase Inhibits the Expression of Vascular Cell Adhesion Molecule-1 and Intracellular Cell Adhesion Molecule-1 Induced by Tumor Necrosis Factor- ${alpha}$ in Human Endothelial Cells Through the JNK/p38 Pathways Shing-Jong Lin, Song-Kun Shyue, Ya-Yun Hung, Yung-Hsiang Chen, Hung-Hai Ku, Jaw-Wen Chen, Ka-Bik Tam, and Yuh-Lien Chen Arterioscler Thromb Vasc Biol. 2005;25:334-340; published online before print December 2 2004, doi:10.1161/01.ATV.0000152114.00114.d8. Abstract \| Full Text \| PDF \| Data Supplement Superoxide dismutase overexpression in endothelial cells attenuates tumor necrosis factor-{alpha}-induced superoxide anion production and adhesion molecule expression, and this effect is mediated by decreased JNK and p38 phosphorylation and AP-1 and nuclear factor {kappa}B inactivation. These results suggest that superoxide dismutase may play an important role in the prevention of atherosclerosis and inflammatory response.
	c-Src and Hydrogen Peroxide Mediate Transforming Growth Factor-ß1–Induced Smooth Muscle Cell–Gene Expression in 10T1/2 Cells Mahito Sato, Keiko Kawai-Kowase, Hiroko Sato, Yuko Oyama, Hiroyoshi Kanai, Yoshio Ohyama, Tatsuo Suga, Toshitaka Maeno, Yasuhiro Aoki, Junichi Tamura, Hironosuke Sakamoto, Ryozo Nagai, and Masahiko Kurabayashi Arterioscler Thromb Vasc Biol. 2005;25:341-347; published online before print December 9 2004, doi:10.1161/01.ATV.0000152608.29351.8f. Abstract \| Full Text \| PDF \| Data Supplement TGF-ß1 controls the expression of numerous genes, including SM22{alpha} and PAI-1. We investigated whether c-Src plays a role in TGF-ß1 signaling. TGF-ß1 induction of such genes was significantly reduced in Src family tyrosine kinase-deficient cells, and Csk and pharmacological inhibitors for Src family kinases or antioxidants inhibit the effects of TGF-ß1. These results indicate that c-Src and hydrogen peroxide are required for TGF-ß1 signaling.
	Modulation of Clusterin Isoforms Is Associated With All-Trans Retinoic Acid–Induced Proliferative Arrest and Apoptosis of Intimal Smooth Muscle Cells Augusto Orlandi, Sabina Pucci, Alessandro Ciucci, Flavia Pichiorri, Amedeo Ferlosio, and Luigi Giusto Spagnoli Arterioscler Thromb Vasc Biol. 2005;25:348-353; published online before print December 9 2004, doi:10.1161/01.ATV.0000152609.28569.e1. Abstract \| Full Text \| PDF \| Data Supplement Clusterin was detected in human arterial myointimal thickening and absent in the underlying media. Rat neointimal cells overexpressed clusterin and clusterin antisense oligonucleotide reduced proliferation and increased apoptosis. All-trans retinoic acid-induced proliferative arrest showed association with s-CLU reduction and n-CLU overexpression with apoptosis, supporting a different biological role of these isoforms.
	Adenovirus-Mediated Intraarterial Delivery of PTEN Inhibits Neointimal Hyperplasia Jianhua Huang, Xi-Lin Niu, Anne M. Pippen, Brian H. Annex, and Christopher D. Kontos Arterioscler Thromb Vasc Biol. 2005;25:354-358; published online before print November 29 2004, doi:10.1161/01.ATV.0000151619.54108.a5. Abstract \| Full Text \| PDF Phosphoinositide (PI) 3-kinase is a critical regulator of neointimal hyperplasia. The inositol 3-phosphatase PTEN modulates PI 3-kinase signaling by hydrolyzing the phospholipid products of PI 3-kinase, and overexpression of PTEN in vascular smooth muscle cells inhibits the cellular processes necessary for neointimal hyperplasia. The effects of adenovirus-mediated PTEN (AdPTEN) overexpression on neointimal hyperplasia were tested in the rat carotid injury model. Compared with control arteries, AdPTEN treatment significantly reduced neointimal area and percent stenosis by enhancing medial cell apoptosis and inhibiting proliferation of the remaining viable cells. Thus, PTEN provides a new target for the treatment of neointimal hyperplasia.
