Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (26 [6])

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Volume 26, Issue 6; June 1, 2006

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

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	Editorials
	Ruptures of Delight?: A New Mouse Model of Plaque Rupture Christopher L. Jackson Arterioscler Thromb Vasc Biol. 2006;26:1191-1192, doi:10.1161/01.ATV.0000222905.77560.c7. Full Text \| PDF
	Plasma Fibronectin Concentration: A Risk Factor for Arterial Thrombosis? Deane F. Mosher Arterioscler Thromb Vasc Biol. 2006;26:1193-1195, doi:10.1161/01.ATV.0000223342.15969.7a. Full Text \| PDF
	Maintenance of Vascular Homeostasis by Bone Marrow–Derived Cells Julie Sainz and Masataka Sata Arterioscler Thromb Vasc Biol. 2006;26:1196-1197, doi:10.1161/01.ATV.0000220378.06854.35. Full Text \| PDF
	Insight Into ABCG1-Mediated Cholesterol Efflux Jonathan D. Smith Arterioscler Thromb Vasc Biol. 2006;26:1198-1200, doi:10.1161/01.ATV.0000221217.86465.66. Full Text \| PDF
	Lipoprotein Metabolism: A Well-Tried Tool to Characterize Dyslipidemic Mechanisms Lars Berglund Arterioscler Thromb Vasc Biol. 2006;26:1201-1203, doi:10.1161/01.ATV.0000217281.06795.61. Full Text \| PDF
	Lipoxygenase Pathways as Mediators of Early Inflammatory Events in Atherosclerosis Colin D. Funk Arterioscler Thromb Vasc Biol. 2006;26:1204-1206, doi:10.1161/01.ATV.0000222960.43792.ff. Full Text \| PDF
	Brief Reviews
	Nitric Oxide and Posttranslational Modification of the Vascular Proteome: S-Nitrosation of Reactive Thiols Diane E. Handy and Joseph Loscalzo Arterioscler Thromb Vasc Biol. 2006;26:1207-1214; published online before print March 16 2006, doi:10.1161/01.ATV.0000217632.98717.a0. Abstract \| Full Text \| PDF Nitric oxide (NO{middle dot}) is known to exert its effects via guanylyl cyclase and cyclic GMP- dependent pathways and by cyclic GMP-independent pathways, including the posttranslational modification of proteins. Much ongoing research is focused on defining the mechanisms of NO{middle dot}-mediated protein modification, the identity and function of the modified proteins, and the significance of these changes in health and disease. Specific findings suggest the utility of using proteomic methods to identify unique targets for protein S-nitrosation to understand further the molecular mechanisms of the effects of NO{middle dot}.
	Endothelium-Derived Hyperpolarizing Factor: Where Are We Now? Michel Félétou and Paul M. Vanhoutte Arterioscler Thromb Vasc Biol. 2006;26:1215-1225; published online before print March 16 2006, doi:10.1161/01.ATV.0000217611.81085.c5. Abstract \| Full Text \| PDF EDHF-mediated responses involve the activation of endothelial potassium channels. The hyperpolarization of the smooth muscle is evoked through myo-endothelial junctions and/or the accumulation of K+ in the intercellular space. Additionally, the endothelium releases factors that can hyperpolarize the smooth muscle cells such as reactive oxygen species and arachidonic acid metabolites.
	Genome-Wide Expression Studies of Atherosclerosis: Critical Issues in Methodology, Analysis, Interpretation of Transcriptomics Data A.P.J.J. Bijnens, E. Lutgens, T. Ayoubi, J. Kuiper, A.J. Horrevoets, and M.J.A.P. Daemen Arterioscler Thromb Vasc Biol. 2006;26:1226-1235; published online before print March 30 2006, doi:10.1161/01.ATV.0000219289.06529.f1. Abstract \| Full Text \| PDF \| Data Supplement This review discusses some critical issues in the methodology, analysis, and interpretation of gene expression studies using vascular specimens from animals and humans. Our analysis demonstrates that future studies may benefit from recent developments in statistical and bioinformatical analysis methods to exploit the full potential of transcriptomics data.
