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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 26, Issue 11; November 1, 2006
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EditorialsBack

Lipoprotein-Associated Phospholipase A2: Novel Biomarker and Causal Mediator of Atherosclerosis?

Nancy Swords Jenny
Arterioscler Thromb Vasc Biol. 2006;26:2417-2418, doi:10.1161/01.ATV.0000248185.26125.28.
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Fibrin Gel Architecture Influences Endogenous Fibrinolysis and May Promote Coronary Artery Disease

Angela Silveira and Anders Hamsten
Arterioscler Thromb Vasc Biol. 2006;26:2419-2420, doi:10.1161/01.ATV.0000245798.26855.88.
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Brief ReviewsBack

Anna-Karin L. Robertson and Göran K Hansson
Arterioscler Thromb Vasc Biol. 2006;26:2421-2432; published online before print September 14 2006, doi:10.1161/01.ATV.0000245830.29764.84.
Abstract | Full Text | PDF
Adaptive immunity, in particular T cells, is highly involved in the development of atherosclerosis. This review summarizes our current knowledge of T cells in atherogenesis and illustrates how they can aggravate or attenuate this disease through cross-talk with other cells within or outside the atherosclerotic plaque.  

Murray W. Huff, Rebecca L. Pollex, and Robert A. Hegele
Arterioscler Thromb Vasc Biol. 2006;26:2433-2438; published online before print September 14 2006, doi:10.1161/01.ATV.0000245791.53245.ee.
Abstract | Full Text | PDF
Niemann-Pick C1-like 1 protein (NPC1L1) was recently shown to be the molecular target of the cholesterol absorption inhibitor, ezetimibe. Evidence in support of a focal physiological role for NPC1L1 in intestinal sterol absorption has been garnered not only through human, animal, and cell studies but also through the use of human genetics.  

An L. Moens and David A. Kass
Arterioscler Thromb Vasc Biol. 2006;26:2439-2444; published online before print August 31 2006, doi:10.1161/01.ATV.0000243924.00970.cb.
Abstract | Full Text | PDF
Tetrahydrobiopterin (BH4) is an essential cofactor for the aromatic amino acid hydroxylases, which are essential in the formation of neurotransmitters, and for nitric oxide synthase (NOS). BH4 replacement may help treat hypertension, ischemia-reperfusion injury, and cardiac hypertrophy with chamber remodeling, by restoring functional NOS. This review discusses BH4 biochemistry, physiology, and evolving uses to treat cardiovascular disease.  

Laurent O. Mosnier and Bonno N. Bouma
Arterioscler Thromb Vasc Biol. 2006;26:2445-2453; published online before print September 7 2006, doi:10.1161/01.ATV.0000244680.14653.9a.
Abstract | Full Text | PDF  

 

Vascular BiologyBack

Nicolas Clavreul, Markus M. Bachschmid, Xiuyun Hou, Chaomei Shi, Azra Idrizovic, Yasuo Ido, David Pimentel, and Richard A. Cohen
Arterioscler Thromb Vasc Biol. 2006;26:2454-2461; published online before print August 24 2006, doi:10.1161/01.ATV.0000242791.28953.4c.
Abstract | Full Text | PDF | Data Supplement
Bovine aortic endothelial cells were exposed to oxLDL. OxLDL induced peroxynitrite production and triggered redox-activation of p21ras via S-glutathiolation of its cysteine-118. Oxidant activation of p21ras was responsible for Erk-dependent phosphorylation of IRS-1 serine-616, which promoted endothelial insulin resistance.  

Valerie Y. Ng, Christophe Morisseau, John R. Falck, Bruce D. Hammock, and Deanna L. Kroetz
Arterioscler Thromb Vasc Biol. 2006;26:2462-2468; published online before print August 17 2006, doi:10.1161/01.ATV.0000242013.29441.81.
Abstract | Full Text | PDF | Data Supplement
Proliferation of smooth muscle cells is implicated in cardiovascular complications. Urea-based alkanoic acids are identified as agonists of the nuclear receptor peroxisome proliferator-activated receptor {alpha} (PPAR{alpha}). These acids attenuate smooth muscle cell proliferation, in part by decreasing cyclin D1 via PPAR{alpha} activation.  

Uma Singh, Sridevi Devaraj, Mohan R. Dasu, Dana Ciobanu, Jane Reusch, and Ishwarlal Jialal
Arterioscler Thromb Vasc Biol. 2006;26:2469-2475; published online before print August 17 2006, doi:10.1161/01.ATV.0000241572.05292.fb.
Abstract | Full Text | PDF | Data Supplement
CRP treatment of HMDMs significantly decreased LPS-induced IL-10 mRNA and intracellular and secreted IL-10 protein and destabilized IL-10 mRNA. CRP significantly decreased intracellular cAMP and pCREB. Thus, CRP inhibits LPS-induced IL-10 secretion via inhibition of cAMP production.  