	In Vitro Angiogenic Effects of Pancreatic Bile Salt-Dependent Lipase Ouafa Rebaï, Josette Le Petit-Thevenin, Nadine Bruneau, Dominique Lombardo, and Alain Vérine Arterioscler Thromb Vasc Biol. 2005;25:359-364; published online before print November 29 2004, doi:10.1161/01.ATV.0000151618.49109.bd. Abstract \| Full Text \| PDF \| Data Supplement We delineate the in vitro effects of pancreatic BSDL on endothelial cells, and we show that BSDL promotes proliferation, migration, capillary network formation, and wound-healing of HUVECs via the displacement of bFGF and VEGF from the ECM, suggesting that BSDL could be involved in angiogenesis.
	Pharmacological Inhibition and Genetic Deficiency of Plasminogen Activator Inhibitor-1 Attenuates Angiotensin II/Salt-Induced Aortic Remodeling Alec D. Weisberg, Francisco Albornoz, Jane P. Griffin, David L. Crandall, Hassan Elokdah, Agnes B. Fogo, Douglas E. Vaughan, and Nancy J. Brown Arterioscler Thromb Vasc Biol. 2005;25:365-371; published online before print December 2 2004, doi:10.1161/01.ATV.0000152356.85791.52. Abstract \| Full Text \| PDF \| Data Supplement In this study, the effect of pharmacological PAI-1 inhibition in a mouse model of Ang II-induced vascular remodeling and cardiac fibrosis was examined. PAI-1 inhibition significantly attenuated Ang II-induced aortic medial and wall thickening, but not cardiac hypertrophy, and enhanced Ang II/salt-induced cardiac fibrosis.
	Matrix Metalloproteinase-9 (MMP-9), MMP-2, and Serum Elastase Activity Are Associated With Systolic Hypertension and Arterial Stiffness Yasmin, Sharon Wallace, Carmel M. McEniery, Zahid Dakham, Pawan Pusalkar, Kaisa Maki-Petaja, Mike J. Ashby, John R. Cockcroft, and Ian B. Wilkinson Arterioscler Thromb Vasc Biol. 2005;25:372-378; published online before print November 18 2004, doi:10.1161/01.ATV.0000151373.33830.41. Abstract \| Full Text \| PDF The relationship between arterial stiffness and elastase activity was examined in isolated systolic hypertension (ISH), and separately in a large cohort of healthy individuals. Aortic stiffness is related to MMP-9, not only in ISH, but also in healthy individuals, suggesting elastases may be involved in the process of arterial stiffening and the development of ISH.
	Betaine and Folate Status as Cooperative Determinants of Plasma Homocysteine in Humans Pål I. Holm, Per M. Ueland, Stein Emil Vollset, Øivind Midttun, Henk J. Blom, Miranda B.A.J. Keijzer, and Martin den Heijer Arterioscler Thromb Vasc Biol. 2005;25:379-385; published online before print November 18 2004, doi:10.1161/01.ATV.0000151283.33976.e6. Abstract \| Full Text \| PDF \| Data Supplement In 500 healthy subjects, postmethionine load increase in tHcy showed a stronger inverse relation to betaine than to folate and vitamin B6, whereas for fasting tHcy, betaine was a weaker determinant than folate. For both tHcy modalities, the association with betaine was most pronounced in subjects with low folate status.
	Atherosclerosis and Lipoproteins