	Lipoprotein Lipase S447X: A Naturally Occurring Gain-of-Function Mutation Jaap Rip, Melchior C. Nierman, Colin J. Ross, Jan Wouter Jukema, Michael R. Hayden, John J.P. Kastelein, Erik S.G. Stroes, and Jan Albert Kuivenhoven Arterioscler Thromb Vasc Biol. 2006;26:1236-1245; published online before print March 30 2006, doi:10.1161/01.ATV.0000219283.10832.43. Abstract \| Full Text \| PDF It is only until recently that we begin to understand the molecular mechanisms that underlie the beneficial effects that are associated with LPLS447X. This review summarizes the current literature on this interesting LPL variant.
	Modulation of Smooth Muscle Cell Migration by Members of the Low-Density Lipoprotein Receptor Family Hideaki Bujo and Yasushi Saito Arterioscler Thromb Vasc Biol. 2006;26:1246-1252; published online before print March 30 2006, doi:10.1161/01.ATV.0000219692.78477.17. Abstract \| Full Text \| PDF LDL receptor family members (LRs) regulate the catabolism of membrane-associated proteins and are expressed in SMCs of atherosclerostic lesions. LRs modulate the activity of the urokinase-type plasminogen activator (uPA) receptor and possibly of the PDGF receptor. Selective modification of the LRs/membrane receptor system may be important for suppression of atherosclerosis.
	Vascular Biology
	Granulocyte Colony Stimulating Factor Directly Inhibits Myocardial Ischemia-Reperfusion Injury Through Akt–Endothelial NO Synthase Pathway Kazutaka Ueda, Hiroyuki Takano, Hiroshi Hasegawa, Yuriko Niitsuma, Yingjie Qin, Masashi Ohtsuka, and Issei Komuro Arterioscler Thromb Vasc Biol. 2006;26:e108-e113; published online before print March 30 2006, doi:10.1161/01.ATV.0000219697.99134.10. Abstract \| Full Text \| PDF Granulocyte colony stimulating factor (G-CSF) has been reported recently to prevent cardiac remodeling and dysfunction after acute myocardial infarction. In this study, we demonstrated in isolated rat hearts that G-CSF administered after reperfusion directly protects the heart from myocardial ischemia-reperfusion injury through the Akt-eNOS pathway.
	Granulocyte Colony Stimulating Factor Directly Inhibits Myocardial Ischemia-Reperfusion Injury Through Akt–Endothelial NO Synthase Pathway Kazutaka Ueda, Hiroyuki Takano, Hiroshi Hasegawa, Yuriko Niitsuma, Yingjie Qin, Masashi Ohtsuka, and Issei Komuro Arterioscler Thromb Vasc Biol. 2006;26:1253. Abstract \| PDF
	Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice Katrin Schäfer, Marco R. Schroeter, Claudia Dellas, Miriam Puls, Mirko Nitsche, Elisabeth Weiss, Gerd Hasenfuss, and Stavros V. Konstantinides Arterioscler Thromb Vasc Biol. 2006;26:1254-1259; published online before print March 2 2006, doi:10.1161/01.ATV.0000215982.14003.b7. Abstract \| Full Text \| PDF \| Data Supplement We performed whole-body irradiation and bone marrow transplantation experiments followed by carotid artery injury with ferric chloride in mice. Our results support the ability of bone marrow-derived cells to modulate neointimal growth after injury, which appears to be partly mediated by the expression of plasminogen activator inhibitor-1
	12/15 Lipoxygenase Mediates Monocyte Adhesion to Aortic Endothelium in Apolipoprotein E–Deficient Mice Through Activation of RhoA and NF- ${kappa}$ B David T. Bolick, Suseela Srinivasan, Angela Whetzel, Lauren C. Fuller, and Catherine C. Hedrick Arterioscler Thromb Vasc Biol. 2006;26:1260-1266; published online before print March 16 2006, doi:10.1161/01.ATV.0000217909.09198.d6. Abstract \| Full Text \| PDF \| Data Supplement L12/15 lipoxygenase (12/15LO) products activate endothelial rhoA and PKC{alpha}. Activation of rhoA and PKC{alpha} causes activation and translocation of NF-{kappa}B to the nucleus, which, in turn, results in induction of ICAM-1. Induction of ICAM-1 on aortic endothelium stimulates monocyte:endothelial adhesion in vivo in apoEKO mice.
