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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 29, Issue 4; April 1, 2009
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Key:  VB = Vascular Biology  AL = Atherosclerosis/Lipoproteins  TH = Thrombosis
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EditorialsBack

TH gif  VEGF and Restenosis: The Rest of the Story

Michael Simons
Arterioscler Thromb Vasc Biol. 2009;29:439-440, doi:10.1161/ATVBAHA.109.183970
Extract | Full Text | PDF Free Article  

TH gif  Interference of Progestins With Endothelial Actions of Estrogens: A Matter of Glucocorticoid Action or Deprivation?

J.F. Arnal, P. Gourdy, and T. Simoncini
Arterioscler Thromb Vasc Biol. 2009;29:441-443; published online before print January 29 2009, doi:10.1161/ATVBAHA.108.182337
Extract | Full Text | PDF Free Article  

TH gif  Caspase-8, a Double-Edged Sword for EPC Functioning

Qingzhong Xiao and Qingbo Xu
Arterioscler Thromb Vasc Biol. 2009;29:444-446, doi:10.1161/ATVBAHA.108.183087
Extract | Full Text | PDF Free Article  

AL gif  Getting Radical About Obesity: New Links Between Fat and Heart Disease

Matthias Barton, Elvira Haas, and Indranil Bhattacharya
Arterioscler Thromb Vasc Biol. 2009;29:447-448, doi:10.1161/ATVBAHA.108.181529
Extract | Full Text | PDF Free Article  

 

History of DiscoveryBack

AL gif  The LDL Receptor

Joseph L. Goldstein and Michael S. Brown
Arterioscler Thromb Vasc Biol. 2009;29:431-438; published online before print April 1 2009, doi:10.1161/ATVBAHA.108.179564
Abstract | Full Text | PDF  

 

Brief ReviewsBack

TH gif   G-Protein–Coupled Receptors as Signaling Targets for Antiplatelet Therapy

Susan S. Smyth, Donna S. Woulfe, Jeffrey I. Weitz, Christian Gachet, Pamela B. Conley, Shaun G. Goodman, Matthew T. Roe, Athan Kuliopulos, David J. Moliterno, Patricia A. French, Steven R. Steinhubl, Richard C. Becker for the 2008 Platelet Colloquium Participants
Arterioscler Thromb Vasc Biol. 2009;29:449-457; published online before print November 20 2008, doi:10.1161/ATVBAHA.108.176388
Abstract | Full Text | PDF
The clinical utility of antagonists of the P2Y12 receptor for ADP suggests that other G protein-coupled receptors and intracellular signaling pathways might be viable targets for novel antiplatelet agents. The mechanistic rationale and available clinical data for agents targeting disruption of ADP-, thrombin-, and thromboxane A2-related signaling pathways are discussed.  

 

Integrative Physiology/Experimental MedicineBack

TH gif  Soluble Flt-1 Gene Transfer Ameliorates Neointima Formation After Wire Injury in flt-1 Tyrosine Kinase–Deficient Mice

Jun-ichiro Koga, Tetsuya Matoba, Kensuke Egashira, Mitsuki Kubo, Miho Miyagawa, Eiko Iwata, Katsuo Sueishi, Masabumi Shibuya, and Kenji Sunagawa
Arterioscler Thromb Vasc Biol. 2009;29:458-464; published online before print January 22 2009, doi:10.1161/ATVBAHA.109.183772
Abstract | Full Text | PDF | Data Supplement  

TH gif  Dominant-Negative Loss of PPAR{gamma} Function Enhances Smooth Muscle Cell Proliferation, Migration, and Vascular Remodeling

Dane Meredith, Manikandan Panchatcharam, Sumitra Miriyala, Yau-Sheng Tsai, Andrew J. Morris, Nobuyo Maeda, George A. Stouffer, and Susan S. Smyth
Arterioscler Thromb Vasc Biol. 2009;29:465-471; published online before print January 29 2009, doi:10.1161/ATVBAHA.109.184234
Abstract | Full Text | PDF
We applied a genetic approach to investigate the normal role of PPAR{gamma} in the regulation of smooth muscle cell (SMC) function. Dominate-negative disruption of PPAR{gamma} function by the P465L mutation increased proliferation, migration, and ETS-1 but not ERK activation, and promoted the development intimal hyperplasia after arterial injury.  