	Asymptomatic Carotid Atherosclerosis Is Associated With Circulating Chlamydia pneumoniae DNA in Younger Normotensive Subjects in a General Population Survey Rolf Mitusch, Jan Luedemann, William G. Wood, Klaus Berger, Ulf Schminke, Matthias Suter, Christof Kessler, Ulrich John, Jan Rupp, Michael Kentsch, and Matthias Maass Arterioscler Thromb Vasc Biol. 2005;25:386-391; published online before print November 18 2004, doi:10.1161/01.ATV.0000151284.49967.a7. Abstract \| Full Text \| PDF C pneumoniae has been implicated in atherogenesis. We determined the association of chlamydial DNA in peripheral blood mononuclear cells with the carotid intima-media thickness from 1032 healthy subjects from a general population survey. A stratified group interaction analysis revealed an independent association in normotensive subjects and those <70 years old.
	Geographic Origin as a Determinant of Carotid Artery Intima-Media Thickness and Brachial Artery Flow-Mediated Dilation: The Cardiovascular Risk in Young Finns Study Markus Juonala, Jorma S.A. Viikari, Mika Kähönen, Leena Taittonen, Tapani Rönnemaa, Tomi Laitinen, Noora Mäki-Torkko, Vera Mikkilä, Leena Räsänen, Hans K. Åkerblom, Erkki Pesonen, and Olli T. Raitakari Arterioscler Thromb Vasc Biol. 2005;25:392-398; published online before print November 11 2004, doi:10.1161/01.ATV.0000150042.43866.7f. Abstract \| Full Text \| PDF \| Data Supplement We studied whether an east-west difference exists in markers of subclinical atherosclerosis in 2264 Finns aged 24 to 39 years. Subjects with family origin in eastern Finland had greater carotid IMT and lower brachial FMD compared with western subjects, suggesting that hereditable factors play a role in excess atherosclerosis risk in eastern Finland.
	Postprandial Lipoprotein Changes in Patients Taking Antiretroviral Therapy for HIV Infection James H. Stein, Michelle A. Merwood, Jennifer B. Bellehumeur, Patrick E. McBride, Donald A. Wiebe, and James M. Sosman Arterioscler Thromb Vasc Biol. 2005;25:399-405; published online before print December 2 2004, doi:10.1161/01.ATV.0000152233.80082.9c. Abstract \| Full Text \| PDF An oral fat load was administered to 55 HIV-positive and 10 HIV-negative individuals. Postprandial clearance of triglyceride-rich lipoproteins was delayed in HIV-positive individuals. Compared with HIV-positive subjects not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial intermediate-density and low-density lipoproteins.
	Acute Effect of High-Fat Meal on Endothelial Function in Moderately Dyslipidemic Subjects C. Giannattasio, A. Zoppo, G. Gentile, M. Failla, A. Capra, F.M. Maggi, A. Catapano, and G. Mancia Arterioscler Thromb Vasc Biol. 2005;25:406-410; published online before print December 2 2004, doi:10.1161/01.ATV.0000152231.93590.17. Abstract \| Full Text \| PDF An oral fat load was administered to 55 HIV-positive and 10 HIV-negative individuals. Postprandial clearance of triglyceride-rich lipoproteins was delayed in HIV-positive individuals. Compared with HIV-positive subjects not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial intermediate-density and low-density lipoproteins.Hypercholesterolemia impairs endothelial function, whereas the effect of hypertriglyceridemia is less clear. In normotensive subjects with an untreated hypertriglyceridemia and hypercholesterolemia, we measured endothelial function before and 6 hours after a high-fat meal. The results demonstrate that in moderately dyslipidemic patients, endothelial function is impaired by acute hypertriglyceridemia.
	Inherited Apolipoprotein A-V Deficiency in Severe Hypertriglyceridemia Claudio Priore Oliva, Livia Pisciotta, Giovanni Li Volti, Maria Paola Sambataro, Alfredo Cantafora, Antonella Bellocchio, Alberico Catapano, Patrizia Tarugi, Stefano Bertolini, and Sebastiano Calandra Arterioscler Thromb Vasc Biol. 2005;25:411-417; published online before print December 9 2004, doi:10.1161/01.ATV.0000153087.36428.dd. Abstract \| Full Text \| PDF Mutations in APOA5 gene might be the cause of severe hypertriglyceridemia in subjects in whom mutations in LPL or APOC2 genes have been excluded. We detected a nonsense mutation in APOA5 gene (Q145X) in a boy with hyperchylomicronemia syndrome. This is the first observation of a complete apoA-V deficiency in humans.