	Apelin Stimulates Myosin Light Chain Phosphorylation in Vascular Smooth Muscle Cells Tatsuo Hashimoto, Minoru Kihara, Junji Ishida, Nozomi Imai, Shin-ichiro Yoshida, Yoshiyuki Toya, Akiyoshi Fukamizu, Hitoshi Kitamura, and Satoshi Umemura Arterioscler Thromb Vasc Biol. 2006;26:1267-1272; published online before print March 23 2006, doi:10.1161/01.ATV.0000218841.39828.91. Abstract \| Full Text \| PDF \| Data Supplement In the vascular smooth muscles, apelin produced APJ-dependent phosphorylation of myosin light chain. This reaction was accompanied with myosin phosphatase target subunit phosphorylation. The apelin-APJ system may play a role in regulating vascular contraction.
	Pleiotrophin Induces Transdifferentiation of Monocytes Into Functional Endothelial Cells Behrooz G. Sharifi, Zhaohui Zeng, Lai Wang, Lei Song, Haiming Chen, Minghui Qin, M. Rocio Sierra-Honigmann, Sebastian Wachsmann-Hogiu, and Prediman K. Shah Arterioscler Thromb Vasc Biol. 2006;26:1273-1280; published online before print April 13 2006, doi:10.1161/01.ATV.0000222017.05085.8e. Abstract \| Full Text \| PDF \| Data Supplement Pleiotrophin (PTN) is a cytokine that is expressed by monocytes/macrophages in the highly vascularized regions of ischemic tissues. We investigated whether exposure of monocytes/macrophages to PTN alter the phenotype of these cells. Using multiple of in vitro and in vivo approaches, we found that exposure of monocytes/macrophages led to downregulation of cell phenotype and upregulation of endothelial cell characteristics. These transdifferentiated cells incorporated into newly developed vasculature and increased blood flow into ischemic hindlimb.
	AMP-Activated Protein Kinase Is Involved in Endothelial NO Synthase Activation in Response to Shear Stress Yingjia Zhang, Tzong-Shyuan Lee, Erik M. Kolb, Kai Sun, Xiao Lu, Frances M. Sladek, Ghassan S. Kassab, Theodore Garland, Jr, and John Y.-J. Shyy Arterioscler Thromb Vasc Biol. 2006;26:1281-1287; published online before print April 6 2006, doi:10.1161/01.ATV.0000221230.08596.98. Abstract \| Full Text \| PDF \| Data Supplement Changes in shear stress, including magnitude and pulsatility, activate AMPK in ECs. The activation of AMPK leads to the shear stress-stimulated eNOS phosphorylation and the ensuing NO production. Elevated phosphorylation of AMPK and eNOS is observed in aortas of mice exhibiting a high level of voluntary running.
	N-Terminal Proteolysis of the Endothelin B Receptor Abolishes Its Ability to Induce EGF Receptor Transactivation and Contractile Protein Expression in Vascular Smooth Muscle Cells Evelina Grantcharova, H. Peter Reusch, Solveig Grossmann, Jenny Eichhorst, Hans-Willi Krell, Michael Beyermann, Walter Rosenthal, and Alexander Oksche Arterioscler Thromb Vasc Biol. 2006;26:1288-1296; published online before print April 6 2006, doi:10.1161/01.ATV.0000220377.51354.30. Abstract \| Full Text \| PDF \| Data Supplement The ETB receptor undergoes agonist-induced N-terminal proteolysis. Postreceptor signaling comprised biphasic ERK1/2 activation, EGF receptor transactivation, and an increased expression of contractile proteins in vascular smooth muscle cells (VSMCs). Thus, the ETB receptor may participate in the differentiation of VSMCs.
