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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 24, Issue 9; September 1, 2004

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EditorialsBack

Myocardin—Not Quite MyoD

Michael S. Parmacek
Arterioscler Thromb Vasc Biol. 2004;24:1535-1537, doi:10.1161/01.ATV.0000141044.03875.7f.
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Unique Pathway for Cholesterol Uptake in Fat Cells

Sergio Fazio and MacRae F. Linton
Arterioscler Thromb Vasc Biol. 2004;24:1538-1539, doi:10.1161/01.ATV.0000140821.25572.1b.
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How Vascular NAD(P)H Oxidase Activity and Nox Isoform Expression are Regulated

Mitsuhiro Yokoyama and Nobutaka Inoue
Arterioscler Thromb Vasc Biol. 2004;24:1540-1541, doi:10.1161/01.ATV.0000142356.48952.33.
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Brief ReviewsBack

Rama Natarajan and Jerry L. Nadler
Arterioscler Thromb Vasc Biol. 2004;24:1542-1548; published online before print May 27 2004, doi:10.1161/01.ATV.0000133606.69732.4c.
Abstract | Full Text | PDF
Evidence suggests that inflammatory responses in the vasculature can be elicited by small oxidized lipids that are components of oxidized low-density lipoprotein or products of the lipoxygenase and cyclooxygenase pathways of arachidonic and linoleic acid metabolism. This review evaluates these inflammatory and proatherogenic pathways in the pathogenesis of diabetic vascular disease.  

Eva M. Muñoz and Robert J. Linhardt
Arterioscler Thromb Vasc Biol. 2004;24:1549-1557; published online before print July 1 2004, doi:10.1161/01.ATV.0000137189.22999.3f.
Abstract | Full Text | PDF
Heparin and structurally related heparan sulfate bind a large number of proteins, taking part in a wide range of biological processes, particularly ones involved in vascular biology. Heparin-binding domains share certain common structural features, but there is no absolute dependency on specific sequences or protein folds.  

Eleanor M. Scott, Robert A.S. Ariëns, and Peter J. Grant
Arterioscler Thromb Vasc Biol. 2004;24:1558-1566; published online before print June 24 2004, doi:10.1161/01.ATV.0000136649.83297.bf.
Abstract | Full Text | PDF
The formation of a fibrin clot is one of the key events in atherothrombotic vascular disease. This review discusses how genetic and environmental factors alter fibrin structure and function and the implications this has for the clinical presentation of vascular disease.  

Teri A. Manolio, Eric Boerwinkle, Christopher J. O’Donnell, and Alexander F. Wilson
Arterioscler Thromb Vasc Biol. 2004;24:1567-1577; published online before print July 15 2004, doi:10.1161/01.ATV.0000138789.11433.c1.
Abstract | Full Text | PDF | Data Supplement
Only 1 genetic variant, MMP 3, has shown consistently positive associations with ultrasonographic carotid disease, although it has not been studied widely. Another, PON1 L55 mol/L, is weakly associated in subgroups only. Genetic variants reported to be associated with clinical cardiovascular disease show weak or no relationship to carotid atherosclerosis.  

J.-C. Tille and M.S. Pepper
Arterioscler Thromb Vasc Biol. 2004;24:1578-1590; published online before print July 1 2004, doi:10.1161/01.ATV.0000137390.56554.df.
Abstract | Full Text | PDF
Increased understanding of the mechanisms of angiogenesis and lymphangiogenesis has provided a glimpse at some of the molecules involved in the pathophysiology of hemangiomas and vascular malformations. This review focuses on recent advances in our understanding of the mechanisms of angiogenesis/lymphangiogenesis and the differentiation of arterial, venous, and lymphatic vessels. We integrate this knowledge with new data obtained from genetic studies in humans, which have revealed a number of heretofore-unsuspected candidates involved in the development of familial vascular anomalies. We present a common infantile vascular tumor, hemangioma, and then focus on hereditary familial vascular and lymphatic malformations. We also summarize transgenic mouse models for some of these malformations. It seems reasonable to believe that novel therapeutic strategies will soon emerge for the treatment of hemangiomas and vascular malformations.  

Khalid Z. Al-Shali and Robert A. Hegele
Arterioscler Thromb Vasc Biol. 2004;24:1591-1595; published online before print June 17 2004, doi:10.1161/01.ATV.0000136392.59656.8b.
Abstract | Full Text | PDF
Dunnigan-type familial partial lipodystrophy and Hutchinson-Gilford progeria syndrome are laminopathies caused by mutation in LMNA that feature atherosclerosis, which is related to proatherogenic metabolic disturbances and to the generalized process of accelerated aging, respectively. These monogenic diseases may provide clues about new pathways for atherogenesis.  