	Genotypic Effect of the –565C>T Polymorphism in the ABCA1 Gene Promoter on ABCA1 Expression and Severity of Atherosclerosis Theodosios Kyriakou, Conrad Hodgkinson, David E. Pontefract, Srikanth Iyengar, W. Martin Howell, Yuk-ki Wong, Per Eriksson, and Shu Ye Arterioscler Thromb Vasc Biol. 2005;25:418-423; published online before print November 4 2004, doi:10.1161/01.ATV.0000149379.72018.20. Abstract \| Full Text \| PDF The study showed that the ABCA1 gene -565C>T polymorphism was associated with severity of coronary atherosclerosis in a cohort of patients from Southern England and that this sequence variant per se had an effect on promoter activity of the ABCA1 gene. The data support the notion that common ABCA1 gene variants can contribute to interindividual variability in atherosclerosis susceptibility and severity.
	Pitavastatin Inhibits Remnant Lipoprotein-Induced Macrophage Foam Cell Formation Through ApoB48 Receptor–Dependent Mechanism Akio Kawakami, Mariko Tani, Tsuyoshi Chiba, Katsumasa Yui, Shohei Shinozaki, Katsuyuki Nakajima, Akira Tanaka, Kentaro Shimokado, and Masayuki Yoshida Arterioscler Thromb Vasc Biol. 2005;25:424-429; published online before print December 9 2004, doi:10.1161/01.ATV.0000152632.48937.2d. Abstract \| Full Text \| PDF \| Data Supplement RLPs induced macrophage foam cell formation via apoB48R. Pitavastatin inhibited RLP-induced macrophage foam cell formation, at least in part, via inhibition of apoB48R expression. Our findings indicate a potential role of apoB48R in atherosclerosis.
	Granulocyte Macrophage–Colony Stimulating Factor Increases the Expression of Histamine and Histamine Receptors in Monocytes/Macrophages in Relation to Arteriosclerosis Yoshitaka Murata, Akihide Tanimoto, Ke-Yong Wang, Masato Tsutsui, Yasuyuki Sasaguri, Filip De Corte, and Hiroshi Matsushita Arterioscler Thromb Vasc Biol. 2005;25:430-435; published online before print October 28 2004, doi:10.1161/01.ATV.0000148705.13411.65. Abstract \| Full Text \| PDF \| Data Supplement The presence of histamine-producing macrophages and gene expression of histamine receptors and GM-CSF was demonstrated in arteriosclerotic lesions. In monocytic U937 cells, GM-CSF upregulated the expression of histamine and HH1R. Coordinated expression of histamine and its receptors by GM-CSF would participate in atherogenesis by affecting monocytic and SMC gene expression.
	Apolipoprotein E Promotes the Regression of Atherosclerosis Independently of Lowering Plasma Cholesterol Levels Robert L. Raffai, Samuel M. Loeb, and Karl H. Weisgraber Arterioscler Thromb Vasc Biol. 2005;25:436-441; published online before print December 9 2004, doi:10.1161/01.ATV.0000152613.83243.12. Abstract \| Full Text \| PDF Using Apoeh/hMx1-Cre mice we have begun to address apolipoprotein E-mediated mechanisms of atherosclerosis regression. We report the existence of a cholesterol-independent role of apolipoprotein E in atherosclerosis regression. This mechanism is critical for lipid removal from the fibrotic component of the plaque but not from the foam cell-rich layer beneath the endothelium.