	Perivascular Adipose Tissue and Mesenteric Vascular Function in Spontaneously Hypertensive Rats Beatriz Gálvez, Javier de Castro, Diana Herold, Galyna Dubrovska, Silvia Arribas, M. Carmen González, Isabel Aranguez, Friedrich C. Luft, M. Pilar Ramos, Maik Gollasch, and Maria S. Fernández Alfonso Arterioscler Thromb Vasc Biol. 2006;26:1297-1302; published online before print April 6 2006, doi:10.1161/01.ATV.0000220381.40739.dd. Abstract \| Full Text \| PDF \| Data Supplement Perivascular adipose tissue of normotensive rats releases a transferable factor that induces relaxation by opening voltage-dependent K+ (Kv) channels. The relevance of these observations to hypertension is unknown. Differences in visceral perivascular adipose tissue mass and function may contribute to the increased vascular resistance observed in SHR.
	Atherosclerosis and Lipoproteins
	Degenerative Aortic Valve Stenosis, but not Coronary Disease, Is Associated With Shorter Telomere Length in the Elderly David J. Kurz, Barbara Kloeckener-Gruissem, Alexander Akhmedov, Franz R. Eberli, Ines Bühler, Wolfgang Berger, Osmund Bertel, and Thomas F. Lüscher Arterioscler Thromb Vasc Biol. 2006;26:e114-e117; published online before print April 20 2006, doi:10.1161/01.ATV.0000222961.24912.69. Abstract \| Full Text \| PDF \| Data Supplement The mechanisms responsible for the age-related increase in the incidence of calcific aortic valve stenosis (CAS) are unclear but may include telomere-driven cellular senescence. Because telomere length varies widely among individuals of the same age, we hypothesized that patients with shorter telomeres would be prone to develop CAS late in life. In the elderly, calcific aortic stenosis, but not coronary disease, is associated with shorter leukocyte telomere length.
	Degenerative Aortic Valve Stenosis, but not Coronary Disease, Is Associated With Shorter Telomere Length in the Elderly David J. Kurz, Barbara Kloeckener-Gruissem, Alexander Akhmedov, Franz R. Eberli, Ines Bühler, Wolfgang Berger, Osmund Bertel, and Thomas F. Lüscher Arterioscler Thromb Vasc Biol. 2006;26:1303. Abstract \| PDF
	A Simple Method of Plaque Rupture Induction in Apolipoprotein E–Deficient Mice Takeshi Sasaki, Masafumi Kuzuya, Kae Nakamura, Xian Wu Cheng, Tami Shibata, Kohji Sato, and Akihisa Iguchi Arterioscler Thromb Vasc Biol. 2006;26:1304-1309; published online before print March 30 2006, doi:10.1161/01.ATV.0000219687.71607.f7. Abstract \| Full Text \| PDF In this study we demonstrate the murine model of human plaque rupture, which is simple, fast, and highly efficient. This model would help us not only to understand the mechanism of human plaque rupture but also to assess various already-known and as-yet-unknown agents in the future.
	LXR-Induced Redistribution of ABCG1 to Plasma Membrane in Macrophages Enhances Cholesterol Mass Efflux to HDL Nan Wang, Mollie Ranalletta, Fumihiko Matsuura, Felix Peng, and Alan R. Tall Arterioscler Thromb Vasc Biol. 2006;26:1310-1316; published online before print March 23 2006, doi:10.1161/01.ATV.0000218998.75963.02. Abstract \| Full Text \| PDF \| Data Supplement This study showed that ABCG1 has a major role in macrophage cholesterol efflux stimulated by LXR activation. LXR activation also induces a parallel redistribution of ABCG1 from intracellular sites to the plasma membrane. ABCG1 appears to act in the plasma membrane to increase the availability of cholesterol to a variety of lipoprotein and nonlipoprotein acceptors while limiting the accumulation of cholesterol in the endoplasmic reticulum.
	The Di-Leucine Motif Contributes to Class A Scavenger Receptor-Mediated Internalization of Acetylated Lipoproteins Yaoyu Chen, Xiaohua Wang, Jingjing Ben, Shen Yue, Hui Bai, Xiaoxiang Guan, Xiaoming Bai, Li Jiang, Yong Ji, Leming Fan, and Qi Chen Arterioscler Thromb Vasc Biol. 2006;26:1317-1322; published online before print March 30 2006, doi:10.1161/01.ATV.0000220171.50282.0c. Abstract \| Full Text \| PDF \| Data Supplement Di-leucine pair exists in human, bovine, and rabbit cytoplasmic domains of class A scavenger receptor. The cells expressing di-leucine mutants showed decreased uptake and unchanged binding of AcLDL. The di-leucine pair was not associated to coated pits. It suggests that di-leucine motif acts as a signal sequence to mediate SR-A into cell.
