Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [9])

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Volume 25, Issue 9; September 1, 2005

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

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	Editorials
	Even Flow: Shear Cues Vascular Development Cam Patterson Arterioscler Thromb Vasc Biol. 2005;25:1761-1762, doi:10.1161/01.ATV.0000175755.93591.56. Full Text \| PDF
	Differential Antiatherogenic Effects of PPAR ${alpha}$ Versus PPAR ${gamma}$ Agonists: Should We Be Surprised? Germán Camejo Arterioscler Thromb Vasc Biol. 2005;25:1763-1764, doi:10.1161/01.ATV.0000181034.54148.8d. Full Text \| PDF
	A Mouse Model of the Perimenopausal Transition: Importance for Cardiovascular Research J. Koudy Williams Arterioscler Thromb Vasc Biol. 2005;25:1765-1766, doi:10.1161/01.ATV.0000175757.28698.c2. Full Text \| PDF
	Brief Reviews
	Rho-Kinase Is an Important Therapeutic Target in Cardiovascular Medicine Hiroaki Shimokawa and Akira Takeshita Arterioscler Thromb Vasc Biol. 2005;25:1767-1775; published online before print July 7 2005, doi:10.1161/01.ATV.0000176193.83629.c8. Abstract \| Full Text \| PDF Rho-Kinase is one of the effectors of the small GTP-binding protein Rho. Translational research on the therapeutic importance of Rho/Rho-kinase pathway from molecular level to clinical studies from authors' and other laboratories is briefly reviewed. The results clearly indicate that Rho-kinase is an important therapeutic target in cardiovascular medicine.
	Atherosclerosis in Patients With Autoimmune Disorders Johan Frostegård Arterioscler Thromb Vasc Biol. 2005;25:1776-1785; published online before print June 23 2005, doi:10.1161/01.ATV.0000174800.78362.ec. Abstract \| Full Text \| PDF The risk of cardiovascular disease is very high in systemic lupus erythematosus and is also raised in other autoimmune diseases like rheumatoid arthritis. This may shed light on the role of immune reactions in atherothrombosis. Traditional risk factors and also non-traditional like inflammation, antiphospholipid antibodies and lipid oxidation are implicated.
	Heme Oxygenase and Atherosclerosis Toshisuke Morita Arterioscler Thromb Vasc Biol. 2005;25:1786-1795; published online before print July 14 2005, doi:10.1161/01.ATV.0000178169.95781.49. Abstract \| Full Text \| PDF Heme oxygenase (HO) is the rate-limiting enzyme which catalyzes heme to carbon monoxide, biliverdin and free ferrous iron. Inducible HO (HO-1) functions as adaptive molecules against oxidative insults. Herein, I highlight the relationship of HO and atherosclerosis and the potential for HO-1 as a novel therapeutic target for cardiovascular diseases.
	Vascular Biology
	Vascular Endothelium Has a Local Anti-Adenovirus Vector System and Glucocorticoid Optimizes Its Gene Transduction Takahisa Murata, Masatoshi Hori, Sheng Lee, Akio Nakamura, Kazuhiro Kohama, Hideaki Karaki, and Hiroshi Ozaki Arterioscler Thromb Vasc Biol. 2005;25:1796-1803; published online before print June 16 2005, doi:10.1161/01.ATV.0000174130.75958.b7. Abstract \| Full Text \| PDF We investigated the mechanisms of this impairment and the effect of DEX on adenovirus-mediated gene transfer into the vascular endothelial cells using organ-cultured pulmonary endothelium. Based on these results, we applied DEX treatment to in vitro and in vivo gene transfection.
	Rapid Effects of Rosiglitazone Treatment on Endothelial Function and Inflammatory Biomarkers Jürgen Hetzel, Bernd Balletshofer, Kilian Rittig, Daniel Walcher, Wolfgang Kratzer, Vinzenz Hombach, Hans-Ulrich Häring, Wolfgang Koenig, and Nikolaus Marx Arterioscler Thromb Vasc Biol. 2005;25:1804-1809; published online before print July 7 2005, doi:10.1161/01.ATV.0000176192.16951.9a. Abstract \| Full Text \| PDF Antidiabetic thiazolidinediones (TZDs), like rosiglitazone or pioglitazone, improve endothelial function in patients with type 2 diabetes or metabolic syndrome, but it is currently unknown whether these beneficial effects of TZDs depend on their metabolic action or may be caused by direct effects on the endothelium. Therefore, the present study examined whether short-term rosiglitazone treatment influences endothelium-dependent vasodilation as well as serum levels of vascular disease biomarkers in healthy, nondiabetic subjects.
	Peroxisome Proliferator-Activated Receptor ${gamma}$ Ligands Stimulate Endothelial Nitric Oxide Production Through Distinct Peroxisome Proliferator-Activated Receptor ${gamma}$ –Dependent Mechanisms John A. Polikandriotis, Louis J. Mazzella, Heidi L. Rupnow, and C. Michael Hart Arterioscler Thromb Vasc Biol. 2005;25:1810-1816; published online before print July 14 2005, doi:10.1161/01.ATV.0000177805.65864.d4. Abstract \| Full Text \| PDF \| Data Supplement This study characterizes the molecular mechanisms underlying peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) ligand-stimulated increases in endothelial nitric oxide production. The data indicate that different PPAR{gamma} ligands increase endothelial cell nitric oxide production by distinct PPAR{gamma}-dependent signaling pathways that could represent novel targets for pharmacological intervention in vascular disease.