	Oral Flavonoid Supplementation Attenuates Atherosclerosis Development in Apolipoprotein E–Deficient Mice Keiichi Hishikawa, Toshio Nakaki, and Toshiro Fujita Arterioscler Thromb Vasc Biol. 2005;25:442-446; published online before print October 21 2004, doi:10.1161/01.ATV.0000148404.24271.fc. Abstract \| Full Text \| PDF In apoE-/- mice, oral caffeic acid phenethyl ester (CAPE) supplementation attenuates the atherosclerotic process and reduces NF-{kappa}B activity and expression of NF-{kappa}B-related genes in the aorta. This may be attributable to direct inhibition of NF-{kappa}B in the lesion and reduction of systemic oxidative stress.
	Differential Effect of Experimental Hypertension and Hypercholesterolemia on Adventitial Remodeling Joerg Herrmann, Saquib Samee, Alejandro Chade, Martin Rodriguez Porcel, Lilach O. Lerman, and Amir Lerman Arterioscler Thromb Vasc Biol. 2005;25:447-453; published online before print December 9 2004, doi:10.1161/01.ATV.0000152606.34120.97. Abstract \| Full Text \| PDF \| Data Supplement Intima-media remodeling is well-described in coronary artery disease in contrast to adventitial remodeling. Results of the current study on coronary arteries of pigs, randomized to 12 weeks of normal diet (N), hypercholesterolemic diet (HC), or renovascular hypertensive (HT), indicate that adventitial remodeling precedes intima-media remodeling early after risk factor exposure with distinct qualitative differences.
	Thrombosis
	Effects of Exercise Training and Deconditioning on Platelet Aggregation Induced by Alternating Shear Stress in Men Jong-Shyan Wang, Yu-San Li, Jin-Chung Chen, and Yu-Wen Chen Arterioscler Thromb Vasc Biol. 2005;25:454-460; published online before print November 29 2004, doi:10.1161/01.ATV.0000151987.04607.24. Abstract \| Full Text \| PDF \| Data Supplement This investigation shows that exercise training decreases resting and severe exercise-promoted platelet aggregation induced by alternating shear stress (ASIPA); moreover, this effect is accompanied by reduced the von Willebrand factor binding and P-selectin expression on platelets. However, the effects of training on ASIPA are reversed to the pretraining state after deconditioning.
	Coagulation Factor Xa Stimulates Interleukin-8 Release in Endothelial Cells and Mononuclear Leukocytes: Implications in Acute Myocardial Infarction Gabi Busch, Isabell Seitz, Birgit Steppich, Sibylle Hess, Robert Eckl, Albert Schömig, and Ilka Ott Arterioscler Thromb Vasc Biol. 2005;25:461-466; published online before print November 18 2004, doi:10.1161/01.ATV.0000151279.35780.2d. Abstract \| Full Text \| PDF \| Data Supplement This study investigates the relationship between the activation of coagulation and systemic inflammatory changes in acute myocardial infarction. Tissue factor pathway inhibitor factor Xa but not F1+2 plasma levels were associated with circulating interleukin-8. In vitro factor Xa stimulated interleukin-8 and monocyte chemoattractant protein-1 release and RNA expression by activation of protease-activated receptors-1 as an underlying mechanism.
	Role of Mitochondrial Permeability Transition Pore in Coated-Platelet Formation Gyula Remenyi, Robert Szasz, Paul Friese, and George L. Dale Arterioscler Thromb Vasc Biol. 2005;25:467-471; published online before print December 9 2004, doi:10.1161/01.ATV.0000152726.49229.bf. Abstract \| Full Text \| PDF Formation of coated-platelets involves a complex set of activation events initiated by dual agonist activation. The mitochondrial permeability transition pore (MPTP) is a key intermediate in apoptosis and has been suggested to impact platelet activation. This report demonstrates that MPTP formation is essential to production of coated-platelets.
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2005;25:472, doi:10.1161/01.ATV.0000157494.59480.2e. Full Text \| PDF