	Transforming Growth Factor-ß–Induced Expression of the Apolipoprotein E Gene Requires c-Jun N-Terminal Kinase, p38 Kinase, and Casein Kinase 2 Nishi N. Singh and Dipak P. Ramji Arterioscler Thromb Vasc Biol. 2006;26:1323-1329; published online before print April 6 2006, doi:10.1161/01.ATV.0000220383.19192.55. Abstract \| Full Text \| PDF \| Data Supplement The mechanisms underlying the regulation of apolipoprotein E expression in monocytes/macrophages by the antiatherogenic cytokine TGF-ß were investigated. We show a novel role for JNK, p38 kinase, CK2, and c-Jun/AP-1 in the response, which have implications to the development of atherosclerosis.
	MMP-9 Microsatellite Polymorphism and Susceptibility to Carotid Arteries Atherosclerosis Nicola Fiotti, Nicola Altamura, Maurizio Fisicaro, Nicola Carraro, Laura Uxa, Gabriele Grassi, Lucio Torelli, Raffaella Gobbato, Gianfranco Guarnieri, B. Timothy Baxter, and Carlo Giansante Arterioscler Thromb Vasc Biol. 2006;26:1330-1336; published online before print March 30 2006, doi:10.1161/01.ATV.0000219233.31702.c9. Abstract \| Full Text \| PDF \| Data Supplement Higher prevalence of long microsatellites (>=22 CA repeats) in MMP-9 promoter was found in patients with ultrasound evidence of carotid atherosclerosis and, among them, in carriers of plaques with a thin fibrous cap and echolucent core. This PM was independent of known risk factors for atherosclerosis and did not influence MMP-9 plasma levels.
	Biological Significance of Decreased HSP27 in Human Atherosclerosis Jose Luis Martin-Ventura, Valentin Nicolas, Xavier Houard, Luis Miguel Blanco-Colio, Anne Leclercq, Jesús Egido, Roger Vranckx, Jean-Baptiste Michel, and Olivier Meilhac Arterioscler Thromb Vasc Biol. 2006;26:1337-1343; published online before print March 30 2006, doi:10.1161/01.ATV.0000220108.97208.67. Abstract \| Full Text \| PDF Decreased HSP27 is a potential sign of atherosclerosis, although its biological significance remains undefined. Extracellular HSP27 is proteolyzed by enzymes released from atherosclerotic plaques. Intracellular HSP27 downregulation decreases VSMC resistance to proteolytic injury. Decreased HSP27 may reflect proteolytic imbalance occurring during pathological vascular remodeling processes.
	In Vivo Low-Density Lipoprotein Exposure Induces Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 Correlated With Activator Protein-1 Expression Lynne Verna, Chintya Ganda, and Michael B. Stemerman Arterioscler Thromb Vasc Biol. 2006;26:1344-1349; published online before print April 13 2006, doi:10.1161/01.ATV.0000222152.83069.3f. Abstract \| Full Text \| PDF Injection of LDL into LDLR-/- mice increased the expression of ICAM-1 and VCAM-1 in their aortic endothelial cells. At the same time, the transcription factor AP-1 proteins c-Jun and c-Fos, but not the NF-{kappa}B protein P65, were observed within the aortic endothelial cell nucleus. This indicated that AP-1, but not NF-{kappa}B, was correlated with adhesion molecule expression in response to elevated blood LDL levels.
