Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (25 [12])

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Volume 25, Issue 12; December 1, 2005

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

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	Editorials
	Mechanisms of Statin-Induced Myopathy: A Role for the Ubiquitin–Proteasome Pathway? M. John Chapman and Alain Carrie Arterioscler Thromb Vasc Biol. 2005;25:2441-2444, doi:10.1161/10.1161/01.ATV.0000194548.11901.a4. Full Text \| PDF
	Apolipoprotein AV: Low Concentration, High Impact Patrick C.N. Rensen, Ko Willems van Dijk, and Louis M. Havekes Arterioscler Thromb Vasc Biol. 2005;25:2445-2447, doi:10.1161/01.ATV.0000193889.65915.f9. Full Text \| PDF
	Killing Two Birds With One Stone: Targeting Chemokine Receptors in Atherosclerosis and HIV Infection Christian Weber Arterioscler Thromb Vasc Biol. 2005;25:2448-2450, doi:10.1161/01.ATV.0000194554.36789.ab. Full Text \| PDF
	Brief Reviews
	Fast Food, Central Nervous System Insulin Resistance, and Obesity Elvira Isganaitis and Robert H. Lustig Arterioscler Thromb Vasc Biol. 2005;25:2451-2462; published online before print September 15 2005, doi:10.1161/01.ATV.0000186208.06964.91. Abstract \| Full Text \| PDF Rates of obesity and insulin resistance have climbed sharply over the past 30 years. These epidemics are temporally related to a dramatic rise in consumption of fast food; until recently, it was not known whether the fast food was driving the obesity, or vice versa. We review the unique properties of fast food that make it the ideal obesigenic foodstuff, and elucidate the mechanisms by which fast food intake contributes to obesity, emphasizing its effects on energy metabolism and on the central regulation of appetite.
	Positive Feedbacks of Coagulation: Their Role in Threshold Regulation Jolyon Jesty and Edward Beltrami Arterioscler Thromb Vasc Biol. 2005;25:2463-2469; published online before print September 22 2005, doi:10.1161/01.ATV.0000187463.91403.b2. Abstract \| Full Text \| PDF The clotting cascade has enormous amplification potential and requires critical regulation. When the positive-feedback reactions of clotting are regulated by inhibitors, thresholds result. These act like switches, with small stimuli and/or nonproductive local conditions generating no response, and larger stimuli or prothrombotic conditions producing a full, explosive response.
	Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in Humans James J. Oliver, David J. Webb, and David E. Newby Arterioscler Thromb Vasc Biol. 2005;25:2470-2479; published online before print October 6 2005, doi:10.1161/01.ATV.0000189309.05924.88. Abstract \| Full Text \| PDF Local release of tissue plasminogen activator from the endothelium is an important defense against intravascular thrombosis and can be assessed in vivo in humans. We describe the rationale and methodology for, and clinical relevance of, assessing acute endothelial tissue plasminogen activator release in humans.
	Adrenomedullin: A Protective Factor for Blood Vessels Johji Kato, Toshihiro Tsuruda, Toshihiro Kita, Kazuo Kitamura, and Tanenao Eto Arterioscler Thromb Vasc Biol. 2005;25:2480-2487; published online before print September 1 2005, doi:10.1161/01.ATV.0000184759.91369.f8. Abstract \| Full Text \| PDF The vasodilator peptide adrenomedullin exerts various vascular actions, and its gene is expressed in three layers of the vascular wall. Both pharmacological and gene-manipulation studies showed an inhibitory effect of adrenomedullin on intimal thickening and perivascular hyperplasia, suggesting a possible role in inhibiting the progression of vascular damage and remodeling.
	Vascular Biology
	${alpha}$ -Lipoic Acid Prevents Endothelial Dysfunction in Obese Rats via Activation of AMP-Activated Protein Kinase Woo Je Lee, In Kyu Lee, Hyoun Sik Kim, Yun Mi Kim, Eun Hee Koh, Jong Chul Won, Sung Min Han, Min-Seon Kim, Inho Jo, Goo Taeg Oh, In-Sun Park, Jang Hyun Youn, Seong-Wook Park, Ki-Up Lee, and Joong-Yeol Park Arterioscler Thromb Vasc Biol. 2005;25:2488-2494; published online before print October 13 2005, doi:10.1161/01.ATV.0000190667.33224.4c. Abstract \| Full Text \| PDF \| Data Supplement We tested whether reduced AMP-activated protein kinase (AMPK) activity in vascular endothelial cells is responsible for endothelial dysfunction in obese rats. {alpha}-Lipoic acid (ALA) improved endothelial dysfunction and normalized AMPK activity in obese rats. This study provides a rationale for the therapeutic use of ALA for vascular dysfunction.