Spotlight

TOC Spotlight File Banner1TOCpage

Volume 25, Issue 2; February 1, 2005

Editorials

Exercise and the Prothrombotic State: A Paradox of Cardiovascular Prevention or an Enhanced Prothrombotic State?

Apolipoprotein E and Atherosclerosis: Beyond Lipid Effect

Are Circulating CD133+ Cells Biomarkers of Vascular Disease?

Brief Reviews

ATVB In Focus: Redox Mechanisms in Blood Vessels

Redox Mechanisms in Blood Vessels

Quantification of Isoprostanes as Indices of Oxidant Stress and the Risk of Atherosclerosis in Humans

Statins and Blood Coagulation

Vascular Biology

Block of Inward Rectifying K+ Channels (KIR) Inhibits Bradykinin-Induced Vasodilatation in Human Forearm Resistance Vasculature

Granulocyte Colony-Stimulating Factor Mobilizes Functional Endothelial Progenitor Cells in Patients With Coronary Artery Disease

Mouse Strain–Specific Differences in Vascular Wall Gene Expression and Their Relationship to Vascular Disease

GATA-6 Regulates Genes Promoting Synthetic Functions in Vascular Smooth Muscle Cells

Prostaglandin E Synthases in Zebrafish

Cytochrome P4502C9-Derived Epoxyeicosatrienoic Acids Induce the Expression of Cyclooxygenase-2 in Endothelial Cells

Fluvastatin Prevents Vascular Hyperplasia by Inhibiting Phenotype Modulation and Proliferation Through Extracellular Signal-Regulated Kinase 1 and 2 and p38 Mitogen-Activated Protein Kinase Inactivation in Organ-Cultured Artery

Superoxide Dismutase Inhibits the Expression of Vascular Cell Adhesion Molecule-1 and Intracellular Cell Adhesion Molecule-1 Induced by Tumor Necrosis Factor- in Human Endothelial Cells Through the JNK/p38 Pathways

c-Src and Hydrogen Peroxide Mediate Transforming Growth Factor-ß1–Induced Smooth Muscle Cell–Gene Expression in 10T1/2 Cells

Modulation of Clusterin Isoforms Is Associated With All-Trans Retinoic Acid–Induced Proliferative Arrest and Apoptosis of Intimal Smooth Muscle Cells

Adenovirus-Mediated Intraarterial Delivery of PTEN Inhibits Neointimal Hyperplasia

In Vitro Angiogenic Effects of Pancreatic Bile Salt-Dependent Lipase

Pharmacological Inhibition and Genetic Deficiency of Plasminogen Activator Inhibitor-1 Attenuates Angiotensin II/Salt-Induced Aortic Remodeling

Matrix Metalloproteinase-9 (MMP-9), MMP-2, and Serum Elastase Activity Are Associated With Systolic Hypertension and Arterial Stiffness

Betaine and Folate Status as Cooperative Determinants of Plasma Homocysteine in Humans

Atherosclerosis and Lipoproteins

Asymptomatic Carotid Atherosclerosis Is Associated With Circulating Chlamydia pneumoniae DNA in Younger Normotensive Subjects in a General Population Survey

Geographic Origin as a Determinant of Carotid Artery Intima-Media Thickness and Brachial Artery Flow-Mediated Dilation: The Cardiovascular Risk in Young Finns Study

Postprandial Lipoprotein Changes in Patients Taking Antiretroviral Therapy for HIV Infection

Acute Effect of High-Fat Meal on Endothelial Function in Moderately Dyslipidemic Subjects

Inherited Apolipoprotein A-V Deficiency in Severe Hypertriglyceridemia

Genotypic Effect of the –565C>T Polymorphism in the ABCA1 Gene Promoter on ABCA1 Expression and Severity of Atherosclerosis

Pitavastatin Inhibits Remnant Lipoprotein-Induced Macrophage Foam Cell Formation Through ApoB48 Receptor–Dependent Mechanism

Granulocyte Macrophage–Colony Stimulating Factor Increases the Expression of Histamine and Histamine Receptors in Monocytes/Macrophages in Relation to Arteriosclerosis

Apolipoprotein E Promotes the Regression of Atherosclerosis Independently of Lowering Plasma Cholesterol Levels

Oral Flavonoid Supplementation Attenuates Atherosclerosis Development in Apolipoprotein E–Deficient Mice

Differential Effect of Experimental Hypertension and Hypercholesterolemia on Adventitial Remodeling

Thrombosis

Effects of Exercise Training and Deconditioning on Platelet Aggregation Induced by Alternating Shear Stress in Men

Coagulation Factor Xa Stimulates Interleukin-8 Release in Endothelial Cells and Mononuclear Leukocytes: Implications in Acute Myocardial Infarction

Role of Mitochondrial Permeability Transition Pore in Coated-Platelet Formation

Corrections

Correction

Spotlight

Are Circulating CD133⁺ Cells Biomarkers of Vascular Disease?

Block of Inward Rectifying K⁺ Channels (K_IR) Inhibits Bradykinin-Induced Vasodilatation in Human Forearm Resistance Vasculature

Superoxide Dismutase Inhibits the Expression of Vascular Cell Adhesion Molecule-1 and Intracellular Cell Adhesion Molecule-1 Induced by Tumor Necrosis Factor- ${alpha}$ in Human Endothelial Cells Through the JNK/p38 Pathways