Hiroko Fujii, Shu-Hong Li, Paul E. Szmitko, Paul W.M. Fedak, and Subodh Verma
Arterioscler Thromb Vasc Biol. 2006;26:2476-2482; published online before print August 24 2006, doi:10.1161/01.ATV.0000242794.65541.02.
Abstract | Full Text | PDF | Data Supplement
CRP has emerged as an important partaker of atherothrombosis. In the present study we demonstrate that CRP, at concentrations known to predict future vascular events, weakens the antioxidant defenses of endothelial progenitor cells, and promotes early senescence through telomerase activation. These data reinforce the role of inflammation in the pathogenesis of vascular disease.  

Takaaki Fujii, Yoshikazu Yonemitsu, Mitsuho Onimaru, Mitsugu Tanii, Toshiaki Nakano, Kensuke Egashira, Takako Takehara, Makoto Inoue, Mamoru Hasegawa, Hiroyuki Kuwano, and Katsuo Sueishi
Arterioscler Thromb Vasc Biol. 2006;26:2483-2489; published online before print September 7 2006, doi:10.1161/01.ATV.0000244684.23499.bf.
Abstract | Full Text | PDF | Data Supplement
MCP-1 is a C-C chemokine that is an inflammatory/arteriogenic factor. Using murine models of limb ischemia, we show that FGF-2 targets nonendothelial mesenchymal cells (NEMCs) enhancing both angiogenic (VEGF) and arteriogenic (MCP-1) signals via independent signal transduction pathways. Therefore, MCP-1/CCR2 plays a critical role in FGF-2-mediated therapeutic neovascularization.  

Peter S. Gargalovic, Nima M. Gharavi, Michael J. Clark, Joanne Pagnon, Wen-Pin Yang, Aiqing He, Amy Truong, Tamar Baruch-Oren, Judith A. Berliner, Todd G. Kirchgessner, and Aldons J. Lusis
Arterioscler Thromb Vasc Biol. 2006;26:2490-2496; published online before print August 24 2006, doi:10.1161/01.ATV.0000242903.41158.a1.
Abstract | Full Text | PDF | Data Supplement
Oxidized 1-palmitoyl-2-arachidonyl-sn-3-glycero-phosphorylcholine (oxPAPC) accumulates in atherosclerotic lesions and in vitro studies suggest that it mediates chronic inflammatory response in endothelial cells (ECs). The goal of our studies was to identify pathways mediating the induction of inflammatory genes by oxPAPC. Our data suggest that the UPR pathway is a general mediator of vascular inflammation and EC dysfunction in atherosclerosis, and, likely, other inflammatory disorders.  

A. Baidoshvili, P.A.J. Krijnen, K. Kupreishvili, C. Ciurana, W. Bleeker, R. Nijmeijer, C.A. Visser, F.C. Visser, C.J.L.M. Meijer, W. Stooker, L. Eijsman, V.W.M. van Hinsbergh, C.E. Hack, H.W.M. Niessen, and C.G. Schalkwijk
Arterioscler Thromb Vasc Biol. 2006;26:2497-2503; published online before print September 14 2006, doi:10.1161/01.ATV.0000245794.45804.ab.
Abstract | Full Text | PDF
We examined a putative relationship between CML and AMI. CML depositions were significantly increased on activated endothelium of intramyocardial blood vessels after AMI and in myocarditis. In vitro and in the rat CML was upregulated by inflammation, not by ischemia. In AMI patients, CML is probably present in advance of the AMI.  

 

Atherosclerosis and LipoproteinsBack

Jukka K. Hakala, Ken A. Lindstedt, Petri T. Kovanen, and Markku O. Pentikäinen
Arterioscler Thromb Vasc Biol. 2006;26:2504-2509; published online before print September 14 2006, doi:10.1161/01.ATV.0000245796.97133.ad.
Abstract | Full Text | PDF
LDL modified by secreted macrophage-derived lysosomal hydrolases (H-LDL) induce secretion of IL-8 by cultured human monocyte-derived macrophages. Secretion of IL-8 by H-LDL-stimulated macrophages depended on the activation of p38 MAPK and NF-{kappa}B transcription factor.  