	Effects of the Cholesteryl Ester Transfer Protein Inhibitor Torcetrapib on Apolipoprotein B100 Metabolism in Humans John S. Millar, Margaret E. Brousseau, Margaret R. Diffenderfer, P. Hugh, R. Barrett, Francine K. Welty, Aisha Faruqi, Megan L. Wolfe, Chorthip Nartsupha, Andres G. Digenio, James P. Mancuso, Gregory G. Dolnikowski, Ernst J. Schaefer, and Daniel J. Rader Arterioscler Thromb Vasc Biol. 2006;26:1350-1356; published online before print March 30 2006, doi:10.1161/01.ATV.0000219695.84644.56. Abstract \| Full Text \| PDF \| Data Supplement The CETP inhibitor torcetrapib reduces apoB-containing lipoproteins in plasma. Torcetrapib alone reduces VLDL, IDL, and LDL apoB100 pool size primarily through increased apoB100 clearance. In contrast, addition of torcetrapib to background treatment with atorvastatin was associated with enhanced VLDL apoB100 clearance and reduced production of IDL and LDL apoB100.
	Hyperinsulinemia Is Associated With Increased Production Rate of Intestinal Apolipoprotein B-48–Containing Lipoproteins in Humans Hélène Duez, Benoît Lamarche, Kristine D. Uffelman, René Valero, Jeffrey S. Cohn, and Gary F. Lewis Arterioscler Thromb Vasc Biol. 2006;26:1357-1363; published online before print April 13 2006, doi:10.1161/01.ATV.0000222015.76038.14. Abstract \| Full Text \| PDF \| Data Supplement In the present study, we investigated whether intestinal lipoprotein particle production rate is related to indices of insulin resistance in humans. ApoB-48-containing lipoprotein metabolism was examined in 14 nondiabetic men with a broad range of BMI and insulin sensitivity. We demonstrate that intestinal apoB-48-containing TRL production rate is increased in hyperinsulinemic, insulin-resistant humans.
	Adiponectin Is an Important Determinant of ApoA-I Catabolism Bruno Vergès, Jean Michel Petit, Laurence Duvillard, Guillaume Dautin, Emmanuel Florentin, Françoise Galland, and Philippe Gambert Arterioscler Thromb Vasc Biol. 2006;26:1364-1369; published online before print March 30 2006, doi:10.1161/01.ATV.0000219611.50066.bd. Abstract \| Full Text \| PDF We show a very significant association between adiponectin and apoA-I FCR independent of other factors, such as HDL triglyceride content or clinical and biological indexes of insulin sensitivity. Plasma adiponectin, on its own, explains 43% of apoA-I FCR variance, suggesting that adiponectin may have a direct role on HDL catabolism.
	Human Lecithin:Cholesterol Acyltransferase Deficiency: In Vivo Kinetics of Low-Density Lipoprotein and Lipoprotein-X Masato Nishiwaki, Katsunori Ikewaki, Giovanni Bader, Hassan Nazih, Minna Hannuksela, Alan T. Remaley, Robert D. Shamburek, and H. Bryan Brewer, Jr Arterioscler Thromb Vasc Biol. 2006;26:1370-1375; published online before print March 16 2006, doi:10.1161/01.ATV.0000217910.90210.99. Abstract \| Full Text \| PDF \| Data Supplement To elucidate the mechanism(s) responsible for the low LDL level in LCAT deficiency (LCAT-def), kinetic studies using radiotracers and a stable isotope were conducted in LCAT-def. Both studies revealed an increased catabolism of LDL. In addition, the radiotracer study showed a decreased catabolism of LpX in LCAT-def.
	Young Adults With Family History of Coronary Heart Disease Have Increased Arterial Vulnerability to Metabolic Risk Factors: The Cardiovascular Risk in Young Finns Study Markus Juonala, Jorma S. A. Viikari, Leena Räsänen, Hans Helenius, Matti Pietikäinen, and Olli T. Raitakari Arterioscler Thromb Vasc Biol. 2006;26:1376-1382; published online before print April 13 2006, doi:10.1161/01.ATV.0000222012.56447.00. Abstract \| Full Text \| PDF \| Data Supplement Family history of coronary heart disease is a risk factor of atherosclerotic disease. We observed that young adults with positive family history have increased carotid IMT. This is partly explained by their increased vulnerability to metabolic risk factors.
