Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
    « Previous Issue | Next Issue »
  Cover Image

Volume 25, Issue 8; August 1, 2005

To see an article, click its "Full Text" or "PDF" link. To review many abstracts, check the boxes to the left of the titles you want, and click the "Get All Checked Abstract(s)" button. To see one abstract at a time, click its "Abstract" link.

button_lock_image article is free immediately upon publication

 

EditorialsBack

CRP—Marker or Maker of Cardiovascular Disease?

Jan Nilsson
Arterioscler Thromb Vasc Biol. 2005;25:1527-1528, doi:10.1161/01.ATV.0000174796.81443.3f.
Full Text | PDF  

Getting a GRP on Tissue Factor Activation

Lindsay M. Pozza and Richard C. Austin
Arterioscler Thromb Vasc Biol. 2005;25:1529-1531, doi:10.1161/01.ATV.0000177041.47444.e2.
Full Text | PDF  

Stored Iron and Vascular Reactivity

Jerome L. Sullivan
Arterioscler Thromb Vasc Biol. 2005;25:1532-1535, doi:10.1161/01.ATV.0000174124.20147.22.
Full Text | PDF  

Kevin Jon Williams and Ira Tabas
Arterioscler Thromb Vasc Biol. 2005;25:1536-1540, doi:10.1161/01.ATV.0000174795.62387.d3.
Abstract | Full Text | PDF  

 

Special ArticleBack

Complex Trait Locus Linkage Mapping in Atherosclerosis: Time to Take a Step Back Before Moving Forward?

Rebecca L. Pollex and Robert A. Hegele
Arterioscler Thromb Vasc Biol. 2005;25:1541-1544; published online before print June 9 2005, doi:10.1161/01.ATV.0000173307.25652.89.
Full Text | PDF  

 

Brief ReviewsBack

Mattias Belting, Jasimuddin Ahamed, and Wolfram Ruf
Arterioscler Thromb Vasc Biol. 2005;25:1545-1550; published online before print May 19 2005, doi:10.1161/01.ATV.0000171155.05809.bf.
Abstract | Full Text | PDF
Activation of coagulation precedes or coincides with angiogenesis in wound healing and post-ischemic tissue regeneration. Advanced cancer is associated with a hypercoagulable state, and tissue factor expression by cancer cells has received widespread attention. Here we review the molecular mechanisms of tissue factor pathways in angiogenesis and tumorigenesis with emphasis on the intriguing role for tissue factor cytoplasmic domain signaling.  

Thomas Münzel, Andreas Daiber, Volker Ullrich, and Alexander Mülsch
Arterioscler Thromb Vasc Biol. 2005;25:1551-1557; published online before print May 5 2005, doi:10.1161/01.ATV.0000168896.64927.bb.
Abstract | Full Text | PDF | Data Supplement  

David A. Vorp and Jonathan P. Vande Geest
Arterioscler Thromb Vasc Biol. 2005;25:1558-1566; published online before print August 1 2005, doi:10.1161/01.ATV.0000174129.77391.55.
Abstract | Full Text | PDF
Careful consideration of the biomechanics of abdominal aortic aneurysm (AAA) may potentially lead to an improved, case-specific prediction of AAA rupture potential, thereby significantly improving the clinical management of these patients. Presented here is an overview of research aimed at improving our understanding of the biomechanics of AAA.  

Catherine L. Higgins, Seth A. Marvel, and Joel D. Morrisett
Arterioscler Thromb Vasc Biol. 2005;25:1567-1576; published online before print May 26 2005, doi:10.1161/01.ATV.0000172017.79441.73.
Abstract | Full Text | PDF  

 

Vascular BiologyBack

Haoyi Zheng, Ritchard Cable, Bryan Spencer, Nancy Votto, and Stuart D. Katz
Arterioscler Thromb Vasc Biol. 2005;25:1577-1583; published online before print June 16 2005, doi:10.1161/01.ATV.0000174126.28201.61.
Abstract | Full Text | PDF
Reduction of iron stores secondary to blood donation has been hypothesized to reduce coronary risk. We prospectively assessed the effects of blood donation frequency on body iron stores and physiological and biochemical biomarkers of vascular function. High-frequency blood donors had decreased body iron stores, decreased oxidative stress, and enhanced vascular function when compared with low-frequency donors.  