 

Vascular BiologyBack

Tadashi Yoshida, Keiko Kawai-Kowase, and Gary K. Owens
Arterioscler Thromb Vasc Biol. 2004;24:1596-1601; published online before print July 1 2004, doi:10.1161/01.ATV.0000137190.63214.c5.
Abstract | Full Text | PDF | Data Supplement
We examined whether myocardin induces the entire smooth muscle cell (SMC) differentiation program. Results of the present study showed that myocardin knockdown or overexpression affected only a subset of SMC marker genes in multipotential cells, indicating that myocardin is required but not sufficient to induce SMC lineage.  

Yuko Oyama, Keiko Kawai-Kowase, Kenichi Sekiguchi, Mahito Sato, Hiroko Sato, Miki Yamazaki, Yoshio Ohyama, Yasushi Aihara, Tatsuya Iso, Eichi Okamaoto, Ryozo Nagai, and Masahiko Kurabayashi
Arterioscler Thromb Vasc Biol. 2004;24:1602-1607; published online before print July 8 2004, doi:10.1161/01.ATV.0000138404.17519.45.
Abstract | Full Text | PDF
This study demonstrates that Hex, a hematopoietically expressed homeobox protein, induces transcription of the SM22{alpha} gene by facilitating the interaction between SRF and its cognate binding site in embryonic fibroblasts. These findings will provide the clue for understanding the mechanisms by which bone marrow-derived SMC precursor cells undergo differentiation.  

Claudia S. Hofmann, Christopher P. Sullivan, Hao-Yuan Jiang, Phillip J. Stone, Paul Toselli, Ernane D. Reis, Igor Chereshnev, Barbara M. Schreiber, and Gail E. Sonenshein
Arterioscler Thromb Vasc Biol. 2004;24:1608-1613; published online before print July 15 2004, doi:10.1161/01.ATV.0000139010.71779.f3.
Abstract | Full Text | PDF | Data Supplement
To analyze B-Myb function in the vasculature, mice overexpressing B-myb were generated. Neonates displayed normal {alpha}1(I) collagen mRNA levels, whereas adults expressed decreased collagen mRNA in aortas and isolated vascular SMCs. On femoral artery denudation, neointima formation was dramatically reduced in B-myb transgenic mice.  

Tomasz J. Guzik, Jerzy Sadowski, Boguslaw Kapelak, Andrzej Jopek, Pawel Rudzinski, Ravi Pillai, Richard Korbut, and Keith M. Channon
Arterioscler Thromb Vasc Biol. 2004;24:1614-1620; published online before print July 15 2004, doi:10.1161/01.ATV.0000139011.94634.9d.
Abstract | Full Text | PDF | Data Supplement
Endothelial dysfunction is characterized by increased superoxide production. NAD(P)H oxidase activity and endothelial function are correlated in veins and arteries in coronary artery disease, suggesting regulation by systemic factors. The expression of the NAD(P)H oxidase subunits p22phox and nox4, although different in veins and arteries, are also correlated.  

Archana Mishra, Ashok Chaudhary, and Sanjeev Sethi
Arterioscler Thromb Vasc Biol. 2004;24:1621-1627; published online before print July 1 2004, doi:10.1161/01.ATV.0000137191.02577.86.
Abstract | Full Text | PDF | Data Supplement  

Karyn L. Hamilton, F.N. Mbai, S. Gupta, and A.A. Knowlton
Arterioscler Thromb Vasc Biol. 2004;24:1628-1633; published online before print July 1 2004, doi:10.1161/01.ATV.0000137188.76195.fb.
Abstract | Full Text | PDF | Data Supplement
We hypothesized that estrogen would increase HSP72 in human coronary artery endothelial cells (HCAEC). Both early and chronic treatment increased HSP72. EMSA showed activation of HSF-1 with early, but not chronic, 17ß-estradiol. Transcription factor decoys blocked estrogen-related HSP72 induction. Estrogen decreased LDH release with hypoxia. An NF-{kappa}B decoy blocked the HSP72 increase and estrogen-associated protection.  

Hiroki Ono, Toshihiro Ichiki, Kae Fukuyama, Naoko Iino, Satoko Masuda, Kensuke Egashira, and Akira Takeshita
Arterioscler Thromb Vasc Biol. 2004;24:1634-1639; published online before print July 8 2004, doi:10.1161/01.ATV.0000138052.86051.0d.
Abstract | Full Text | PDF | Data Supplement
Migration of vascular smooth muscle cells (VSMCs) contributes to formation of vascular stenotic lesions. TNF-{alpha}, a potent migration factor for VSMCs, activated CREB through p38 mitogen-activated protein kinase (p38-MAPK). CREB inhibition suppressed TNF-{alpha}-induced VSMC migration and Rac1 expression. These results suggest p38-MAPK/CREB/Rac1 pathway mediates TNF-{alpha}-induced VSMC migration.  