	Hypercholesterolemia Reduces Collateral Artery Growth More Dominantly Than Hyperglycemia or Insulin Resistance in Mice Vincent van Weel, Margreet de Vries, Peter J. Voshol, Robert E. Verloop, Paul H.C. Eilers, Victor W.M. van Hinsbergh, J. Hajo van Bockel, and Paul H.A. Quax Arterioscler Thromb Vasc Biol. 2006;26:1383-1390; published online before print March 30 2006, doi:10.1161/01.ATV.0000219234.78165.85. Abstract \| Full Text \| PDF \| Data Supplement Collateral formation (arteriogenesis) may be deregulated by vascular risk factors, eg, diabetes or hypercholesterolemia. Here, we found that hypercholesterolemia reduces arteriogenesis more dominantly than hyperglycemia or hyperinsulinemia in mice. This suggests that a disturbed lipid metabolism as observed in diabetics might be crucial for deregulation of arteriogenesis.
	Thrombosis
	Decreased Plasma Fibronectin Leads to Delayed Thrombus Growth in Injured Arterioles Jana Matuskova, Anil K. Chauhan, Beatrice Cambien, Sophie Astrof, Vandana S. Dole, Crystal L. Piffath, Richard O. Hynes, and Denisa D. Wagner Arterioscler Thromb Vasc Biol. 2006;26:1391-1396; published online before print March 9 2006, doi:10.1161/01.ATV.0000216282.58291.c6. Abstract \| Full Text \| PDF We show that mice with half the normal plasma fibronectin levels have a striking defect in thrombus growth specifically at arterial shear rate attributed to a decrease of plasma fibronectin. Our study emphasizes the fundamental role of this protein in thrombosis.
	Plasma Homocysteine Affects Fibrin Clot Permeability and Resistance to Lysis in Human Subjects Anetta Undas, Jan Brozek, Milosz Jankowski, Zbigniew Siudak, Andrew Szczeklik, and Hieronim Jakubowski Arterioscler Thromb Vasc Biol. 2006;26:1397-1404; published online before print March 30 2006, doi:10.1161/01.ATV.0000219688.43572.75. Abstract \| Full Text \| PDF We hypothesized that plasma homocysteine affects fibrin clot structure in vivo. In healthy men and CAD patients, but not in those with diabetes or hypercholesterolemia, elevated homocysteine levels were associated with reduced clot permeability and increased resistance to lysis. In contrast to methionine load, folic acid treatment improved clot properties.
	Common Genetic Variation in Five Thrombosis Genes and Relations to Plasma Hemostatic Protein Level and Cardiovascular Disease Risk Sekar Kathiresan, Qiong Yang, Martin G. Larson, Amy L. Camargo, Geoffrey H. Tofler, Joel N. Hirschhorn, Stacey B. Gabriel, and Christopher J. O’Donnell Arterioscler Thromb Vasc Biol. 2006;26:1405-1412; published online before print April 13 2006, doi:10.1161/01.ATV.0000222011.13026.25. Abstract \| Full Text \| PDF \| Data Supplement We hypothesized that cis-acting SNPs influence hemostatic protein levels or CVD risk. In Framingham Heart Study participants, a single FGB SNP explained 1% of fibrinogen level variance, and 2 F7 SNPs together explained 10% of F7 level variance. PLAT gene haplotypes were associated with CVD.
	Letters to the Editor
	Longitudinal Differences in Familial Combined Hyperlipidemia Quantitative Trait Loci Martijn C.G.J. Brouwers, Naoko Kono, Marleen M.J. van Greevenbroek, Carla J.H. van der Kallen, Aldons J. Lusis, Tjerk W.A. de Bruin, and Rita M. Cantor Arterioscler Thromb Vasc Biol. 2006;26:e118-e119, doi:10.1161/01.ATV.0000221232.79877.c7. Full Text \| PDF
	Longitudinal Differences in Familial Combined Hyperlipidemia Quantitative Trait Loci Rebecca L. Pollex and Robert A. Hegele Arterioscler Thromb Vasc Biol. 2006;26:e120, doi:10.1161/01.ATV.0000222010.98018.6b. Full Text \| PDF
	Rosiglitazone Cools Down Inflammation in the Metabolic Syndrome Katherine Esposito, Miryam Ciotola, Domenico Merante, and Dario Giugliano Arterioscler Thromb Vasc Biol. 2006;26:1413-1414, doi:10.1161/01.ATV.0000223874.94624.11. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 26, Issue 6; June 1, 2006