Kai Wang, Xiaorong Zhou, Zhongmin Zhou, Niladri Mal, Liming Fan, Ming Zhang, A. Michael Lincoff, Edward F. Plow, Eric J. Topol, and Marc S. Penn
Arterioscler Thromb Vasc Biol. 2005;25:1584-1589; published online before print June 9 2005, doi:10.1161/01.ATV.0000172687.01179.d4.
Abstract | Full Text | PDF | Data Supplement
The relative importance of platelet and endothelial P-selectins to neointimal formation after vascular injury was determined by bone marrow transplantation. Significantly less neointima was observed from EC-Psel mice when compared with Plt-Psel mice and WT mice. Decreased neointimal formation was accompanied by reduced inflammation.  

Zsolt Bagi, John A. Frangos, Jiunn-Chern Yeh, Charles R. White, Gabor Kaley, and Akos Koller
Arterioscler Thromb Vasc Biol. 2005;25:1590-1595; published online before print May 12 2005, doi:10.1161/01.ATV.0000170136.71970.5f.
Abstract | Full Text | PDF | Data Supplement
We found that in isolated skeletal muscle arterioles of PECAM-1 knockout mice the NO-mediated dilations to high temporal gradients of wall shear stress is reduced. Thus, we propose a role for PECAM-1 in the ability of the endothelium to sense high temporal gradients of shear stress which is coupled with NO-mediated vasodilation.  

James L. Park, Robert D. Loberg, Damon Duquaine, Hongyu Zhang, Baljit K. Deo, Noelia Ardanaz, Jami Coyle, Kevin B. Atkins, MaryLee Schin, Maureen J. Charron, Arno K. Kumagai, Patrick J. Pagano, and Frank C. Brosius, III
Arterioscler Thromb Vasc Biol. 2005;25:1596-1602; published online before print May 12 2005, doi:10.1161/01.ATV.0000170137.41079.ab.
Abstract | Full Text | PDF | Data Supplement
We found that GLUT4 is a predominant transporter in VSMCs, and that GLUT4, as well as non-GLUT4 transporters, are necessary for agonist-induced VSMC contraction. However, each transporter participates in VSMC contraction selectively, depending on the agonist. Decreased GLUT4 expression may account for some functional changes associated with vascular diseases such as hypertension.  

Stephan Schiekofer, Gennaro Galasso, Kaori Sato, Benjamin J. Kraus, and Kenneth Walsh
Arterioscler Thromb Vasc Biol. 2005;25:1603-1609; published online before print May 26 2005, doi:10.1161/01.ATV.0000171994.89106.ca.
Abstract | Full Text | PDF | Data Supplement
Angiogenic repair of ischemic hindlimbs was impaired in diabetic Leprdb/db and WT mice as evaluated by laser Doppler measurements. cDNA expression profiles were created from adductor muscle of Leprdb/db and WT mice before and after hindlimb ischemia illustrating the dysregulation of a complex angiogenesis-regulatory network in diabetic mice.  

Zsolt Bagi, Nora Erdei, Attila Toth, Wei Li, Thomas H. Hintze, Akos Koller, and Gabor Kaley
Arterioscler Thromb Vasc Biol. 2005;25:1610-1616; published online before print June 9 2005, doi:10.1161/01.ATV.0000172688.26838.9f.
Abstract | Full Text | PDF
Here we report that mice with type 2 diabetes mellitus have elevated systolic blood pressures and increased peripheral vascular resistance. In type 2 diabetic mice, these alterations are associated with enhanced skeletal muscle arteriolar tone, which is likely attributable to increased release of COX-2-derived constrictor prostaglandins within the arteriolar wall.  