	Shear Stress Induces Endothelial Differentiation From a Murine Embryonic Mesenchymal Progenitor Cell Line Hao Wang, Gordon M. Riha, Shaoyu Yan, Min Li, Hong Chai, Hui Yang, Qizhi Yao, and Changyi Chen Arterioscler Thromb Vasc Biol. 2005;25:1817-1823; published online before print June 30 2005, doi:10.1161/01.ATV.0000175840.90510.a8. Abstract \| Full Text \| PDF \| Data Supplement Shear stress significantly induces expression of endothelial cell-specific markers such as CD31, vWF, and VE-cadherin in C3H/10T1/2, a murine embryonic mesenchymal progenitor cell line. In addition, shear induces augmentation of functional markers of the mature endothelial phenotype such as uptake of ac-LDL and formation of capillary-like structures on Matrigel.
	Caveolin-1 Is Essential for Activation of Rac1 and NAD(P)H Oxidase After Angiotensin II Type 1 Receptor Stimulation in Vascular Smooth Muscle Cells: Role in Redox Signaling and Vascular Hypertrophy Lian Zuo, Masuko Ushio-Fukai, Satoshi Ikeda, Lula Hilenski, Nikolay Patrushev, and R. Wayne Alexander Arterioscler Thromb Vasc Biol. 2005;25:1824-1830; published online before print June 23 2005, doi:10.1161/01.ATV.0000175295.09607.18. Abstract \| Full Text \| PDF \| Data Supplement Angiotensin II (Ang II)-induced vascular hypertrophy is dependent on caveolae/lipid rafts and reactive oxygen species (ROS) derived from NAD(P)H oxidase. Using caveolin-1 siRNA, we demonstrate that caveolin-1 plays an essential role in AT1 receptor targeting into caveolae/lipid rafts and Rac1 activation, which are required for ROS-dependent, growth-related Ang II signaling.
	Signal-Crosstalk Between Rho/ROCK and c-Jun NH₂-Terminal Kinase Mediates Migration of Vascular Smooth Muscle Cells Stimulated by Angiotensin II Haruhiko Ohtsu, Mizuo Mifune, Gerald D. Frank, Shuichi Saito, Tadashi Inagami, Shokei Kim-Mitsuyama, Yoh Takuwa, Terukatsu Sasaki, Jeffrey D. Rothstein, Hiroyuki Suzuki, Hidekatsu Nakashima, Elethia A. Woolfolk, Evangeline D. Motley, and Satoru Eguchi Arterioscler Thromb Vasc Biol. 2005;25:1831-1836; published online before print June 30 2005, doi:10.1161/01.ATV.0000175749.41799.9b. Abstract \| Full Text \| PDF \| Data Supplement By using vascular smooth muscle cells (VSMCs) in culture, we have investigated signal cross-talk in mediating VSMC migration induced by angiotensin II. We found that Rho-kinase/ROCK activated by PYK2 and PKC-delta specifically mediate angiotensin II-induced VSMC migration via JNK activation, providing a potential cascade in mediating vascular remodeling.
	Pentraxin 3 Inhibits Fibroblast Growth Factor 2–Dependent Activation of Smooth Muscle Cells In Vitro and Neointima Formation In Vivo Maura Camozzi, Serena Zacchigna, Marco Rusnati, Daniela Coltrini, Genaro Ramirez-Correa, Barbara Bottazzi, Alberto Mantovani, Mauro Giacca, and Marco Presta Arterioscler Thromb Vasc Biol. 2005;25:1837-1842; published online before print July 14 2005, doi:10.1161/01.ATV.0000177807.54959.7d. Abstract \| Full Text \| PDF \| Data Supplement Human long-pentraxin 3 inhibits human coronary artery smooth muscle cell proliferation and migration driven by endogenous and exogenous fibroblast growth factor-2. Accordingly, long-pentraxin 3 overexpression after recombinant adeno-associated virus gene transfer affects smooth muscle cell proliferation and survival in vitro and intimal thickening after arterial injury in vivo.
	CD34⁺ Cells Home, Proliferate, and Participate in Capillary Formation, and in Combination With CD34^– Cells Enhance Tube Formation in a 3-Dimensional Matrix Maarten B. Rookmaaker, Marianne C. Verhaar, Cindy J.M. Loomans, Robert Verloop, Erna Peters, Peter E. Westerweel, Toyoaki Murohara, Frank J.T. Staal, Anton Jan van Zonneveld, Pieter Koolwijk, Ton J. Rabelink, and Victor W.M. van Hinsbergh Arterioscler Thromb Vasc Biol. 2005;25:1843-1850; published online before print July 14 2005, doi:10.1161/01.ATV.0000177808.92494.14. Abstract \| Full Text \| PDF \| Data Supplement In an in vitro 3D neovascularization model, homing, proliferation, differentiation, and participation of purified CD34+ cells in capillary tube formation as well as a modest stimulatory effect on neovascularization were shown. Coaddition of CD34[minus] cells markedly enhanced capillary growth. This suggests a potential role for CD34+ cells as vectors for gene therapy and indicates an important supportive role for CD34- cells in neovascularization.
	Identification and Characterization of Vascular Calcification–Associated Factor, a Novel Gene Upregulated During Vascular Calcification In Vitro and In Vivo M. Yvonne Alexander, Fiona L. Wilkinson, John Paul Kirton, Claire Farrington Rock, Georgina D.M. Collett, Maria Jeziorska, J. Vincent Smyth, Anthony M. Heagerty, and Ann E. Canfield Arterioscler Thromb Vasc Biol. 2005;25:1851-1857; published online before print June 30 2005, doi:10.1161/01.ATV.0000175750.94742.46. Abstract \| Full Text \| PDF Vascular calcification presents an important and unresolved dilemma in the clinic. We aim to identify molecules involved in this process to develop strategies for treatment. We isolated a novel cDNA (VCAF) from mineralized pericytes and demonstrate its association with calcification in vitro and in vivo.