TH gif  New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia: Activation of Glycogen Synthase Kinase-3β Followed by Inhibition of MMP-9

Choon-Soo Lee, Yoo-Wook Kwon, Han-Mo Yang, Sung-Hwan Kim, Tae-Youn Kim, Jin Hur, Kyung-Woo Park, Hyun-Jai Cho, Hyun-Jae Kang, Young-Bae Park, and Hyo-Soo Kim
Arterioscler Thromb Vasc Biol. 2009;29:472-479; published online before print February 5 2009, doi:10.1161/ATVBAHA.108.176230
Abstract | Full Text | PDF
Rosiglitazone regulated both VSMC viability and migration through activation of GSK-3β, resulting in reduced neointimal hyperplasia after vascular injury. The mechanism to inhibit migration was that rosiglitazone suppressed MMP-9 via GSK-3β mediated inhibition of NF-{kappa}B DNA binding activity. Our results demonstrate new action mechanism of rosiglitazone to reduce neointimal hyperplasia and may provide rosiglitazone as a new therapeutic approach for proliferative vascular disease.  

TH gif  Mechanisms of Vascular Smooth Muscle NADPH Oxidase 1 (Nox1) Contribution to Injury-Induced Neointimal Formation

Moo Yeol Lee, Alejandra San Martin, Puja K. Mehta, Anna E. Dikalova, Abel Martin Garrido, S. Raju Datla, Erin Lyons, Karl-Heinz Krause, Botond Banfi, J. David Lambeth, Bernard Lassègue, and Kathy K. Griendling
Arterioscler Thromb Vasc Biol. 2009;29:480-487; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.181925
Abstract | Full Text | PDF | Data Supplement
The role of specific NADPH oxidase (Nox) proteins in vascular disease is incompletely understood. We show here that Nox1 plays a critical role in neointima formation by mediating VSMC migration, proliferation, and extracellular matrix production, and that cofilin is a major effector of Nox1-mediated migration.  

TH gif  Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries

Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N. Keswani, Sankaranarayanan Kannan, Xiao-ming Liu, Hong Wang, David A. Tulis, and William Durante
Arterioscler Thromb Vasc Biol. 2009;29:488-494; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.183392
Abstract | Full Text | PDF
Arginase is the central enzyme of the urea cycle that converts L-arginine to L-ornithine and urea. We now report that arginase contributes to cell cycle progression and neointima formation after arterial injury, and identify arginase as a promising therapeutic target in treating vasculoproliferative disorders.  

TH gif  Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis

Shengchuan Dai, Yun He, Haifeng Zhang, Luyang Yu, Ting Wan, Zhe Xu, Dennis Jones, Hong Chen, and Wang Min
Arterioscler Thromb Vasc Biol. 2009;29:495-502; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.180349
Abstract | Full Text | PDF | Data Supplement  

TH gif  Cell Therapy Based on Adipose Tissue-Derived Stromal Cells Promotes Physiological and Pathological Wound Healing

T.G. Ebrahimian, F. Pouzoulet, C. Squiban, V. Buard, M. André, B. Cousin, P. Gourmelon, M. Benderitter, L. Casteilla, and R. Tamarat
Arterioscler Thromb Vasc Biol. 2009;29:503-510; published online before print February 5 2009, doi:10.1161/ATVBAHA.108.178962
Abstract | Full Text | PDF
Adipose tissue-derived stroma cell (ADSC) administration promoted wound healing. Interestingly, GFP-positive ADSCs incorporated in dermal and epidermal tissue in vivo and expressed epidermal markers K5 and K14. ADSCs also improved skin blood perfusion and capillary density, at least through their ability to incorporate into capillary structures in vivo.  

TH gif  Vehicular Emissions Induce Vascular MMP-9 Expression and Activity Associated With Endothelin-1–Mediated Pathways

Amie K. Lund, JoAnn Lucero, Selitá Lucas, Michael C. Madden, Jacob D. McDonald, Jean-Clare Seagrave, Travis L. Knuckles, and Matthew J. Campen
Arterioscler Thromb Vasc Biol. 2009;29:511-517; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.176107
Abstract | Full Text | PDF | Data Supplement  

AL gif  Leukotriene Receptor Antagonism and the Prevention of Extracellular Matrix Degradation During Atherosclerosis and In-Stent Stenosis

Hanna Hlawaty, Marie-Paule Jacob, Liliane Louedec, Didier Letourneur, Charles Brink, Jean-Baptiste Michel, Laurent Feldman, and Magnus Bäck
Arterioscler Thromb Vasc Biol. 2009;29:518-524; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.181750
Abstract | Full Text | PDF | Data Supplement
In the present study, hypercholesteremic rabbits subjected to carotid artery balloon dilatation and stent implantation displayed significantly reduced in-stent intimal hyperplasia after leukotriene receptor antagonist treatment. This effect was in part mediated through reduced MMP activities. The results suggest antileukotrienes as a therapeutic strategy in atherosclerosis and interventional cardiology.  