C.A. Gunnett, D.D. Lund, A.K. McDowell, F.M. Faraci, and D.D. Heistad
Arterioscler Thromb Vasc Biol. 2005;25:1617-1622; published online before print June 2 2005, doi:10.1161/01.ATV.0000172626.00296.ba.
Abstract | Full Text | PDF
Inducible nitric oxide synthase (iNOS) is expressed in arteries during inflammation and may impair vascular contraction of rabbit carotid artery by activation of soluble guanylate cyclase. iNOS also impairs vascular relaxation by limiting availability of BH4. Furthermore, expression of iNOS in endothelium impairs vascular function more than expression of iNOS in adventitia.  

J. Scott McNally, Archana Saxena, Hua Cai, Sergey Dikalov, and David G. Harrison
Arterioscler Thromb Vasc Biol. 2005;25:1623-1628; published online before print May 19 2005, doi:10.1161/01.ATV.0000170827.16296.6e.
Abstract | Full Text | PDF | Data Supplement
In this study we found that H2O2-dependent calcium release from the ER caused conversion of XDH to XO, and that this was prevented by nitric oxide. This may represent a feed-forward mechanism in many disease processes whereby H2O2 can stimulate further ROS production through XDH-to-XO conversion.  

Leon J. Schurgers, Kirsten J.F. Teunissen, Marjo H.J. Knapen, Martijn Kwaijtaal, Rob van Diest, Ad Appels, Chris P. Reutelingsperger, Jack P.M. Cleutjens, and Cees Vermeer
Arterioscler Thromb Vasc Biol. 2005;25:1629-1633; published online before print June 16 2005, doi:10.1161/01.ATV.0000173313.46222.43.
Abstract | Full Text | PDF | Data Supplement
MGP is a strong inhibitor of arterial calcification; its function depends on vitamin K status. In this work, we demonstrate that: (1) undercarboxylated MGP is associated with arterial calcification, and (2) patients with angioplasty tend to have low serum MGP.  

 

Atherosclerosis and LipoproteinsBack

Peter F. Bodary, Shufang Gu, Yuechun Shen, Alyssa H. Hasty, Joshua M. Buckler, and Daniel T. Eitzman
Arterioscler Thromb Vasc Biol. 2005;25:e119-e122; published online before print June 9 2005, doi:10.1161/01.ATV.0000173306.47722.ec.
Abstract | Full Text | PDF
The direct role of leptin in vascular disease remains controversial. Our studies indicate that exogenous leptin promotes atherosclerosis and thrombosis and support the concept that elevations of leptin may increase the risk for cardiovascular disease.  

Peter F. Bodary, Shufang Gu, Yuechun Shen, Alyssa H. Hasty, Joshua M. Buckler, and Daniel T. Eitzman
Arterioscler Thromb Vasc Biol. 2005;25:1634.
Abstract | Full Text | PDF  

A. Trion, M.P.M. de Maat, J.W. Jukema, A. van der Laarse, M.C. Maas, E.H. Offerman, L.M. Havekes, A.J. Szalai, H.M.G. Princen, and J.J. Emeis
Arterioscler Thromb Vasc Biol. 2005;25:1635-1640; published online before print May 26 2005, doi:10.1161/01.ATV.0000171992.36710.1e.
Abstract | Full Text | PDF | Data Supplement
C-reactive protein (CRP) is associated with incidence and severity of cardiovascular disease (CVD). Whether CRP is causally involved in atherosclerosis, the underlying cause of CVD, is unclear. This study in apolipoprotein E*3-Leiden transgenic mice demonstrated that mildly elevated levels of CRP in plasma did not contribute to atherosclerosis development.  

Kurt Reifenberg, Hans-Anton Lehr, Daniela Baskal, Elena Wiese, Stephan C. Schaefer, Steven Black, David Samols, Michael Torzewski, Karl J. Lackner, Matthias Husmann, Maria Blettner, and Sucharit Bhakdi
Arterioscler Thromb Vasc Biol. 2005;25:1641-1646; published online before print May 26 2005, doi:10.1161/01.ATV.0000171983.95612.90.
Abstract | Full Text | PDF | Data Supplement
Transgenic mice expressing rabbit CRP were crossbred onto apolipoprotein E knockout animals, and the animals were monitored for the development of atherosclerotic lesions. We failed to detect a significant influence of CRP transgenesis on atherogenesis in apoE knockout mice.  