	Tumor Necrosis Factor- ${alpha}$ –Induced Iron Sequestration and Oxidative Stress in Human Endothelial Cells Masayoshi Nanami, Tomomi Ookawara, Yoshinaga Otaki, Katsukiyo Ito, Rintarou Moriguchi, Koji Miyagawa, Yukiko Hasuike, Masaaki Izumi, Hironobu Eguchi, Keiichiro Suzuki, and Takeshi Nakanishi Arterioscler Thromb Vasc Biol. 2005;25:2495-2501; published online before print October 13 2005, doi:10.1161/01.ATV.0000190610.63878.20. Abstract \| Full Text \| PDF TNF-{alpha} induced upregulation of iron import proteins and downregulation of iron export protein in human endothelial cells via a posttranscriptional mechanism. These modifications could cause accumulation of iron in endothelium, increasing oxidative stress that might contribute importantly to the pathophysiologic processes of atherosclerosis.
	Vascular Neuronal NO Synthase Is Selectively Upregulated by Platelet-Derived Growth Factor: Involvement of the MEK/ERK Pathway Sei Nakata, Masato Tsutsui, Hiroaki Shimokawa, Masahito Tamura, Hiromi Tasaki, Tsuyoshi Morishita, Osamu Suda, Susumu Ueno, Yumiko Toyohira, Yasuhide Nakashima, and Nobuyuki Yanagihara Arterioscler Thromb Vasc Biol. 2005;25:2502-2508; published online before print October 13 2005, doi:10.1161/01.ATV.0000190663.88143.97. Abstract \| Full Text \| PDF \| Data Supplement This study demonstrates that vascular neuronal NO synthase (nNOS) expression is selectively upregulated in response to platelet-derived growth factor via activation of the ERK cascade. Upregulated nNOS may play an important compensatory role in the presence of reduced endothelial NOS activity (eg, arteriosclerosis) to maintain vascular homeostasis.
	Effect of Nuclear Actin on Endothelial Nitric Oxide Synthase Expression Hesheng Ou, Ying H. Shen, Budi Utama, Jian Wang, Xinwen Wang, Joseph Coselli, and Xing Li Wang Arterioscler Thromb Vasc Biol. 2005;25:2509-2514; published online before print October 6 2005, doi:10.1161/01.ATV.0000189306.99112.4c. Abstract \| Full Text \| PDF \| Data Supplement The 27nt repeat element in eNOS intron 4 functions as a cis-acting enhancer regulating eNOS expression. We found that nuclear actin binds on the 27nt DNA fragment and upregulates eNOS expression. Whereas nuclear actin may upregulate several other genes, its effect on eNOS depends on the presence of the 27nt enhancer
	Hyperhomocystinemia Impairs Endothelial Function and eNOS Activity via PKC Activation Xiaohua Jiang, Fan Yang, Hongmei Tan, Dan Liao, Robert M. Bryan, Jr, Jaspreet K. Randhawa, Rolando E. Rumbaut, William Durante, Andrew I. Schafer, Xiaofeng Yang, and Hong Wang Arterioscler Thromb Vasc Biol. 2005;25:2515-2521; published online before print October 6 2005, doi:10.1161/01.ATV.0000189559.87328.e4. Abstract \| Full Text \| PDF \| Data Supplement A risk factor for cardiovascular disease, hyperhomocystinemia (HHcy), is associated with endothelial dysfunction. In this study, we examined the mechanistic role of HHcy in endothelial dysfunction. Our data suggest that HHcy impairs endothelial function and eNOS activity, primarily through PKC activation.
	Upregulation of Proinflammatory Proteins Through NF- ${kappa}$ B Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity Angela Tesse, M. Carmen Martínez, Bénédicte Hugel, Karel Chalupsky, Christian D. Muller, Ferhat Meziani, Delia Mitolo-Chieppa, Jean-Marie Freyssinet, and Ramaroson Andriantsitohaina Arterioscler Thromb Vasc Biol. 2005;25:2522-2527; published online before print October 6 2005, doi:10.1161/01.ATV.0000189298.62240.5d. Abstract \| Full Text \| PDF \| Data Supplement Microparticles are membrane vesicles with procoagulant and proinflammatory properties released during cell activation. T cell-derived microparticles induce in vivo and in vitro vascular hyporeactivity associated with NO and prostacyclin production. Microparticles induce inducible NO synthase and cyclooxygenase-2, and evoke NF-{kappa}B activation through Fas/FasLigand pathway. Microparticles promote vascular dysfunction during inflammatory diseases.