AL gif  Suppressors of Cytokine Signaling Modulate JAK/STAT-Mediated Cell Responses During Atherosclerosis

Guadalupe Ortiz-Muñoz, Jose Luis Martin-Ventura, Purificacion Hernandez-Vargas, Beñat Mallavia, Virginia Lopez-Parra, Oscar Lopez-Franco, Begoña Muñoz-Garcia, Paula Fernandez-Vizarra, Luis Ortega, Jesus Egido, and Carmen Gomez-Guerrero
Arterioscler Thromb Vasc Biol. 2009;29:525-531; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.173781
Abstract | Full Text | PDF | Data Supplement
We demonstrated an increased expression of SOCS proteins in human and experimental atherosclerotic plaques. In vitro, STAT activation, gene expression, and cell growth were prevented by SOCS overexpression and were increased by SOCS downregulation. In vivo, antisense oligonucleotides targeting SOCS aggravated the atherosclerotic process. This suggests an important role of SOCS as negative regulators of inflammation during atherosclerosis.  

AL gif  The Capacity of Group V sPLA2 to Increase Atherogenicity of ApoE–/– and LDLR–/– Mouse LDL In Vitro Predicts its Atherogenic Role In Vivo

Boris Boyanovsky, Melissa Zack, Kathy Forrest, and Nancy R. Webb
Arterioscler Thromb Vasc Biol. 2009;29:532-538; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.183038
Abstract | Full Text | PDF | Data Supplement  

AL gif  ApoE-Dependent Modulation of HDL and Atherosclerosis by G2A in LDL Receptor–Deficient Mice Independent of Bone Marrow–Derived Cells

Brian W. Parks, Roshni Srivastava, Shaohua Yu, and Janusz H.S. Kabarowski
Arterioscler Thromb Vasc Biol. 2009;29:539-547; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.179937
Abstract | Full Text | PDF | Data Supplement
G2A promotes atherosclerosis in LDLR knockout mice. Atheroprotection in G2A-deficient LDLR knockout mice was dependent on ApoE and associated with HDL elevation and increased hepatocyte ApoA1 secretion. G2A deficiency in resident tissues, not bone marrow-derived cells, elevated HDL and suppressed atherosclerosis. Modulation of HDL might contribute to G2A proatherogenic action.  

AL gif  Tissue-Specific Roles of ABCA1 Influence Susceptibility to Atherosclerosis

Liam R. Brunham, Roshni R. Singaraja, MyNgan Duong, Jenelle M. Timmins, Catherine Fievet, Nagat Bissada, Martin H. Kang, Amrit Samra, Jean-Charles Fruchart, Bruce McManus, Bart Staels, John S. Parks, and Michael R. Hayden
Arterioscler Thromb Vasc Biol. 2009;29:548-554; published online before print February 5 2009, doi:10.1161/ATVBAHA.108.182303
Abstract | Full Text | PDF | Data Supplement
We investigated the role of ABCA1 in atherosclerosis. Global ABCA1 overexpression reduced atherosclerosis. Deletion of hepatic Abca1 significantly accelerated atherosclerosis, indicating that the liver is an important site at which Abca1 plays an antiatherogenic role. In contrast, macrophage-specific inactivation of Abca1 displayed no change in atherosclerosis.  

AL gif  n-3 Fatty Acids Reduce Arterial LDL-Cholesterol Delivery and Arterial Lipoprotein Lipase Levels and Lipase Distribution

Chuchun L. Chang, Toru Seo, Mika Matsuzaki, Tilla S. Worgall, and Richard J. Deckelbaum
Arterioscler Thromb Vasc Biol. 2009;29:555-561; published online before print February 5 2009, doi:10.1161/ATVBAHA.108.182287
Abstract | Full Text | PDF | Data Supplement
In C57BL/6 mice fed a chow, saturated fatty acid (SAT)-rich, or n-3 diets for 12 weeks, SAT increased arterial LDL-cholesterol uptake. In contrast, n-3 markedly reduced LDL-cholesterol. Patterns of arterial cholesterol deposition parallel distribution and expression of arterial LpL.  

 

Cell Biology/SignalingBack

TH gif  FXR Promotes Endothelial Cell Motility Through Coordinated Regulation of FAK and MMP-9

Amitava Das, Usman Yaqoob, Dolly Mehta, and Vijay H. Shah
Arterioscler Thromb Vasc Biol. 2009;29:562-570; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.182725
Abstract | Full Text | PDF | Data Supplement
The signaling pathways linking bile acid receptor FXR and its transcriptional target MMP-9 to changes in actin cytoskeleton, responsible for EC migration remains unexplored. Here, using a variety of complementary cell biological and biochemical approaches, we demonstrate a key role for tyrosine phosphorylation of FAK at Y397 in the process of FXR-induced MMP-9-dependent endothelial cell motility and in vitro vascular tube formation.  