Vladimir R. Babaev, Patricia G. Yancey, Sergey V. Ryzhov, Valentina Kon, Matthew D. Breyer, Mark A. Magnuson, Sergio Fazio, and MacRae F. Linton
Arterioscler Thromb Vasc Biol. 2005;25:1647-1653; published online before print June 9 2005, doi:10.1161/01.ATV.0000173413.31789.1a.
Abstract | Full Text | PDF | Data Supplement
To investigate the contribution of macrophage PPAR{gamma} on atherogenesis, we generated macrophage-specific PPAR{gamma} knockout (MacPPAR{gamma}KO) mice. C57BL/6 and low-density lipoprotein (LDL) receptor-deficient mice were reconstituted with MacPPAR{gamma}KO marrow. These mice had significantly larger atherosclerotic lesions than control recipients. MacPPAR{gamma}KO macrophages had decreased uptake of oxidized LDL and increased CCR2 expression levels.  

Tobias Pischon, Jennifer K. Pai, JoAnn E. Manson, Frank B. Hu, Kathryn M. Rexrode, David Hunter, and Eric B. Rimm
Arterioscler Thromb Vasc Biol. 2005;25:1654-1658; published online before print May 26 2005, doi:10.1161/01.ATV.0000171993.78135.7e.
Abstract | Full Text | PDF
This study did not find a decreased risk of CHD among carriers of the PPARG2 A12 allele in 2 nested case control studies of women and men. Overweight but not normal weight carriers of the A12 allele were at increased risk of CHD; however, these results require confirmation from future studies.  

Giuseppina Caligiuri, Emilie Groyer, Jamila Khallou-Laschet, Ayman Al Haj Zen, Julie Sainz, Dominique Urbain, Anh-Thu Gaston, Mathilde Lemitre, Antonino Nicoletti, and Antoine Lafont
Arterioscler Thromb Vasc Biol. 2005;25:1659-1664; published online before print June 2 2005, doi:10.1161/01.ATV.0000172660.24580.b4.
Abstract | Full Text | PDF
Lymphocyte activation plays a major role in the pathogenesis of plaque thrombosis. CD31+ T cells regulate T cells activation. We found that circulating CD31+ T cells were reduced in apolipoprotein E knockout mice with plaque thrombosis. Our data suggest that CD31+ T cells may play a regulatory role in plaque thrombosis.  

Francesco Cipollone, Andrea Mezzetti, Maria Luigia Fazia, Chiara Cuccurullo, Annalisa Iezzi, Sante Ucchino, Francesco Spigonardo, Marco Bucci, Franco Cuccurullo, Stephen M. Prescott, and Diana M. Stafforini
Arterioscler Thromb Vasc Biol. 2005;25:1665-1670; published online before print June 2 2005, doi:10.1161/01.ATV.0000172632.96987.2d.
Abstract | Full Text | PDF
Plaque instability involves the participation of numerous genes, the most of which are still unknown. We conducted analyses of 5-lipoxygenase expression in human carotid plaques. 5-Lipoxygenase was overexpressed in symptomatic compared with asymptomatic plaques and correlated with increased leukotriene B4 and metalloproteinase production expression. Thus, this study indicates a potential role for 5-lipoxygenase in plaque instability.  

Dan Gavrila, Wei Gen Li, Michael L. McCormick, Manesh Thomas, Alan Daugherty, Lisa A. Cassis, Francis J. Miller, Jr, Larry W. Oberley, Kevin C. Dellsperger, and Neal L. Weintraub
Arterioscler Thromb Vasc Biol. 2005;25:1671-1677; published online before print June 2 2005, doi:10.1161/01.ATV.0000172631.50972.0f.
Abstract | Full Text | PDF | Data Supplement
We investigated the effects of vitamin E on angiotensin II-induced abdominal aortic aneurysms (AAAs) in apolipoprotein E-deficient mice. Vitamin E reduced AAA maximal diameter and weight while attenuating aortic 8-isoprostane formation, macrophage infiltration, and osteopontin expression (P<0.05, respectively). Vitamin E also decreased the combined end point of fatal plus nonfatal artic rupture by 44% (P<0.05). Vitamin E did not affect lipid profile, systolic blood pressure, or the extent of aortic root atherosclerosis. We conclude that vitamin E inhibits AAA formation and improves clinical end points in this experimental model.  