	T Cell Modulation of Intimal Thickening After Vascular Injury: The Bimodal Role of IFN- ${gamma}$ in Immune Deficiency Paul C. Dimayuga, Hongyan Li, Kuang-Yuh Chyu, Gunilla Nordin Fredrikson, Jan Nilsson, Michael C. Fishbein, Prediman K. Shah, and Bojan Cercek Arterioscler Thromb Vasc Biol. 2005;25:2528-2534; published online before print October 13 2005, doi:10.1161/01.ATV.0000190606.41121.00. Abstract \| Full Text \| PDF \| Data Supplement Immune deficiency results in exuberant intimal thickening after arterial injury. We investigated the modulatory role of T cells and IFN-{gamma} in the response to injury in normal and immune-deficient Rag-1KO mice. The study adds novel insight in defining factors that contribute to vascular disease in conditions of immune deficiency.
	Therapeutic Angiogenesis With Intramuscular Injection of Low-Dose Recombinant Granulocyte-Colony Stimulating Factor Mejeong Lee, Mika Aoki, Takahisa Kondo, Koichi Kobayashi, Kenji Okumura, Kimihiro Komori, and Toyoaki Murohara Arterioscler Thromb Vasc Biol. 2005;25:2535-2541; published online before print October 13 2005, doi:10.1161/01.ATV.0000190609.28293.17. Abstract \| Full Text \| PDF \| Data Supplement G-CSF receptor was expressed in human umbilical vein endothelial cells (HUVECs). rhG-CSF (100 ng/mL) enhanced migration and tube formation but not proliferation of HUVECs. Moreover, local injection of low doses rhG-CSF augmented ischemia-induced angiogenesis in vivo. This treatment regimen of low-dose rhG-CSF may become a new and safe modality for therapeutic angiogenesis.
	Novel Autologous Cell Therapy in Ischemic Limb Disease Through Growth Factor Secretion by Cultured Adipose Tissue–Derived Stromal Cells Hironori Nakagami, Kazuhisa Maeda, Ryuichi Morishita, Sota Iguchi, Tomoyuki Nishikawa, Yoichi Takami, Yasushi Kikuchi, Yukihiro Saito, Katsuto Tamai, Toshio Ogihara, and Yasufumi Kaneda Arterioscler Thromb Vasc Biol. 2005;25:2542-2547; published online before print October 13 2005, doi:10.1161/01.ATV.0000190701.92007.6d. Abstract \| Full Text \| PDF \| Data Supplement The adipose tissue-derived cells (ADSCs) induced angiogenesis through secretion of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in coculture with endothelial cells or ischemic mouse hindlimb model. These results demonstrated the potential of ADSC as angiogenic cell therapy for ischemic disease.
	Role of Focal Adhesion Kinase in Flow-Induced Dilation of Coronary Arterioles Ryoji Koshida, Petra Rocic, Shuichi Saito, Takahiko Kiyooka, Cuihua Zhang, and William M. Chilian Arterioscler Thromb Vasc Biol. 2005;25:2548-2553; published online before print September 29 2005, doi:10.1161/01.ATV.0000188511.84138.9b. Abstract \| Full Text \| PDF Although NO-mediated flow-induced dilation (FID) has been observed by many groups, the signal transduction pathway is still not totally resolved. We sought to determine the role of focal adhesion kinase in FID by loading endothelial cells of intact, isolated coronary resistance vessels with an anti-FAK that prevented its downstream signaling. Anti-FAK blocked FID but not dilation to endothelium-dependent and -independent agonists. Anti-FAK also prevented the flow-dependent phosphorylation of Akt and eNOS, 2 enzymes essential for FID. We conclude that FAK plays a pivotal role in NO-mediated FID.
	Mechanisms of Increased Vascular Superoxide Production in an Experimental Model of Idiopathic Dilated Cardiomyopathy Hanke Mollnau, Matthias Oelze, Michael August, Maria Wendt, Andreas Daiber, Eberhard Schulz, Stephan Baldus, Andrei L. Kleschyov, Anke Materne, Philip Wenzel, Ulrich Hink, Georg Nickenig, Ingrid Fleming, and Thomas Münzel Arterioscler Thromb Vasc Biol. 2005;25:2554-2559; published online before print October 13 2005, doi:10.1161/01.ATV.0000190673.41925.9B. Abstract \| Full Text \| PDF \| Data Supplement In vessels from cardiomyopathic hamsters, we identified NOSIII and NADPH oxidase as significant superoxide sources. Oxidative stress was associated with a decrease in vascular NO production and NOSIII expression, leading to inhibition of NO downstream signaling. Captopril treatment prevented these phenomena, indicating a crucial role of the renin-angiotensin-aldosterone system.
	Atherosclerosis and Lipoproteins