TH gif  Caspase-8 Is Involved in Neovascularization-Promoting Progenitor Cell Functions

Dörte Scharner, Lothar Rössig, Guillaume Carmona, Emmanouil Chavakis, Carmen Urbich, Ariane Fischer, Tae-Bong Kang, David Wallach, Yungping Jeffrey Chiang, Yonathan Lissanu Deribe, Ivan Dikic, Andreas M. Zeiher, and Stefanie Dimmeler
Arterioscler Thromb Vasc Biol. 2009;29:571-578; published online before print January 2 2009, doi:10.1161/ATVBAHA.108.182006
Abstract | Full Text | PDF | Data Supplement
The neovascularization-promoting potential of progenitor cells depends on survival and retention of the infused cells to the tissue. Here we provide evidence that caspase-8 is essential for progenitor cell adhesion, migration, and in vivo homing demonstrating a novel apoptosis-unrelated role of caspase-8 in proangiogenic cells.  

AL gif  Mechanisms Targeting Apolipoprotein B100 to Proteasomal Degradation: Evidence That Degradation Is Initiated by BiP Binding at the N Terminus and the Formation of a p97 Complex at the C Terminus

Angela C. Rutledge, Wei Qiu, Rianna Zhang, Rita Kohen-Avramoglu, Nina Nemat-Gorgani, and Khosrow Adeli
Arterioscler Thromb Vasc Biol. 2009;29:579-585; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.181859
Abstract | Full Text | PDF | Data Supplement
Proteasomal targeting mechanisms mediating cotranslational degradation of apolipoprotein B100 (apoB) were investigated. BiP and p97 were found to respectively bind the N and C termini of apoB cotranslationally and initiate the formation of a degradative complex. p97 was essential for proteasomal degradation of a C-terminal portion of apoB.  

TH gif  Certain Progestins Prevent the Enhancing Effect of 17β-Estradiol on NO-Mediated Inhibition of Platelet Aggregation by Endothelial Cells

Murielle Zerr-Fouineau, Marie Jourdain, Caroline Boesch, Markus Hecker, Christian Bronner, and Valérie B. Schini-Kerth
Arterioscler Thromb Vasc Biol. 2009;29:586-593; published online before print December 18 2008, doi:10.1161/ATVBAHA.108.178004
Abstract | Full Text | PDF
This study examined whether progestins antagonize the beneficial effect of 17β-estradiol on the endothelial formation of NO. The present findings indicate that certain progestins overcome the 17β-E-induced NO-mediated inhibition of platelet aggregation by endothelial cells, in part, by preventing the expression of eNOS and GTPCH I.  

 

Clinical and Population StudiesBack

AL gif  Associations of Pentraxin 3 With Cardiovascular Disease and All-Cause Death: The Cardiovascular Health Study

Nancy Swords Jenny, Alice M. Arnold, Lewis H. Kuller, Russell P. Tracy, and Bruce M. Psaty
Arterioscler Thromb Vasc Biol. 2009;29:594-599; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.178947
Abstract | Full Text | PDF
We examined associations of pentraxin 3 (PTX3), a specific marker of vascular inflammation, with cardiovascular disease (CVD) and all-cause death in older adults. PTX3 was associated with CVD-related and all-cause death but not nonfatal CVD events. PTX3 may provide insight into vascular health in aging.  

TH gif   Identification of Quantitative Trait Loci for Fibrin Clot Phenotypes: The EuroCLOT Study

Frances M.K. Williams, Angela M. Carter, Bernet Kato, Mario Falchi, Lise Bathum, Gabriela Surdulescu, Kirsten Ohm Kyvik, Aarno Palotie, Tim D. Spector, Peter J. Grant on Behalf of the EuroCLOT Investigators
Arterioscler Thromb Vasc Biol. 2009;29:600-605; published online before print January 15 2009, doi:10.1161/ATVBAHA.108.178103
Abstract | Full Text | PDF | Data Supplement
Linkage analysis of fibrin phenotypes in UK and Danish twin pairs has revealed 6 chromosomal regions with LOD >3. The results indicate genetic contributions to variability in fibrin phenotypes and highlight regions in the human genome which warrant further investigation in relation to cardiovascular disease.  

TH gif  The Brachial Artery Remodels to Maintain Local Shear Stress Despite the Presence of Cardiovascular Risk Factors

William B. Chung, Naomi M. Hamburg, Monika Holbrook, Sherene M. Shenouda, Mustali M. Dohadwala, Dellara F. Terry, Noyan Gokce, and Joseph A. Vita
Arterioscler Thromb Vasc Biol. 2009;29:606-612; published online before print January 22 2009, doi:10.1161/ATVBAHA.108.181495
Abstract | Full Text | PDF
We investigated whether risk factors induce maladaptive remodeling in the brachial artery by measuring diameter and flow by ultrasound in 1583 subjects. Diameter and flow were higher, but shear stress was unaffected by risk factors. These findings suggest that enlargement of the brachial artery in the setting of risk factors reflects adaptive remodeling.  

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