Katariina Öörni, Pirjo Posio, Mika Ala-Korpela, Matti Jauhiainen, and Petri T. Kovanen
Arterioscler Thromb Vasc Biol. 2005;25:1678-1683; published online before print May 5 2005, doi:10.1161/01.ATV.0000168912.42941.60.
Abstract | Full Text | PDF | Data Supplement
Lipolysis of small VLDL and IDL particles by sphingomyelinase induces their aggregation and fusion and enhances binding of the particles to proteoglycans. The results suggest that sphingomyelinase-induced modification of small VLDL and IDL particles can lead to increased retention of the atherogenic triglyceride-rich lipoprotein particles in the arterial intima.  

Katherine Choy, Konstanze Beck, Francoise Y. Png, Ben J. Wu, Steven B. Leichtweis, Shane R. Thomas, Jing Y. Hou, Kevin D. Croft, Trevor A. Mori, and Roland Stocker
Arterioscler Thromb Vasc Biol. 2005;25:1684-1690; published online before print June 16 2005, doi:10.1161/01.ATV.0000174125.89058.b6.
Abstract | Full Text | PDF | Data Supplement
We investigated how the antioxidant probucol increases lesion size at the sinus and decreases atherosclerosis at distal sites in apolipoprotein E-deficient mice. Probucol affected atherosclerosis independent of arterial lipid oxidation. Rather, probucol decreased accumulation of macrophages in lesions, and it promoted a more stable lesion composition at the aortic sinus.  

Nirupa R. Matthan, Susan M. Jalbert, Stefania Lamon-Fava, Gregory G. Dolnikowski, Francine K. Welty, Hugh R. Barrett, Ernst J. Schaefer, and Alice H. Lichtenstein
Arterioscler Thromb Vasc Biol. 2005;25:1691-1696; published online before print June 2 2005, doi:10.1161/01.ATV.0000172629.12846.b8.
Abstract | Full Text | PDF | Data Supplement
Postmenopausal women have higher VLDL-C and LDL-C levels compared with premenopausal women. To determine mechanism, apolipoprotein kinetic studies were conducted in 24 women. Postmenopausal women had higher TRL and LDL pool sizes, which were accounted for by lower TRL and LDL apoB-100 catabolic rates. No significant difference in plasma HDL-C levels or apoA-I kinetics parameters were observed between groups.  

Martin Adiels, Jan Borén, Muriel J. Caslake, Philip Stewart, Aino Soro, Jukka Westerbacka, Bernt Wennberg, Sven-Olof Olofsson, Chris Packard, and Marja-Riitta Taskinen
Arterioscler Thromb Vasc Biol. 2005;25:1697-1703; published online before print June 9 2005, doi:10.1161/01.ATV.0000172689.53992.25.
Abstract | Full Text | PDF | Data Supplement
Analysis of the synthesis and metabolism of VLDL1 and VLDL2 in patients with type 2 diabetes and healthy controls revealed that type 2 diabetes and insulin resistance are associated with excess hepatic production of VLDL1 particles similar in size and composition to those of nondiabetic subjects.  

Cecilia M. Devlin, Sung-Joon Lee, George Kuriakose, Craig Spencer, Lev Becker, Itamar Grosskopf, Carol Ko, Li-Shin Huang, Marlys L. Koschinsky, Allen D. Cooper, and Ira Tabas
Arterioscler Thromb Vasc Biol. 2005;25:1704-1710; published online before print May 19 2005, doi:10.1161/01.ATV.0000170819.57945.03.
Abstract | Full Text | PDF | Data Supplement
Humans with high expression of apolipoprotein(a) [apo(a)] and high plasma levels of lipoprotein(a) [Lp(a)] are at increased risk for atherosclerosis, but the mechanism is not known. We propose that high levels of apo(a)/Lp(a), perhaps acting via a specific cell-surface binding domain, inhibit hepatic clearance of remnants, leading to high plasma levels of RLPs and markedly enhanced atherosclerosis. We speculate that the KIV5-8 region of apo(a) competes with one or more receptors for remnant clearance in the liver and that this process may represent one mechanism accounting for increased atherosclerosis in humans with high secretion levels of apo(a).  