	Changes in Ubiquitin Proteasome Pathway Gene Expression in Skeletal Muscle With Exercise and Statins Maria L. Urso, Priscilla M. Clarkson, Dustin Hittel, Eric P. Hoffman, and Paul D. Thompson Arterioscler Thromb Vasc Biol. 2005;25:2560-2566; published online before print October 13 2005, doi:10.1161/01.ATV.0000190608.28704.71. Abstract \| Full Text \| PDF \| Data Supplement Statins are safe medications but have side effects including myalgia and rhabdomyolysis. How statins provoke muscle damage is not known, but this effect is exacerbated by exercise. This is the first investigation to our knowledge to implicate involvement of the UPP in skeletal muscle in response to combined exercise and statin treatment, possibly explaining the onset of myalgia with exertion. Statins may alter the response of muscle to exercise stress by altering the action of the UPP, protein folding, and catabolism, disrupting the balance between protein degradation and repair.
	Expression of Fractalkine (CX3CL1) and its Receptor, CX3CR1, Is Elevated in Coronary Artery Disease and Is Reduced During Statin Therapy Jan K. Damås, Agnes Boullier, Torgun Wæhre, Camilla Smith, Wiggo J. Sandberg, Simone Green, Pål Aukrust, and Oswald Quehenberger Arterioscler Thromb Vasc Biol. 2005;25:2567-2572; published online before print October 13 2005, doi:10.1161/01.ATV.0000190672.36490.7b. Abstract \| Full Text \| PDF \| Data Supplement We show increased plasma levels of CX3CL1 and enhanced expression of its cognate receptor, CX3CR1, on T cells in patients with coronary artery disease. These changes were accompanied by an increased chemotactic and adhesive response to CX3CL1. Statin therapy reduced the CX3CL1/CX3CR1 levels and normalized the functional responses to CX3CL1.
	Apolipoprotein A-V Deficiency Results in Marked Hypertriglyceridemia Attributable to Decreased Lipolysis of Triglyceride-Rich Lipoproteins and Removal of Their Remnants Itamar Grosskopf, Nadine Baroukh, Sung-Joon Lee, Yehuda Kamari, Dror Harats, Edward M. Rubin, Len A. Pennacchio, and Allen D. Cooper Arterioscler Thromb Vasc Biol. 2005;25:2573-2579; published online before print September 15 2005, doi:10.1161/01.ATV.0000186189.26141.12. Abstract \| Full Text \| PDF \| Data Supplement Absence of apoAV in mice slows lipolysis of triglyceride-rich lipoproteins and the removal of their remnants by regulating their apoproteins. In humans decreased apoAV could be atherogenic by increasing remnant residence time in the circulation. As this is elucidated the potential of apoAV as a therapeutic target will be clarified.
	Measures of Oxidized Low-Density Lipoprotein and Oxidative Stress Are Not Related and Not Elevated in Otherwise Healthy Men With the Metabolic Syndrome Per Sjogren, Samar Basu, Magdalena Rosell, Angela Silveira, Ulf de Faire, Bengt Vessby, Anders Hamsten, Mai-Lis Hellenius, and Rachel M. Fisher Arterioscler Thromb Vasc Biol. 2005;25:2580-2586; published online before print October 13 2005, doi:10.1161/01.ATV.0000190675.08857.3d. Abstract \| Full Text \| PDF Increases of oxLDL and measures of oxidative stress have been proposed to be related to the metabolic syndrome. However, in this study, oxLDL and measures of oxidative stress were not increased in otherwise healthy individuals with the metabolic syndrome. Furthermore, no relationships between oxLDL and measures of oxidative stress were found.
	Plasma Level of Endogenous Secretory RAGE Is Associated With Components of the Metabolic Syndrome and Atherosclerosis Hidenori Koyama, Takuhito Shoji, Hisayo Yokoyama, Kohka Motoyama, Katsuhito Mori, Shinya Fukumoto, Masanori Emoto, Tetsuo Shoji, Hironori Tamei, Hirokazu Matsuki, Shigeru Sakurai, Yasuhiko Yamamoto, Hideto Yonekura, Takuo Watanabe, Hiroshi Yamamoto, and Yoshiki Nishizawa Arterioscler Thromb Vasc Biol. 2005;25:2587-2593; published online before print October 13 2005, doi:10.1161/01.ATV.0000190660.32863.cd. Abstract \| Full Text \| PDF Endogenous secretory RAGE, esRAGE, has been identified as an alternatively spliced form of RAGE, and shown to act as a decoy receptor for AGE. Here, we show that plasma esRAGE was inversely and independently associated with carotid atherosclerosis or components of the metabolic syndrome, even in the absence of diabetes.