Dmitry Namgaladze and Bernhard Brüne
Arterioscler Thromb Vasc Biol. 2006;26:2510-2516; published online before print September 14 2006, doi:10.1161/01.ATV.0000245797.76062.2e.
Abstract | Full Text | PDF | Data Supplement
Monocyte survival is an important determinant in the development of atherosclerotic lesions. We show that phospholipase A2-modified LDL activates phosphatidylinositol 3-kinase-Akt signaling and increases survival of monocytic cells. Our data provide a mechanistic explanation to understand pro-atherogenic actions of phospholipase A2.  

Yariv Gerber, Joseph P. McConnell, Allan S. Jaffe, Susan A. Weston, Jill M. Killian, and Véronique L. Roger
Arterioscler Thromb Vasc Biol. 2006;26:2517-2522; published online before print August 10 2006, doi:10.1161/01.ATV.0000240406.89440.0c.
Abstract | Full Text | PDF
We evaluated the role of lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory biomarker, in defining risk after myocardial infarction (MI). Among community subjects presenting with MI, increased Lp-PLA2 levels measured early after MI are strongly and independently associated with mortality and provide incremental value in risk discrimination over traditional predictors.  

Frank D. Kolodgie, Allen P. Burke, Kristi S. Skorija, Elena Ladich, Robert Kutys, Addisalem Taye Makuria, and Renu Virmani
Arterioscler Thromb Vasc Biol. 2006;26:2523-2529; published online before print September 7 2006, doi:10.1161/01.ATV.0000244681.72738.bc.
Abstract | Full Text | PDF
The expression of lipoprotein-associated phospholipase A2 (Lp-PLA2) was assessed in early through late, unstable coronary plaques from sudden death victims. Lp-PLA2 was mostly present in plaque ruptures and thin-cap fibroatheromas in necrotic cores and surrounding areas of apoptotic macrophages. The present study suggests Lp-PLA2 may be an important biomarker for plaque instability.  

Matteo Pirro, Giuseppe Schillaci, Rita Paltriccia, Francesco Bagaglia, Cinzia Menecali, Massimo R. Mannarino, Marusca Capanni, Andrea Velardi, and Elmo Mannarino
Arterioscler Thromb Vasc Biol. 2006;26:2530-2535; published online before print August 31 2006, doi:10.1161/01.ATV.0000243941.72375.15.
Abstract | Full Text | PDF
Atherosclerosis may be caused by increased endothelial damage and loss of endothelial repair by circulating progenitors. We found that hypercholesterolemic patients have a stiffer aorta, more CD31+/CD42- microparticles, and less endothelial progenitors than normocholesterolemic subjects. An increased ratio of CD31+/CD42- microparticles to endothelial progenitors independently predicted increased aortic stiffness.  

Friedrich Mittermayer, Katarzyna Krzyzanowska, Markus Exner, Wolfgang Mlekusch, Jasmin Amighi, Schila Sabeti, Erich Minar, Markus Müller, Michael Wolzt, and Martin Schillinger
Arterioscler Thromb Vasc Biol. 2006;26:2536-2540; published online before print August 24 2006, doi:10.1161/01.ATV.0000242801.38419.48.
Abstract | Full Text | PDF
Concentrations of the nitric oxide synthase inhibitor asymmetrical dimethylarginine (ADMA) are elevated in states of increased cardiovascular risk. We prospectively examined the relationship between ADMA and major adverse cardiovascular events (MACE) in patients with peripheral artery disease. High ADMA independently predicted MACE supporting its role as new cardiovascular risk marker.  

Stylianos Kapiotis, Gregor Holzer, Georg Schaller, Markus Haumer, Harald Widhalm, Daniel Weghuber, Bernd Jilma, Georg Röggla, Michael Wolzt, Kurt Widhalm, and Oswald F. Wagner
Arterioscler Thromb Vasc Biol. 2006;26:2541-2546; published online before print September 14 2006, doi:10.1161/01.ATV.0000245795.08139.70.
Abstract | Full Text | PDF
Obesity is generally accepted as a risk factor for premature atherosclerosis. Subclinical inflammation as quantified by blood levels of C-reactive protein contributes to the development and progression of atherosclerosis. We hypothesized that inflammation in obese children is related to functional and early morphological vascular changes.  

Andrew Steptoe, Ann E. Donald, Katie O’Donnell, Michael Marmot, and John E. Deanfield
Arterioscler Thromb Vasc Biol. 2006;26:2547-2551; published online before print August 24 2006, doi:10.1161/01.ATV.0000242792.93486.0d.
Abstract | Full Text | PDF
Delayed blood pressure recovery after psychological stress was associated with carotid intima-media thickness (IMT) in men and women of low but not high socioeconomic status independently of conventional risk factors. Variations in poststress recovery reflect dysfunction of biological regulatory processes, and may partly mediate psychosocial influences on cardiovascular disease.  