Fabien Forcheron, Liliana Legedz, Guiletta Chinetti, Patrick Feugier, Dominique Letexier, Giampierro Bricca, and Michel Beylot
Arterioscler Thromb Vasc Biol. 2005;25:1711-1717; published online before print June 16 2005, doi:10.1161/01.ATV.0000174123.19103.52.
Abstract | Full Text | PDF
We measured in human atheroma and nearby tissue the expression of perilipin and ADRP, which are key factors of cholesterol metabolism. We show the presence and induction of perilipin in atheroma and coordinated modifications of the expression of regulatory factors for cholesterol metabolism that favor its uptake and storage and reduce its efflux.  

Claudia Imke, Beatriz L. Rodriguez, John S. Grove, Judith R. McNamara, Carol Waslien, Alan R. Katz, Bradley Willcox, Katsuhiko Yano, and J. David Curb
Arterioscler Thromb Vasc Biol. 2005;25:1718-1722; published online before print June 9 2005, doi:10.1161/01.ATV.0000173310.85845.7b.
Abstract | Full Text | PDF
Remnant-like particles (RLPs) have been proposed as a new risk factor for coronary heart disease. The association between RLP levels and coronary heart disease (CHD) was evaluated in a cohort of the Honolulu Heart Program that included 1156 Japanese-American men aged 60 to 82. RLP levels were significantly related to 17-year incidence of CHD independently of nonlipid cardiovascular risk factors and of total cholesterol or HDL and LDL cholesterol. RLP levels did not provide additional information about risk of CHD over and above total triglyceride levels. Therefore, this study does not support the need for testing of remnants if measures of fasting triglycerides are available.  

James G. Terry, J. Jeffrey Carr, Rong Tang, Gregory W. Evans, Ethel O. Kouba, Rong Shi, Delilah R. Cook, Jose L.C. Vieira, Mark A. Espeland, Michele F. Mercuri, and John R. Crouse, III
Arterioscler Thromb Vasc Biol. 2005;25:1723-1728; published online before print June 9 2005, doi:10.1161/01.ATV.0000173418.42264.19.
Abstract | Full Text | PDF
We compared coronary artery calcium (CAC) and carotid intima-media thickness (IMT) as indices of coronary artery disease (CAD). Elevated IMT doubled the odds of CAD, but elevated CAC increased risk of CAD 28-fold. CAC compares well to the "gold standard" carotid IMT as a noninvasive index of prevalent CAD.  

Ronald L. Wolf, Suzanne L. Wehrli, Andra M. Popescu, John H. Woo, Hee Kwon Song, Alexander C. Wright, Emile R. Mohler, III, John D. Harding, Eric L. Zager, Ronald M. Fairman, Michael A. Golden, Omaida C. Velazquez, Jeffrey P. Carpenter, and Felix W. Wehrli
Arterioscler Thromb Vasc Biol. 2005;25:1729-1735; published online before print June 9 2005, doi:10.1161/01.ATV.0000173311.39867.65.
Abstract | Full Text | PDF
High-resolution MRI was compared with micro-CT for evaluating quantity and pattern of mineral deposition in 20 carotid endarterectomy specimens. Mineral volumes generated from CT and MR data were highly correlated. Patterns of mineralization were more clearly depicted on CT. Extent and morphology of mineralization may help assess plaque stability.  