	Production of Chemokines by Perivascular Adipose Tissue: A Role in the Pathogenesis of Atherosclerosis? Elvire Henrichot, Cristiana E. Juge-Aubry, Agnès Pernin, Jean-Claude Pache, Valdimir Velebit, Jean-Michel Dayer, Paolo Meda, Carlo Chizzolini, and Christoph A. Meier Arterioscler Thromb Vasc Biol. 2005;25:2594-2599; published online before print September 29 2005, doi:10.1161/01.ATV.0000188508.40052.35. Abstract \| Full Text \| PDF \| Data Supplement Perivascular adipose tissue (pWAT) is found in close proximity of the vascular wall of aortas. This strategic location suggests an impact of pWAT on vascular wall function. Indeed, supernatant from human pWAT has a net chemotactic effect on blood leukocytes, which is mainly mediated via the secretion of chemokines.
	Effect of Fenofibrate on Plasma Lipoprotein Composition and Kinetics in Patients With Complete Hepatic Lipase Deficiency Isabelle L. Ruel, Benoît Lamarche, Jean-François Mauger, Karen O. Badellino, Jeffrey S. Cohn, Michel Marcil, and Patrick Couture Arterioscler Thromb Vasc Biol. 2005;25:2600-2607; published online before print October 13 2005, doi:10.1161/01.ATV.0000190700.76493.bb. Abstract \| Full Text \| PDF Fenofibrate treatment in 2 patients with complete HL deficiency was associated with a marked reduction in plasma triglyceride concentration and an improvement in the composition and metabolism of all apoB-containing lipoproteins, indicating that fenofibrate can have pronounced antiatherogenic effects on plasma lipoprotein metabolism even in the complete absence of HL.
	A Novel Inhibitor of Oxidosqualene:Lanosterol Cyclase Inhibits Very Low–Density Lipoprotein Apolipoprotein B100 (ApoB100) Production and Enhances Low-Density Lipoprotein ApoB100 Catabolism Through Marked Reduction in Hepatic Cholesterol Content Dawn E. Telford, Sara M. Lipson, P. Hugh R. Barrett, Brian G. Sutherland, Jane Y. Edwards, Johannes D. Aebi, Henrietta Dehmlow, Olivier H. Morand, and Murray W. Huff Arterioscler Thromb Vasc Biol. 2005;25:2608-2614; published online before print October 6 2005, doi:10.1161/01.ATV.0000189158.28455.94. Abstract \| Full Text \| PDF \| Data Supplement In miniature pigs, a novel OSC inhibitor, RO0717625, decreased VLDL and LDL apoB100 through decreased VLDL production and increased LDL receptor-mediated LDL apoB clearance. Cholesterol synthesis and postprandial cholesterol transport in chylomicrons decreased, resulting in a marked reduction in hepatic cholesterol concentration. Thus, OSC is a potential therapeutic target for dyslipidemia.
	Delayed In Vivo Catabolism of Intermediate-Density Lipoprotein and Low-Density Lipoprotein in Hemodialysis Patients as Potential Cause of Premature Atherosclerosis Katsunori Ikewaki, Juergen R. Schaefer, Michael E. Frischmann, Keio Okubo, Tatsuo Hosoya, Seibu Mochizuki, Benjamin Dieplinger, Evi Trenkwalder, Horst Schweer, Florian Kronenberg, Paul Koenig, and Hans Dieplinger Arterioscler Thromb Vasc Biol. 2005;25:2615-2622; published online before print September 29 2005, doi:10.1161/01.ATV.0000188555.60475.c2. Abstract \| Full Text \| PDF The metabolism of atherogenic LDL in hemodialysis (HD) patients who are at high risk for cardiovascular disease (CVD) is still poorly understood. We here report a severely impaired catabolism of LDL and IDL (misleadingly masked by normal plasma cholesterol levels) in 12 HD patients compared with 13 controls, investigated by stable-isotope technology. The resulting markedly prolonged residence times of both IDL and LDL particles might thus significantly contribute to the well-documented high risk for premature CVD in HD patients.
	Peroxynitrite Causes Endoplasmic Reticulum Stress and Apoptosis in Human Vascular Endothelium: Implications in Atherogenesis Jeffrey G. Dickhout, Gazi S. Hossain, Lindsay M. Pozza, Ji Zhou, Sárka Lhoták, and Richard C. Austin Arterioscler Thromb Vasc Biol. 2005;25:2623-2629; published online before print October 6 2005, doi:10.1161/01.ATV.0000189159.96900.d9. Abstract \| Full Text \| PDF \| Data Supplement Peroxynitrite induces ER stress in human vascular endothelial cells, depletes ER-Ca2+, and induces programmed cell death. Overexpression of GRP78 prevents peroxynitrite-induced apoptosis. Consistent with these findings, 3-nitrotyrosine and GRP78 overexpression colocalize in early atherosclerotic lesions from apoE-/- mice.