	Mast Cell Tryptase in Mast Cell Granules Enhances MCP-1 and Interleukin-8 Production in Human Endothelial Cells Makoto Kinoshita, Masaharu Okada, Masatake Hara, Yutaka Furukawa, and Akira Matsumori Arterioscler Thromb Vasc Biol. 2005;25:1858-1863; published online before print June 23 2005, doi:10.1161/01.ATV.0000174797.71708.97. Abstract \| Full Text \| PDF \| Data Supplement The role of mast cells in the pathogenesis of cardiovascular disorders has been recently highlighted. However, the mechanism remains unclear. This study demonstrates that degranulation of mast cells causes chemokine production in endothelial cells. These observations suggest the link between mast cells and atherosclerosis via endothelial production of chemokine.
	Mechanisms of the Inhibitory Effect of Epigallocatechin-3-Gallate on Cultured Human Vascular Smooth Muscle Cell Invasion Xian Wu Cheng, Masafumi Kuzuya, Kae Nakamura, Zexuan Liu, Qun Di, Jun Hasegawa, Mitsunaga Iwata, Toyoaki Murohara, Mitsuhiro Yokota, and Akihisa Iguchi Arterioscler Thromb Vasc Biol. 2005;25:1864-1870; published online before print July 28 2005, doi:10.1161/01.ATV.0000179675.49619.9b. Abstract \| Full Text \| PDF \| Data Supplement Molecular mechanisms of administration of catechins that reduce the neointimal hyperplasia remain largely unknown. We demonstrated EGCG inhibited SMC invasion through upregulation TIMP-2 expression to modulate MMP activity. These findings provide new insights into the mechanisms of action of EGCG as restenosis-preventive agent.
	Critical Role of Mst1 in Vascular Remodeling After Injury Hiroki Ono, Toshihiro Ichiki, Hideki Ohtsubo, Kae Fukuyama, Ikuyo Imayama, Yasuko Hashiguchi, Junichi Sadoshima, and Kenji Sunagawa Arterioscler Thromb Vasc Biol. 2005;25:1871-1876; published online before print June 16 2005, doi:10.1161/01.ATV.0000174588.50971.1a. Abstract \| Full Text \| PDF \| Data Supplement Apoptosis of vascular smooth muscle cells (VSMCs) is believed to contribute to the vascular remodeling process. Mst1 mediated VSMC apoptosis in vitro and vivo and suppressed neointimal formation in balloon-injured artery, suggesting that Mst1 mediates the vascular remodeling process and may be a potential therapeutic target for vascular proliferative diseases.
	Important Role of Apoptosis Signal-Regulating Kinase 1 in Ischemia-Induced Angiogenesis Yasukatsu Izumi, Shokei Kim-Mitsuyama, Minoru Yoshiyama, Takashi Omura, Masayuki Shiota, Atsushi Matsuzawa, Tokihito Yukimura, Toyoaki Murohara, Motohiro Takeya, Hidenori Ichijo, Junichi Yoshikawa, and Hiroshi Iwao Arterioscler Thromb Vasc Biol. 2005;25:1877-1883; published online before print June 23 2005, doi:10.1161/01.ATV.0000174801.76234.bd. Abstract \| Full Text \| PDF We examined the significance of apoptosis signal-regulating kinase 1 (ASK1) in ischemia-induced angiogenesis in vivo. Well-developed collateral vessels and angiogenesis were observed in wild-type mice in response to hindlimb ischemia, whereas these responses were reduced in mice deficient in ASK1. Thus, the activation of ASK1 leads to angiogenesis.
	Heparin-Binding Epidermal Growth Factor–Like Growth Factor, Collateral Vessel Development, and Angiogenesis in Skeletal Muscle Ischemia Dan Chalothorn, Scott M. Moore, Hua Zhang, Susan W. Sunnarborg, David C. Lee, and James E. Faber Arterioscler Thromb Vasc Biol. 2005;25:1884-1890; published online before print June 30 2005, doi:10.1161/01.ATV.0000175761.59602.16. Abstract \| Full Text \| PDF \| Data Supplement We examined whether HB-EGF participates in arteriogenesis and angiogenesis after femoral ligation in HB-EGF-null (-/-) mice. No attenuation occurred in hind-limb perfusion recovery, collateral growth, or angiogenesis. Renin and arterial pressure were unaltered in HB-EGF-/-. Although EGFR phosphorylation was decreased in HB-EGF-/-, HB-EGF is not required for arteriogenesis or angiogenesis.
	Aldehyde Dehydrogenase 2 Plays a Role in the Bioactivation of Nitroglycerin in Humans Isla S. Mackenzie, Kaisa M. Maki-Petaja, Carmel M. McEniery, Yi Ping Bao, Sharon M. Wallace, Joseph Cheriyan, Sue Monteith, Morris J. Brown, and Ian B. Wilkinson Arterioscler Thromb Vasc Biol. 2005;25:1891-1895; published online before print July 28 2005, doi:10.1161/01.ATV.0000179599.71086.89. Abstract \| Full Text \| PDF This study investigates the role of aldehyde dehydrogenase type 2 (ALDH2) in the bioactivation of nitrates in humans. We show that genetic and pharmacological reduction of ALDH2 activity decreases in vivo vascular responses to nitroglycerin, suggesting that ALDH2 is a mediator of the bioactivation of nitrates in humans.
	Atherosclerosis and Lipoproteins
	Overexpression of Human Apolipoprotein A-II in Transgenic Mice Does Not Impair Macrophage-Specific Reverse Cholesterol Transport In Vivo Noemí Rotllan, Vicent Ribas, Laura Calpe-Berdiel, Jesús M. Martín-Campos, Francisco Blanco-Vaca, and Joan Carles Escolà-Gil Arterioscler Thromb Vasc Biol. 2005;25:e128-e132; published online before print June 30 2005, doi:10.1161/01.ATV.0000175760.28378.80. Abstract \| Full Text \| PDF Macrophage-specific reverse cholesterol transport was measured in human apoA-II transgenic mice. Increased fecal [3H]cholesterol excretion was found in chow-fed transgenic mice, a situation in which there is no increased atherosclerosis. No significant differences were observed in atherogenic-fed mice, a situation in which there is a marked increase in atherosclerosis.