 

ThrombosisBack

J. Khallou-Laschet, G. Caligiuri, E. Tupin, A.-T. Gaston, B. Poirier, E. Groyer, D. Urbain, S. Maisnier-Patin, R. Sarkar, S.V. Kaveri, S. Lacroix-Desmazes, and A. Nicoletti
Arterioscler Thromb Vasc Biol. 2005;25:e123-e126; published online before print May 26 2005, doi:10.1161/01.ATV.0000171995.22284.9a.
Abstract | Full Text | PDF
The contribution of coagulation factor VIII (FVIII)-dependent pathway in atherogenesis was addressed in hemophilic apolipoprotein E-deficient mice (E{degrees}/FVIII{degrees}).  

J. Khallou-Laschet, G. Caligiuri, E. Tupin, A.-T. Gaston, B. Poirier, E. Groyer, D. Urbain, S. Maisnier-Patin, R. Sarkar, S.V. Kaveri, S. Lacroix-Desmazes, and A. Nicoletti
Arterioscler Thromb Vasc Biol. 2005;25:1736.
Abstract | Full Text | PDF  

Gourab Bhattacharjee, Jasimuddin Ahamed, Brian Pedersen, Amr El-Sheikh, Nigel Mackman, Wolfram Ruf, Cheng Liu, and Thomas S. Edgington
Arterioscler Thromb Vasc Biol. 2005;25:1737-1743; published online before print June 9 2005, doi:10.1161/01.ATV.0000173419.31242.56.
Abstract | Full Text | PDF
The present study examines the interaction between the 78-kDa glucose-regulated protein (Grp78) and tissue factor (TF). The results demonstrate that Grp78 negatively regulates TF functional activity via direct binding to and functional inhibition of TF on the cell surface.  

Khalid Al-Nedawi, Janusz Szemraj, and Czeslaw S. Cierniewski
Arterioscler Thromb Vasc Biol. 2005;25:1744-1749; published online before print May 26 2005, doi:10.1161/01.ATV.0000172007.86541.76.
Abstract | Full Text | PDF
We showed that mast cell-derived exosomes induce PAI-1 expression in endothelial cells. Proteomic analysis of exosomes identified components of the prothrombinase complex that after activation are responsible for upregulation of PAI-1.  

Angelika Gillitzer, Mario Peluso, Karl-Ludwig Laugwitz, Götz Münch, Steffen Massberg, Ildiko Konrad, Meinrad Gawaz, and Martin Ungerer
Arterioscler Thromb Vasc Biol. 2005;25:1750-1755; published online before print June 2 2005, doi:10.1161/01.ATV.0000172659.01157.c6.
Abstract | Full Text | PDF | Data Supplement
A novel selection method allowed us to produce recombinant transgene-expressing culture-derived platelets in sufficient amounts to study genetically modified platelets in vitro and in vivo. These platelets maintain the physiological characteristics of freshly isolated platelets.  

Nadine Ajzenberg, Clarisse Berroeta, Ivan Philip, Bernard Grandchamp, Pierre Ducellier, Virginie Huart, Patrice Verpillat, Marie-Claude Guillin, and Joelle Benessiano
Arterioscler Thromb Vasc Biol. 2005;25:1756-1760; published online before print June 9 2005, doi:10.1161/01.ATV.0000173308.13054.4f.
Abstract | Full Text | PDF
An important combined effect of the -92C and 807T polymorphisms of the {alpha}2 gene in increasing the expression of human platelet {alpha}2ß1 receptors has been observed, suggesting that this haplotype could modulate variations in {alpha}2ß1 receptor density.  

 

Letters to the EditorBack

Circulating Matrix Metalloproteinase-9 Levels as a Possible Marker of Aortic Stiffness

Jose E. Tanus-Santos and Raquel F. Gerlach
Arterioscler Thromb Vasc Biol. 2005;25:e127, doi:10.1161/01.ATV.0000172661.60304.57.
Full Text | PDF  

 

CorrectionsBack

Correction


Arterioscler Thromb Vasc Biol. 2005;25:e128.
Full Text | PDF  

Correction


Arterioscler Thromb Vasc Biol. 2005;25:e129.
Full Text | PDF  

Correction


Arterioscler Thromb Vasc Biol. 2005;25:e130.
Full Text | PDF  

Spotlight

TOC Spotlight File Banner1TOCpage

Banner2TOCpage