	Smoking, Endothelial Function, and Rho-Kinase in Humans Kensuke Noma, Chikara Goto, Kenji Nishioka, Keiko Hara, Masashi Kimura, Takashi Umemura, Daisuke Jitsuiki, Keigo Nakagawa, Tetsuya Oshima, Kazuaki Chayama, Masao Yoshizumi, and Yukihito Higashi Arterioscler Thromb Vasc Biol. 2005;25:2630-2635; published online before print October 6 2005, doi:10.1161/01.ATV.0000189304.32725.bd. Abstract \| Full Text \| PDF Smoking is associated with endothelial dysfunction and activated Rho-kinase in vascular smooth muscle cells (VSMCs) in humans. The purpose of this study was to elucidate the relationship between endothelial function and Rho-kinase activity in forearm VSMCs in healthy young men. Our findings suggest that smoking is involved in not only endothelial dysfunction but also activation of Rho-kinase in VSMCs in forearm circulation, and that there is a significant correlation between endothelial function and Rho-kinase activity in VSMCs.
	Transfer of Endothelial Progenitor and Bone Marrow Cells Influences Atherosclerotic Plaque Size and Composition in Apolipoprotein E Knockout Mice Jacob George, Arnon Afek, Anastasia Abashidze, Haim Shmilovich, Varda Deutsch, Juri Kopolovich, Hylton Miller, and Gad Keren Arterioscler Thromb Vasc Biol. 2005;25:2636-2641; published online before print September 29 2005, doi:10.1161/01.ATV.0000188554.49745.9e. Abstract \| Full Text \| PDF Transfer of EPCs and BM cells significantly increased plaque size in apoE KO mice, whereas only the former treatment was associated with destabilization of the lesions. BM cell and EPC transfer reduced aortic expression of IL-10. Thus, cell therapy with BM cells should be used with caution in clinical trials.
	HIV Entry Inhibitor TAK-779 Attenuates Atherogenesis in Low-Density Lipoprotein Receptor–Deficient Mice Eva J.A. van Wanrooij, Hester Happé, Arnaud D. Hauer, Paula de Vos, Takeshi Imanishi, Hiromi Fujiwara, Theo J.C. van Berkel, and Johan Kuiper Arterioscler Thromb Vasc Biol. 2005;25:2642-2647; published online before print October 20 2005, doi:10.1161/01.ATV.0000192018.90021.c0. Abstract \| Full Text \| PDF \| Data Supplement The HIV entry inhibitor TAK-779, a CCR5/CXCR3 antagonist, reduced atherogenesis by blocking the influx of Th1 cells into the plaque. We conclude that HIV entry inhibitors, because of their antiatherogenic properties, are preferred for treatment of HIV-positive patients.
	Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum S. Claiborne Johnston, Hui Zhang, Louis M. Messina, Michael T. Lawton, and Deborah Dean Arterioscler Thromb Vasc Biol. 2005;25:2648-2653; published online before print October 6 2005, doi:10.1161/01.ATV.0000189157.88630.d1. Abstract \| Full Text \| PDF Serum interleukin-6 (IL-6) and C-reactive protein (CRP) are risk factors for stroke. Carotid plaque Chlamydia pneumoniae (Cpn) burden may contribute to these factors. Burden was significantly associated with IL-6 plaque expression, which was associated with serum IL-6 and CRP. Cpn is associated with inflammation and atherogenesis via upregulation of local and systemic inflammatory markers.
	Severe Hypercholesterolemia in Four British Families With the D374Y Mutation in the PCSK9 Gene: Long-Term Follow-Up and Treatment Response Rossi P. Naoumova, Isabella Tosi, Dilip Patel, Clare Neuwirth, Stuart D. Horswell, A. David Marais, Charles van Heyningen, and Anne K. Soutar Arterioscler Thromb Vasc Biol. 2005;25:2654-2660; published online before print October 13 2005, doi:10.1161/01.ATV.0000190668.94752.ab. Abstract \| Full Text \| PDF \| Data Supplement Thirteen British patients with the D374Y mutation of PCSK9 were compared with 36 similar patients with heterozygous familial hypercholesterolemia caused by LDLR mutations and were found to have higher total cholesterol levels, pretreatment and on-treatment with statins, and were affected >10 years earlier by severe atherosclerosis.
	Thrombosis
	Platelet Nitric Oxide Responsiveness: A Novel Prognostic Marker in Acute Coronary Syndromes Scott R. Willoughby, Simon Stewart, Andrew S. Holmes, Yuliy Y. Chirkov, and John D. Horowitz Arterioscler Thromb Vasc Biol. 2005;25:2661-2666; published online before print October 27 2005, doi:10.1161/01.ATV.0000193622.77294.57. Abstract \| Full Text \| PDF \| Data Supplement We tested the hypotheses that platelet hyporesponsiveness to nitric oxide (NO) at time of admission is a predictor cardiovascular readmission and/or death and all-cause mortality in high-risk patients (n=51) with ACS. Impaired NO responsiveness was associated with an {approx}3-fold increased risk of the combination of cardiovascular readmission and/or death and {approx}6-fold incremental risk of all-cause mortality. Severe impairment of platelet responsiveness to NO is, thus, an independent prognostic marker in such patients and may more directly reflect risk of vascular events than measures of endothelial dysfunction.