	Overexpression of Human Apolipoprotein A-II in Transgenic Mice Does Not Impair Macrophage-Specific Reverse Cholesterol Transport In Vivo Noemí Rotllan, Vicent Ribas, Laura Calpe-Berdiel, Jesús M. Martín-Campos, Francisco Blanco-Vaca, and Joan Carles Escolà-Gil Arterioscler Thromb Vasc Biol. 2005;25:1896. Abstract \| Full Text \| PDF
	PPAR ${alpha}$ , but not PPAR ${gamma}$ , Activators Decrease Macrophage-Laden Atherosclerotic Lesions in a Nondiabetic Mouse Model of Mixed Dyslipidemia Nathalie Hennuyer, Anne Tailleux, Gérard Torpier, Hafid Mezdour, Jean-Charles Fruchart, Bart Staels, and Catherine Fiévet Arterioscler Thromb Vasc Biol. 2005;25:1897-1902; published online before print June 30 2005, doi:10.1161/01.ATV.0000175756.56818.ee. Abstract \| Full Text \| PDF In a dyslipidemic nondiabetic murine model characterized by macrophage-laden atherosclerotic lesions, we show that fenofibrate, but not rosiglitazone or pioglitazone, delays lesional lipid and macrophage accumulation.
	Rosiglitazone Attenuates Atherosclerosis in a Model of Insulin Insufficiency Independent of Its Metabolic Effects Anna C. Calkin, Josephine M. Forbes, Craig M. Smith, Markus Lassila, Mark E. Cooper, Karin A. Jandeleit-Dahm, and Terri J. Allen Arterioscler Thromb Vasc Biol. 2005;25:1903-1909; published online before print July 14 2005, doi:10.1161/01.ATV.0000177813.99577.6b. Abstract \| Full Text \| PDF \| Data Supplement To assess the independent vascular effects of rosiglitazone, we treated streptozotocin-diabetic apolipoprotein E-deficient mice with rosiglitazone for 20 weeks. Rosiglitazone significantly reduced plaque area in the absence of changes in glucose, insulin, or cholesterol levels. These results may implicate a role for thiazolidinediones in the absence of insulin resistance.
	Atherosclerotic Lesion Development in a Novel Ovary-Intact Mouse Model of Perimenopause Loretta P. Mayer, Cheryl A. Dyer, Rebecca L. Eastgard, Patricia B. Hoyer, and Carole L. Banka Arterioscler Thromb Vasc Biol. 2005;25:1910-1916; published online before print June 30 2005, doi:10.1161/01.ATV.0000175767.46520.6a. Abstract \| Full Text \| PDF The goal was to determine whether estrogen treatment altered atherosclerosis development in follicle-deplete ovary-intact mice compared with ovariectomized mice. Ovarian contribution of androgen appeared to augment the protective effects of estrogen, suggesting this new model may provide an improved experimental system to analyze atherosclerosis drugs for perimenopausal and postmenopausal women.
	Genetic Deletion or Antibody Blockade of ${alpha}$ 1ß1 Integrin Induces a Stable Plaque Phenotype in ApoE–/– Mice Kitty Schapira, Esther Lutgens, Antonin de Fougerolles, Andrew Sprague, Anouk Roemen, Humphrey Gardner, Victor Koteliansky, Mat Daemen, and Sylvia Heeneman Arterioscler Thromb Vasc Biol. 2005;25:1917-1924; published online before print June 23 2005, doi:10.1161/01.ATV.0000174807.90292.2f. Abstract \| Full Text \| PDF \| Data Supplement The role of {alpha}1ß1 integrin was investigated in atherosclerosis. {alpha}1ß1 integrin is involved in atherosclerosis by mediating the migration of leukocytes to lesions via adhesion to collagen IV. Blocking this integrin reduces atherosclerosis and induces a more stable plaque phenotype.
	Association Between Prostaglandin E Receptor Subtype EP4 Overexpression and Unstable Phenotype in Atherosclerotic Plaques in Human Francesco Cipollone, Maria Luigia Fazia, Annalisa Iezzi, Chiara Cuccurullo, Domenico De Cesare, Sante Ucchino, Francesco Spigonardo, Antonio Marchetti, Fiamma Buttitta, Leonardo Paloscia, Marco Mascellanti, Franco Cuccurullo, and Andrea Mezzetti Arterioscler Thromb Vasc Biol. 2005;25:1925-1931; published online before print July 14 2005, doi:10.1161/01.ATV.0000177814.41505.41. Abstract \| Full Text \| PDF \| Data Supplement We investigated which of the 4 PGE2 receptors mediates PGE2-dependent metalloproteinase (MMP) generation in carotid plaques from symptomatic and asymptomatic patients. Only EP4 and EP2 were detected in plaques. EP4 was higher in symptomatic plaques and linearly correlated with MMPs. This study indicates a role for EP4 in PGE2-dependent plaque destabilization.
	An Oral ApoJ Peptide Renders HDL Antiinflammatory in Mice and Monkeys and Dramatically Reduces Atherosclerosis in Apolipoprotein E–Null Mice Mohamad Navab, G.M. Anantharamaiah, Srinivasa T. Reddy, Brian J. Van Lenten, Alan C. Wagner, Susan Hama, Greg Hough, Eugene Bachini, David W. Garber, Vinod K. Mishra, Mayakonda N. Palgunachari, and Alan M. Fogelman Arterioscler Thromb Vasc Biol. 2005;25:1932-1937; published online before print June 16 2005, doi:10.1161/01.ATV.0000174589.70190.e2. Abstract \| Full Text \| PDF Oral D- [113-122]apoJ, a peptide synthesized from D-amino acids corresponding to residues 113 to 122 in apolipoprotein J, significantly improves HDL inflammatory properties in mice and monkeys and inhibits lesion formation in apoE-null mice.