Editorials

Ruptures of Delight?: A New Mouse Model of Plaque Rupture

Plasma Fibronectin Concentration: A Risk Factor for Arterial Thrombosis?

Maintenance of Vascular Homeostasis by Bone Marrow–Derived Cells

Insight Into ABCG1-Mediated Cholesterol Efflux

Lipoprotein Metabolism: A Well-Tried Tool to Characterize Dyslipidemic Mechanisms

Lipoxygenase Pathways as Mediators of Early Inflammatory Events in Atherosclerosis

Brief Reviews

Nitric Oxide and Posttranslational Modification of the Vascular Proteome: S-Nitrosation of Reactive Thiols

Endothelium-Derived Hyperpolarizing Factor: Where Are We Now?

Genome-Wide Expression Studies of Atherosclerosis: Critical Issues in Methodology, Analysis, Interpretation of Transcriptomics Data

Lipoprotein Lipase S447X: A Naturally Occurring Gain-of-Function Mutation

Modulation of Smooth Muscle Cell Migration by Members of the Low-Density Lipoprotein Receptor Family

Vascular Biology

Granulocyte Colony Stimulating Factor Directly Inhibits Myocardial Ischemia-Reperfusion Injury Through Akt–Endothelial NO Synthase Pathway

Granulocyte Colony Stimulating Factor Directly Inhibits Myocardial Ischemia-Reperfusion Injury Through Akt–Endothelial NO Synthase Pathway

Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice

12/15 Lipoxygenase Mediates Monocyte Adhesion to Aortic Endothelium in Apolipoprotein E–Deficient Mice Through Activation of RhoA and NF-B

Apelin Stimulates Myosin Light Chain Phosphorylation in Vascular Smooth Muscle Cells

Pleiotrophin Induces Transdifferentiation of Monocytes Into Functional Endothelial Cells

AMP-Activated Protein Kinase Is Involved in Endothelial NO Synthase Activation in Response to Shear Stress

N-Terminal Proteolysis of the Endothelin B Receptor Abolishes Its Ability to Induce EGF Receptor Transactivation and Contractile Protein Expression in Vascular Smooth Muscle Cells

Perivascular Adipose Tissue and Mesenteric Vascular Function in Spontaneously Hypertensive Rats

Atherosclerosis and Lipoproteins

Degenerative Aortic Valve Stenosis, but not Coronary Disease, Is Associated With Shorter Telomere Length in the Elderly

Degenerative Aortic Valve Stenosis, but not Coronary Disease, Is Associated With Shorter Telomere Length in the Elderly

A Simple Method of Plaque Rupture Induction in Apolipoprotein E–Deficient Mice

LXR-Induced Redistribution of ABCG1 to Plasma Membrane in Macrophages Enhances Cholesterol Mass Efflux to HDL

The Di-Leucine Motif Contributes to Class A Scavenger Receptor-Mediated Internalization of Acetylated Lipoproteins

Transforming Growth Factor-ß–Induced Expression of the Apolipoprotein E Gene Requires c-Jun N-Terminal Kinase, p38 Kinase, and Casein Kinase 2

MMP-9 Microsatellite Polymorphism and Susceptibility to Carotid Arteries Atherosclerosis

Biological Significance of Decreased HSP27 in Human Atherosclerosis

In Vivo Low-Density Lipoprotein Exposure Induces Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 Correlated With Activator Protein-1 Expression

Effects of the Cholesteryl Ester Transfer Protein Inhibitor Torcetrapib on Apolipoprotein B100 Metabolism in Humans

Hyperinsulinemia Is Associated With Increased Production Rate of Intestinal Apolipoprotein B-48–Containing Lipoproteins in Humans

Adiponectin Is an Important Determinant of ApoA-I Catabolism

Human Lecithin:Cholesterol Acyltransferase Deficiency: In Vivo Kinetics of Low-Density Lipoprotein and Lipoprotein-X

Young Adults With Family History of Coronary Heart Disease Have Increased Arterial Vulnerability to Metabolic Risk Factors: The Cardiovascular Risk in Young Finns Study

Hypercholesterolemia Reduces Collateral Artery Growth More Dominantly Than Hyperglycemia or Insulin Resistance in Mice

Thrombosis

Decreased Plasma Fibronectin Leads to Delayed Thrombus Growth in Injured Arterioles

Plasma Homocysteine Affects Fibrin Clot Permeability and Resistance to Lysis in Human Subjects

Common Genetic Variation in Five Thrombosis Genes and Relations to Plasma Hemostatic Protein Level and Cardiovascular Disease Risk

Letters to the Editor

Longitudinal Differences in Familial Combined Hyperlipidemia Quantitative Trait Loci

Longitudinal Differences in Familial Combined Hyperlipidemia Quantitative Trait Loci

Rosiglitazone Cools Down Inflammation in the Metabolic Syndrome

Spotlight

12/15 Lipoxygenase Mediates Monocyte Adhesion to Aortic Endothelium in Apolipoprotein E–Deficient Mice Through Activation of RhoA and NF- ${kappa}$ B