	Genetic Variations in the Tissue Factor Gene Are Associated With Clinical Outcome in Acute Coronary Syndrome and Expression Levels in Human Monocytes Anders Mälarstig, Taavo Tenno, Nina Johnston, Bo Lagerqvist, Tomas Axelsson, Ann-Christine Syvänen, Lars Wallentin, and Agneta Siegbahn Arterioscler Thromb Vasc Biol. 2005;25:2667-2672; published online before print October 20 2005, doi:10.1161/01.ATV.0000191637.48129.9b. Abstract \| Full Text \| PDF \| Data Supplement Polymorphisms in the tissue factor gene were investigated concerning association with risk and outcome in patients with acute coronary syndrome. The TF 5466 AG genotype was associated with cardiovascular death. In vitro endotoxin induced a relative increase in monocytic TF activity, which was significantly higher in AG compared with AA carriers.
	The Glycoprotein VI-Phospholipase C ${gamma}$ 2 Signaling Pathway Controls Thrombus Formation Induced by Collagen and Tissue Factor In Vitro and In Vivo Imke C.A. Munnix, Amrei Strehl, Marijke J.E. Kuijpers, Jocelyn M. Auger, Paola E.J. van der Meijden, Marc A.M. van Zandvoort, Mirjam G.A. oude Egbrink, Bernhard Nieswandt, and Johan W.M. Heemskerk Arterioscler Thromb Vasc Biol. 2005;25:2673-2678; published online before print October 27 2005, doi:10.1161/01.ATV.0000193568.71980.4a. Abstract \| Full Text \| PDF \| Data Supplement We investigated the contribution of the signaling modules glycoprotein VI, FcR {gamma}-chain, Src-kinases, LAT, and phospholipase C{gamma}2 in collagen- and tissue factor-induced thrombus formation. This signaling pathway regulated the formation of procoagulant platelets on collagen, collagen-enhanced thrombin generation, and fibrin clot formation under flow in vitro and in vivo.
	Fibrinogen Contains Cryptic PAI-1 Binding Sites That Are Exposed on Binding to Solid Surfaces or Limited Proteolysis Katarzyna Smolarczyk, Joanna Boncela, Jacek Szymanski, Ann Gils, and Czeslaw S. Cierniewski Arterioscler Thromb Vasc Biol. 2005;25:2679-2684; published online before print October 6 2005, doi:10.1161/01.ATV.0000189305.84297.8b. Abstract \| Full Text \| PDF \| Data Supplement We showed that PAI-1 is directly bound to the {alpha}(20-88) and thus its concentration on fibrinogen/fibrin, particularly at sites of injury and inflammation, may account for the recent observations that both its active and latent forms stimulate cell migration and wound healing.
	Letters to the Editor
	Letter to the Editor: Cell-Based Ex Vivo Delivery of Angiogenic Growth Factors for Cardiac Repair Husnain Kh. Haider, Eugene K.W. Sim, Ye Lei, and Muhammad Ashraf Arterioscler Thromb Vasc Biol. 2005;25:e144, doi:10.1161/01.ATV.0000190665.72652.d7. Full Text \| PDF
	Early Anticoagulant Effect of Atorvastatin Pasquale Pignatelli, Valerio Sanguigni, Barbara Buchetti, Luisa Lenti, Francesco Violi, Anetta Undas, and Kenneth G. Mann Arterioscler Thromb Vasc Biol. 2005;25:e145-e146, doi:10.1161/01.ATV.0000190697.74465.ab. Full Text \| PDF
	Letter to the Editor: Dissociation Between the Short-Term Effects of Nocturnal Hemodialysis on Endothelium Dependent Vasodilation and Plasma ADMA Christopher T. Chan, Paula J. Harvey, Rainer Böger, Andreas Pierratos, and John S. Floras Arterioscler Thromb Vasc Biol. 2005;25:2685-2686, doi:10.1161/01.ATV.0000193890.94720.1a. Full Text \| PDF \| Data Supplement
	Letter to the Editor: Associations Between Liver Histology and Carotid Intima-Media Thickness in Patients With Nonalcoholic Fatty Liver Disease Giovanni Targher, Lorenzo Bertolini, Roberto Padovani, Giacomo Zoppini, Luciano Zenari, and Giancarlo Falezza Arterioscler Thromb Vasc Biol. 2005;25:2687-2688, doi:10.1161/01.ATV.0000189299.61568.79. Full Text \| PDF
	Letter to the Editor: Heparin Cofactor II Levels Do Not Predict the Development of Coronary Heart Disease: The Atherosclerosis Risk in Communities (ARIC) Study Tusar K. Giri, Chul W. Ahn, Kenneth K. Wu, and Douglas M. Tollefsen Arterioscler Thromb Vasc Biol. 2005;25:2689-2690, doi:10.1161/01.ATV.0000193888.71297.f3. Full Text \| PDF \| Data Supplement