	Cytoplasmic Expression and Extracellular Deposition of an Antiangiogenic Factor, Pigment Epithelium-Derived Factor, in Human Atherosclerotic Plaques Hiromitsu Baba, Yoshikazu Yonemitsu, Toshiaki Nakano, Mitsuho Onimaru, Masanori Miyazaki, Yasuhiro Ikeda, Shinji Sumiyoshi, Yasuji Ueda, Mamoru Hasegawa, Ichiro Yoshino, Yoshihiko Maehara, and Katsuo Sueishi Arterioscler Thromb Vasc Biol. 2005;25:1938-1944; published online before print June 30 2005, doi:10.1161/01.ATV.0000175759.78338.1e. Abstract \| Full Text \| PDF \| Data Supplement To obtain the evidence of antiangiogenic factor in atherosclerotic plaque, we investigated the localization of pigment epithelium-derived factor (PEDF). Extracellular deposition of PEDF was negatively correlated with the number of microvessels, suggesting that PEDF functions as an antiangiogenic factor when it is deposited onto the extracellular matrix in human subjects.
	Cytosolic Lipid Droplets Increase in Size by Microtubule-Dependent Complex Formation Pontus Boström, Mikael Rutberg, Johanna Ericsson, Peter Holmdahl, Linda Andersson, Michael A. Frohman, Jan Borén, and Sven-Olof Olofsson Arterioscler Thromb Vasc Biol. 2005;25:1945-1951; published online before print July 28 2005, doi:10.1161/01.ATV.0000179676.41064.d4. Abstract \| Full Text \| PDF \| Data Supplement Lipid droplets increase in size by a triglyceride biosynthesis-independent process after their assembly. Confocal microscopy and time-lapse recordings of 3T3 NIH cells, microinjected with ADRP-GFP or stained with Nile Red, indicated that complex formation between droplets could explain this increase in size. This process is dependent on intact microtubules.
	Effects of Diet and Simvastatin on Fatty Acid Composition in Hypercholesterolemic Men: A Randomized Controlled Trial Antti Jula, Jukka Marniemi, Tapani Rönnemaa, Arja Virtanen, and Risto Huupponen Arterioscler Thromb Vasc Biol. 2005;25:1952-1959; published online before print July 14 2005, doi:10.1161/01.ATV.0000177812.84927.fa. Abstract \| Full Text \| PDF Effects of diet and simvastatin on serum fatty acids in hypercholesterolemic men were studied in a randomized controlled trial. Simvastatin increased the formation of long-chain polyunsaturated fatty acids. Increased formation of long-chain polyunsaturated fatty acids and their metabolites may contribute a substantial part of the pleiotropic effects of simvastatin.
	Tendon Xanthomas in Familial Hypercholesterolemia Are Associated With Cardiovascular Risk Independently of the Low-Density Lipoprotein Receptor Gene Mutation Fernando Civeira, Sergio Castillo, Rodrigo Alonso, Erardo Meriño-Ibarra, Ana Cenarro, Marta Artied, Paula Martín-Fuentes, Emilio Ros, Miguel Pocoví, Pedro Mata for the Spanish Familial Hypercholesterolemia Group Arterioscler Thromb Vasc Biol. 2005;25:1960-1965; published online before print July 14 2005, doi:10.1161/01.ATV.0000177811.14176.2b. Abstract \| Full Text \| PDF \| Data Supplement In 951 subjects with hFH, significance of TX was studied. 278 (29.2%) presented TX (TX+) and 102 TX+ reported premature CVD (36.7%) versus 93 TX- (13.8%) (P=0.001). Age, male sex, LDL cholesterol, and hypertension showed positive association and body mass index showed negative association with TX.
	Relationship of Monocyte Count and Peripheral Arterial Disease: Results From the National Health and Nutrition Examination Survey 1999–2002 Khurram Nasir, Eliseo Guallar, Ana Navas-Acien, Michael H. Criqui, and João A.C. Lima Arterioscler Thromb Vasc Biol. 2005;25:1966-1971; published online before print June 23 2005, doi:10.1161/01.ATV.0000175296.02550.e4. Abstract \| Full Text \| PDF In this study of 3949 individuals 40 years of age without known cardiovascular disease participating in the 1999 to 2002 National Health and Nutrition Examination Survey, monocytes were the only white blood cell types significantly and independently associated with peripheral arterial disease after adjustment for other inflammatory markers.
	The Molecular Basis of Lecithin:Cholesterol Acyltransferase Deficiency Syndromes: A Comprehensive Study of Molecular and Biochemical Findings in 13 Unrelated Italian Families Laura Calabresi, Livia Pisciotta, Anna Costantin, Ilaria Frigerio, Ivano Eberini, Paola Alessandrini, Marcello Arca, Gabriele Bittolo Bon, Giuliano Boscutti, Ghil Busnach, Giovanni Frascà, Loreto Gesualdo, Maddalena Gigante, Graziana Lupattelli, Anna Montali, Stefano Pizzolitto, Ivana Rabbone, Marina Rolleri, Giacomo Ruotolo, Tiziana Sampietro, Adalberto Sessa, Gaetano Vaudo, Alfredo Cantafora, Fabrizio Veglia, Sebastiano Calandra, Stefano Bertolini, and Guido Franceschini Arterioscler Thromb Vasc Biol. 2005;25:1972-1978; published online before print June 30 2005, doi:10.1161/01.ATV.0000175751.30616.13. Abstract \| Full Text \| PDF \| Data Supplement The impact of mutations in the LCAT gene on the plasma lipid/lipoprotein profile was investigated in 13 families carrying 17 different LCAT mutations. The inheritance of a mutated LCAT genotype causes a gene- dose-dependent alteration in the lipid/lipoprotein profile, which is remarkably similar between subjects classified as FLD or FED.