Marit Westerterp, Caroline C. van der Hoogt, Willeke de Haan, Erik H. Offerman, Geesje M. Dallinga-Thie, J. Wouter Jukema, Louis M. Havekes, and Patrick C.N. Rensen
Arterioscler Thromb Vasc Biol. 2006;26:2552-2559; published online before print August 31 2006, doi:10.1161/01.ATV.0000243925.65265.3c.
Abstract | Full Text | PDF | Data Supplement
The effect of CETP on lipoprotein metabolism and atherosclerosis development was investigated in APOE*3-Leiden mice with a humanized lipoprotein profile. CETP expression shifted the distribution of cholesterol from HDL to VLDL/LDL, and severely aggravated atherosclerosis. The CETP{middle dot}E3L mouse may be a valuable model for the preclinical evaluation of HDL-raising interventions on atherosclerosis development.  

A. Susanne M. Zadelaar, Lianne S.M. Boesten, J. Wouter Jukema, Bart J.M. van Vlijmen, Teake Kooistra, Jef J. Emeis, Erik Lundholm, German Camejo, and Louis M. Havekes
Arterioscler Thromb Vasc Biol. 2006;26:2560-2566; published online before print August 24 2006, doi:10.1161/01.ATV.0000242904.34700.66.
Abstract | Full Text | PDF | Data Supplement
We investigated whether the dual PPAR{alpha}/{gamma} agonist tesaglitazar has anti-atherogenic effects in ApoE*3Leiden transgenic mice with reduced insulin sensitivity. Tesaglitazar has anti-atherosclerotic effects that go beyond plasma cholesterol-lowering. This may be caused by a combination of altered lipoprotein profiles and anti-inflammatory vascular effects.  

 

ThrombosisBack

J.P. Collet, Y. Allali, C. Lesty, M.L. Tanguy, J. Silvain, A. Ankri, B. Blanchet, R. Dumaine, J. Gianetti, L. Payot, J.W. Weisel, and G. Montalescot
Arterioscler Thromb Vasc Biol. 2006;26:2567-2573; published online before print August 17 2006, doi:10.1161/01.ATV.0000241589.52950.4c.
Abstract | Full Text | PDF
Hypofibrinolysis promotes atherosclerosis and recurrent ischemic events in premature coronary artery disease (CAD). In the present investigation, plasma fibrin of young CAD patients was found to be significantly stiffer and more resistant to lysis as compared with matched controls. In addition, plasma fibrin stiffness was an independent correlate for both premature CAD and hypofibrinolysis, suggesting an important pathophysiological role of altered fibrin properties.  

 

Letters to the EditorBack

Cell Surface Localization of ABCG1 Does Not Require LXR Activation

Qian Xie, Thomas Engel, Michael Schnoor, Julia Niehaus, Oliver Hofnagel, Insa Buers, Paul Cullen, Udo Seedorf, Gerd Assmann, and Stefan Lorkowski
Arterioscler Thromb Vasc Biol. 2006;26:e143-e144, doi:10.1161/01.ATV.0000245790.47112.b2.
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Cell Surface Localization of ABCG1 Does Not Require LXR Activation

Nan Wang, Mollie Ranalletta, and Alan R. Tall
Arterioscler Thromb Vasc Biol. 2006;26:e145, doi:10.1161/01.ATV.0000245788.94998.29.
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Assessment of a Serum Assay for Quantification of Abdominal Aortic Calcification

Paula Clancy, Lisa Oliver, Rumal Jayalath, Petra Buttner, and Jonathan Golledge
Arterioscler Thromb Vasc Biol. 2006;26:2574-2576, doi:10.1161/01.ATV.0000242799.81434.7d.
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Alpha-Linolenic Acid–Rich Wheat Germ Oil Decreases Oxidative Stress and CD40 Ligand in Patients With Mild Hypercholesterolemia

Cesare Alessandri, Pasquale Pignatelli, Lorenzo Loffredo, Luisa Lenti, Maria Del Ben, Roberto Carnevale, Alessandro Perrone, Domenico Ferro, Francesco Angelico, and Francesco Violi
Arterioscler Thromb Vasc Biol. 2006;26:2577-2578, doi:10.1161/01.ATV.0000242795.08322.fb.
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CorrectionsBack

Correction


Arterioscler Thromb Vasc Biol. 2006;26:e146, doi:10.1161/01.ATV.0000250807.31172.92.
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