Spotlight

TOC Spotlight File

Volume 25, Issue 12; December 1, 2005

Editorials

Mechanisms of Statin-Induced Myopathy: A Role for the Ubiquitin–Proteasome Pathway?

Apolipoprotein AV: Low Concentration, High Impact

Killing Two Birds With One Stone: Targeting Chemokine Receptors in Atherosclerosis and HIV Infection

Brief Reviews

Fast Food, Central Nervous System Insulin Resistance, and Obesity

Positive Feedbacks of Coagulation: Their Role in Threshold Regulation

Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in Humans

Adrenomedullin: A Protective Factor for Blood Vessels

Vascular Biology

-Lipoic Acid Prevents Endothelial Dysfunction in Obese Rats via Activation of AMP-Activated Protein Kinase

Tumor Necrosis Factor-–Induced Iron Sequestration and Oxidative Stress in Human Endothelial Cells

Vascular Neuronal NO Synthase Is Selectively Upregulated by Platelet-Derived Growth Factor: Involvement of the MEK/ERK Pathway

Effect of Nuclear Actin on Endothelial Nitric Oxide Synthase Expression

Hyperhomocystinemia Impairs Endothelial Function and eNOS Activity via PKC Activation

Upregulation of Proinflammatory Proteins Through NF-B Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity

T Cell Modulation of Intimal Thickening After Vascular Injury: The Bimodal Role of IFN- in Immune Deficiency

Therapeutic Angiogenesis With Intramuscular Injection of Low-Dose Recombinant Granulocyte-Colony Stimulating Factor

Novel Autologous Cell Therapy in Ischemic Limb Disease Through Growth Factor Secretion by Cultured Adipose Tissue–Derived Stromal Cells

Role of Focal Adhesion Kinase in Flow-Induced Dilation of Coronary Arterioles

Mechanisms of Increased Vascular Superoxide Production in an Experimental Model of Idiopathic Dilated Cardiomyopathy

Atherosclerosis and Lipoproteins

Changes in Ubiquitin Proteasome Pathway Gene Expression in Skeletal Muscle With Exercise and Statins

Expression of Fractalkine (CX3CL1) and its Receptor, CX3CR1, Is Elevated in Coronary Artery Disease and Is Reduced During Statin Therapy

Apolipoprotein A-V Deficiency Results in Marked Hypertriglyceridemia Attributable to Decreased Lipolysis of Triglyceride-Rich Lipoproteins and Removal of Their Remnants

Measures of Oxidized Low-Density Lipoprotein and Oxidative Stress Are Not Related and Not Elevated in Otherwise Healthy Men With the Metabolic Syndrome

Plasma Level of Endogenous Secretory RAGE Is Associated With Components of the Metabolic Syndrome and Atherosclerosis

Production of Chemokines by Perivascular Adipose Tissue: A Role in the Pathogenesis of Atherosclerosis?

Effect of Fenofibrate on Plasma Lipoprotein Composition and Kinetics in Patients With Complete Hepatic Lipase Deficiency

A Novel Inhibitor of Oxidosqualene:Lanosterol Cyclase Inhibits Very Low–Density Lipoprotein Apolipoprotein B100 (ApoB100) Production and Enhances Low-Density Lipoprotein ApoB100 Catabolism Through Marked Reduction in Hepatic Cholesterol Content

Delayed In Vivo Catabolism of Intermediate-Density Lipoprotein and Low-Density Lipoprotein in Hemodialysis Patients as Potential Cause of Premature Atherosclerosis

Peroxynitrite Causes Endoplasmic Reticulum Stress and Apoptosis in Human Vascular Endothelium: Implications in Atherogenesis

Smoking, Endothelial Function, and Rho-Kinase in Humans

Transfer of Endothelial Progenitor and Bone Marrow Cells Influences Atherosclerotic Plaque Size and Composition in Apolipoprotein E Knockout Mice

HIV Entry Inhibitor TAK-779 Attenuates Atherogenesis in Low-Density Lipoprotein Receptor–Deficient Mice

Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Severe Hypercholesterolemia in Four British Families With the D374Y Mutation in the PCSK9 Gene: Long-Term Follow-Up and Treatment Response

Thrombosis

Platelet Nitric Oxide Responsiveness: A Novel Prognostic Marker in Acute Coronary Syndromes

Genetic Variations in the Tissue Factor Gene Are Associated With Clinical Outcome in Acute Coronary Syndrome and Expression Levels in Human Monocytes

The Glycoprotein VI-Phospholipase C2 Signaling Pathway Controls Thrombus Formation Induced by Collagen and Tissue Factor In Vitro and In Vivo

Fibrinogen Contains Cryptic PAI-1 Binding Sites That Are Exposed on Binding to Solid Surfaces or Limited Proteolysis

Letters to the Editor

Letter to the Editor: Cell-Based Ex Vivo Delivery of Angiogenic Growth Factors for Cardiac Repair

Early Anticoagulant Effect of Atorvastatin

Letter to the Editor: Dissociation Between the Short-Term Effects of Nocturnal Hemodialysis on Endothelium Dependent Vasodilation and Plasma ADMA

Letter to the Editor: Associations Between Liver Histology and Carotid Intima-Media Thickness in Patients With Nonalcoholic Fatty Liver Disease

Letter to the Editor: Heparin Cofactor II Levels Do Not Predict the Development of Coronary Heart Disease: The Atherosclerosis Risk in Communities (ARIC) Study

Spotlight

${alpha}$ -Lipoic Acid Prevents Endothelial Dysfunction in Obese Rats via Activation of AMP-Activated Protein Kinase

Tumor Necrosis Factor- ${alpha}$ –Induced Iron Sequestration and Oxidative Stress in Human Endothelial Cells

Upregulation of Proinflammatory Proteins Through NF- ${kappa}$ B Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity

T Cell Modulation of Intimal Thickening After Vascular Injury: The Bimodal Role of IFN- ${gamma}$ in Immune Deficiency

The Glycoprotein VI-Phospholipase C ${gamma}$ 2 Signaling Pathway Controls Thrombus Formation Induced by Collagen and Tissue Factor In Vitro and In Vivo