	Hepatic and Cardiovascular Consequences of Familial Hypobetalipoproteinemia Raaj R. Sankatsing, Sigrid W. Fouchier, Stefan de Haan, Barbara A. Hutten, Eric de Groot, John J.P. Kastelein, and Erik S.G. Stroes Arterioscler Thromb Vasc Biol. 2005;25:1979-1984; published online before print July 7 2005, doi:10.1161/01.ATV.0000176191.64314.07. Abstract \| Full Text \| PDF \| Data Supplement We investigated the risk for fatty liver disease (FLD) and cardiovascular disease (CVD) in familial hypobetalipoproteinemia (FHBL) subjects and in healthy controls. Whereas the prevalence of FLD was increased in FHBL, carotid arterial wall stiffness, a surrogate marker for CVD, was decreased suggesting that these subjects are relatively protected against developing CVD.
	Familial Combined Hyperlipidemia in Mexicans: Association With Upstream Transcription Factor 1 and Linkage on Chromosome 16q24.1 Adriana Huertas-Vazquez, Carlos Aguilar-Salinas, Aldons J. Lusis, Rita M. Cantor, Samuel Canizales-Quinteros, Jenny C. Lee, Lizzette Mariana-Nuñez, Roopa-Metha Laura Riba-Ramirez, Anne Jokiaho, Teresa Tusie-Luna, and Päivi Pajukanta Arterioscler Thromb Vasc Biol. 2005;25:1985-1991; published online before print June 23 2005, doi:10.1161/01.ATV.0000175297.37214.a0. Abstract \| Full Text \| PDF \| Data Supplement To investigate the genetic component of familial combined hyperlipidemia (FCHL) in Mexican FCHL families, we analyzed the upstream transcription factor 1 (USF1) gene and 7 chromosomal loci previously identified for FCHL. In Mexicans, USF1 was associated with FCHL and triglycerides, and a locus on 16q24.1 linked to total cholesterol.
	Thrombosis
	Recurrence Rate After a First Venous Thrombosis in Patients With Familial Thrombophilia Carla Y. Vossen, Isobel D. Walker, Peter Svensson, Juan C. Souto, Inge Scharrer, F. Eric Preston, Gualtiero Palareti, Ingrid Pabinger, Felix J.M. van der Meer, Mike Makris, Jordi Fontcuberta, Jacqueline Conard, and Frits R. Rosendaal Arterioscler Thromb Vasc Biol. 2005;25:1992-1997; published online before print June 23 2005, doi:10.1161/01.ATV.0000174806.76629.7b. Abstract \| Full Text \| PDF \| Data Supplement We prospectively determined the recurrence rate in patients with familial thrombophilia. The overall incidence of a second venous thromboembolic event was 5.0%/year. Extra care after a first event is required for men with a deficiency in natural anticoagulants or multiple defects and women with antithrombin deficiency.
	Protective Mechanisms of Inosine in Platelet Activation and Cerebral Ischemic Damage George Hsiao, Kuang H. Lin, Yi Chang, Ta L. Chen, Nien H. Tzu, Duen S. Chou, and Joen R. Sheu Arterioscler Thromb Vasc Biol. 2005;25:1998-2004; published online before print June 23 2005, doi:10.1161/01.ATV.0000174798.25085.d6. Abstract \| Full Text \| PDF Inosine inhibited platelet aggregation, phosphoinositide breakdown, [Ca+2]i, PKC activation, TxA2, and hydroxyl radical formation stimulated by collagen. Inosine increased levels of cyclic GMP-induced VASP Ser157 phosphorylation. Inosine inhibited platelet plug formation and attenuated focal cerebral ischemia in vivo. Thus, inosine treatment may represent a novel approach to lowering the risk of thromboembolic-related disorders.
	Endogenous NO Blockade Enhances Tissue Factor Expression via Increased Ca²⁺ Influx Through MCP-1 in Endothelial Cells by Monocyte Adhesion Takayuki Sakamoto, Toshiyuki Ishibashi, Nobuo Sakamoto, Koichi Sugimoto, Kensuke Egashira, Hiroshi Ohkawara, Kenji Nagata, Keiko Yokoyama, Masashi Kamioka, Toshihiro Ichiki, Naotoshi Sugimoto, Masahiko Kurabayashi, Koji Suzuki, Yoh Takuwa, and Yukio Maruyama Arterioscler Thromb Vasc Biol. 2005;25:2005-2011; published online before print July 14 2005, doi:10.1161/01.ATV.0000178171.61754.cd. Abstract \| Full Text \| PDF Endogenous NO blockade increased Ca2+ influx and TF expression in ECs when monocytes adhered to them. This was inhibited by the mutant MCP-1, 7ND. These suggest a role for MCP-1/CCR2 in endogenous NO blockade in procoagulant activity via Ca2+ influx-dependent TF expression in monocyte-EC interaction.
	Letters to the Editor
	Consequences of Cholesteryl Ester Transfer Protein Inhibition in Patients With Familial Hypoalphalipoproteinemia Radjesh J. Bisoendial, G. Kees Hovingh, Karim El Harchaoui, Johannes H.M. Levels, Sotirios Tsimikas, Kewei Pu, Aeilko E. Zwinderman, Jan Albert Kuivenhoven, John J.P. Kastelein, and Erik S.G. Stroes Arterioscler Thromb Vasc Biol. 2005;25:e133-e134, doi:10.1161/01.ATV.0000179009.60612.28. Full Text \| PDF
	Toll-Like Receptors, Endocrine Stress Response, and Arteriosclerosis Stefan R. Bornstein, Henning Morawietz, Mahmood R. Kazemi, Carl Grunfeld, and Kenneth R. Feingold Arterioscler Thromb Vasc Biol. 2005;25:e135, doi:10.1161/01.ATV.0000178996.91277.fb. Full Text \| PDF
	Lipopolysaccharide (LPS) Contamination Plays the Real Role in C-Reactive Protein–Induced IL-6 Secretion From Human Endothelial Cells In Vitro Sandhya S. Nerurkar, Patrick J. McDevitt, Gilbert F. Scott, Kyung O. Johanson, Robert N. Willette, and Tian-Li Yue Arterioscler Thromb Vasc Biol. 2005;25:e136, doi:10.1161/01.ATV.0000175753.82842.cc. Full Text \| PDF
	Association of C-Reactive Protein With Blood Pressure Leonelo E. Bautista, George Davey Smith, Debbie A. Lawlor, Roger Harbord, Nick Timpson, Anne Rumley, Gordon D.O. Lowe, Ian N.M. Day, and Shah Ebrahim Arterioscler Thromb Vasc Biol. 2005;25:e137-e138, doi:10.1161/01.ATV.0000176190.80460.ba. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 25, Issue 9; September 1, 2005

Editorials

Even Flow: Shear Cues Vascular Development

Differential Antiatherogenic Effects of PPAR Versus PPAR Agonists: Should We Be Surprised?

A Mouse Model of the Perimenopausal Transition: Importance for Cardiovascular Research

Brief Reviews

Rho-Kinase Is an Important Therapeutic Target in Cardiovascular Medicine

Atherosclerosis in Patients With Autoimmune Disorders

Heme Oxygenase and Atherosclerosis

Vascular Biology

Vascular Endothelium Has a Local Anti-Adenovirus Vector System and Glucocorticoid Optimizes Its Gene Transduction

Rapid Effects of Rosiglitazone Treatment on Endothelial Function and Inflammatory Biomarkers

Peroxisome Proliferator-Activated Receptor Ligands Stimulate Endothelial Nitric Oxide Production Through Distinct Peroxisome Proliferator-Activated Receptor –Dependent Mechanisms

Shear Stress Induces Endothelial Differentiation From a Murine Embryonic Mesenchymal Progenitor Cell Line

Caveolin-1 Is Essential for Activation of Rac1 and NAD(P)H Oxidase After Angiotensin II Type 1 Receptor Stimulation in Vascular Smooth Muscle Cells: Role in Redox Signaling and Vascular Hypertrophy

Signal-Crosstalk Between Rho/ROCK and c-Jun NH2-Terminal Kinase Mediates Migration of Vascular Smooth Muscle Cells Stimulated by Angiotensin II

Pentraxin 3 Inhibits Fibroblast Growth Factor 2–Dependent Activation of Smooth Muscle Cells In Vitro and Neointima Formation In Vivo

CD34+ Cells Home, Proliferate, and Participate in Capillary Formation, and in Combination With CD34– Cells Enhance Tube Formation in a 3-Dimensional Matrix

Identification and Characterization of Vascular Calcification–Associated Factor, a Novel Gene Upregulated During Vascular Calcification In Vitro and In Vivo

Mast Cell Tryptase in Mast Cell Granules Enhances MCP-1 and Interleukin-8 Production in Human Endothelial Cells

Mechanisms of the Inhibitory Effect of Epigallocatechin-3-Gallate on Cultured Human Vascular Smooth Muscle Cell Invasion

Critical Role of Mst1 in Vascular Remodeling After Injury

Important Role of Apoptosis Signal-Regulating Kinase 1 in Ischemia-Induced Angiogenesis

Heparin-Binding Epidermal Growth Factor–Like Growth Factor, Collateral Vessel Development, and Angiogenesis in Skeletal Muscle Ischemia

Aldehyde Dehydrogenase 2 Plays a Role in the Bioactivation of Nitroglycerin in Humans

Atherosclerosis and Lipoproteins

Overexpression of Human Apolipoprotein A-II in Transgenic Mice Does Not Impair Macrophage-Specific Reverse Cholesterol Transport In Vivo

Overexpression of Human Apolipoprotein A-II in Transgenic Mice Does Not Impair Macrophage-Specific Reverse Cholesterol Transport In Vivo

PPAR, but not PPAR, Activators Decrease Macrophage-Laden Atherosclerotic Lesions in a Nondiabetic Mouse Model of Mixed Dyslipidemia

Rosiglitazone Attenuates Atherosclerosis in a Model of Insulin Insufficiency Independent of Its Metabolic Effects

Atherosclerotic Lesion Development in a Novel Ovary-Intact Mouse Model of Perimenopause

Genetic Deletion or Antibody Blockade of 1ß1 Integrin Induces a Stable Plaque Phenotype in ApoE–/– Mice

Association Between Prostaglandin E Receptor Subtype EP4 Overexpression and Unstable Phenotype in Atherosclerotic Plaques in Human

An Oral ApoJ Peptide Renders HDL Antiinflammatory in Mice and Monkeys and Dramatically Reduces Atherosclerosis in Apolipoprotein E–Null Mice

Cytoplasmic Expression and Extracellular Deposition of an Antiangiogenic Factor, Pigment Epithelium-Derived Factor, in Human Atherosclerotic Plaques

Cytosolic Lipid Droplets Increase in Size by Microtubule-Dependent Complex Formation

Effects of Diet and Simvastatin on Fatty Acid Composition in Hypercholesterolemic Men: A Randomized Controlled Trial

Tendon Xanthomas in Familial Hypercholesterolemia Are Associated With Cardiovascular Risk Independently of the Low-Density Lipoprotein Receptor Gene Mutation

Relationship of Monocyte Count and Peripheral Arterial Disease: Results From the National Health and Nutrition Examination Survey 1999–2002

The Molecular Basis of Lecithin:Cholesterol Acyltransferase Deficiency Syndromes: A Comprehensive Study of Molecular and Biochemical Findings in 13 Unrelated Italian Families

Hepatic and Cardiovascular Consequences of Familial Hypobetalipoproteinemia

Familial Combined Hyperlipidemia in Mexicans: Association With Upstream Transcription Factor 1 and Linkage on Chromosome 16q24.1

Thrombosis

Recurrence Rate After a First Venous Thrombosis in Patients With Familial Thrombophilia

Protective Mechanisms of Inosine in Platelet Activation and Cerebral Ischemic Damage

Endogenous NO Blockade Enhances Tissue Factor Expression via Increased Ca2+ Influx Through MCP-1 in Endothelial Cells by Monocyte Adhesion

Letters to the Editor

Consequences of Cholesteryl Ester Transfer Protein Inhibition in Patients With Familial Hypoalphalipoproteinemia

Toll-Like Receptors, Endocrine Stress Response, and Arteriosclerosis

Lipopolysaccharide (LPS) Contamination Plays the Real Role in C-Reactive Protein–Induced IL-6 Secretion From Human Endothelial Cells In Vitro

Association of C-Reactive Protein With Blood Pressure

Spotlight

Differential Antiatherogenic Effects of PPAR ${alpha}$ Versus PPAR ${gamma}$ Agonists: Should We Be Surprised?

Peroxisome Proliferator-Activated Receptor ${gamma}$ Ligands Stimulate Endothelial Nitric Oxide Production Through Distinct Peroxisome Proliferator-Activated Receptor ${gamma}$ –Dependent Mechanisms

Signal-Crosstalk Between Rho/ROCK and c-Jun NH₂-Terminal Kinase Mediates Migration of Vascular Smooth Muscle Cells Stimulated by Angiotensin II

CD34⁺ Cells Home, Proliferate, and Participate in Capillary Formation, and in Combination With CD34^– Cells Enhance Tube Formation in a 3-Dimensional Matrix

PPAR ${alpha}$ , but not PPAR ${gamma}$ , Activators Decrease Macrophage-Laden Atherosclerotic Lesions in a Nondiabetic Mouse Model of Mixed Dyslipidemia

Genetic Deletion or Antibody Blockade of ${alpha}$ 1ß1 Integrin Induces a Stable Plaque Phenotype in ApoE–/– Mice

Endogenous NO Blockade Enhances Tissue Factor Expression via Increased Ca²⁺ Influx Through MCP-1 in Endothelial Cells by Monocyte Adhesion