Wakako Takabe, Yoshikatsu Kanai, Arthit Chairoungdua, Noriyuki Shibata, Sono Toi, Makio Kobayashi, Tatsuhiko Kodama, and Noriko Noguchi
Arterioscler Thromb Vasc Biol. 2004;24:1640-1645; published online before print June 3 2004, doi:10.1161/01.ATV.0000134377.17680.26.
Abstract | Full Text | PDF | Data Supplement  

Jaroslav Pelisek, Andreas Kuehnl, Pierre H. Rolland, Choukri Mekkaoui, Alexandra Fuchs, Greg F. Walker, Manfred Ogris, Ernst Wagner, and Sigrid Nikol
Arterioscler Thromb Vasc Biol. 2004;24:1646-1651; published online before print July 1 2004, doi:10.1161/01.ATV.0000137387.78515.61.
Abstract | Full Text | PDF | Data Supplement
Functional analysis of various C-type natriuretic peptide (CNP) sequences on growth of vascular cells. For the first time, dual therapeutic effects of CNP with inhibition of smooth muscle cell proliferation and stimulation of re-endothelialization were demonstrated in a pig restenosis model using liposome-mediated gene transfer and local adventitial delivery.  

Takeo Anazawa, Paul C. Dimayuga, Hongyan Li, Shigemasa Tani, Jason Bradfield, Kuang-Yuh Chyu, Sanjay Kaul, Prediman K. Shah, and Bojan Cercek
Arterioscler Thromb Vasc Biol. 2004;24:1652-1658; published online before print July 22 2004, doi:10.1161/01.ATV.0000139925.84444.ad.
Abstract | Full Text | PDF
We investigated the role of inducible nitric oxide synthase (iNOS) in intimal thickening with exposure to cigarette smoke (CS) exposure in WT mice was associated with increased arterial iNOS expression, superoxide production, AP-1 activation, serum NO, and intimal thickening. Inhibition or deletion of iNOS abrogated the effects of CS.  

Hiroshi Shibata, Toru Nabika, Hidehiko Moriyama, Junichi Masuda, and Shotai Kobayashi
Arterioscler Thromb Vasc Biol. 2004;24:1659-1663; published online before print July 1 2004, doi:10.1161/01.ATV.0000137415.67349.3c.
Abstract | Full Text | PDF
Oxidative stress and NO levels were evaluated in a general population with or without mild periventricular hyperintensity under a cross-sectional study design. Serum NOx (NO metabolites) and urinary 8-iso-PG F2{alpha} (a marker for oxidative stress) correlated with the severity of periventricular hyperintensity in a multivariate analysis.  

Frederic Pipp, Stefanie Boehm, Wei-Jun Cai, Farzin Adili, Bela Ziegler, Gordana Karanovic, Ralf Ritter, Jörn Balzer, Christian Scheler, Wolfgang Schaper, and Thomas Schmitz-Rixen
Arterioscler Thromb Vasc Biol. 2004;24:1664-1668; published online before print July 8 2004, doi:10.1161/01.ATV.0000138028.14390.e4.
Abstract | Full Text | PDF | Data Supplement
The role of fluid shear stress on the development of a collateral circulation was studied by abruptly increasing collateral blood flow by a distal femoral artery-to-vein anastomosis. This increased number and size of collateral vessels to a hitherto unknown degree. Fluid shear stress is the primary and strongest arteriogenic stimulus.  

 

Atherosclerosis and LipoproteinsBack

Gerard Vassiliou and Ruth McPherson
Arterioscler Thromb Vasc Biol. 2004;24:1669-1675; published online before print June 3 2004, doi:10.1161/01.ATV.0000134295.09932.60.
Abstract | Full Text | PDF
In adipocytes, the LDL receptor-related protein contributes to selective uptake when it recaptures and internalizes HDL-derived cholesteryl esters that are otherwise lost by apoE-mediated efflux. This novel "efflux-recapture" process explains some conflicting observations of selective uptake and underscores the bi-directional nature of efflux.  

Srinivasa T. Reddy, Julie T. Nguyen, Victor Grijalva, Greg Hough, Susan Hama, Mohamad Navab, and Alan M. Fogelman
Arterioscler Thromb Vasc Biol. 2004;24:1676-1681; published online before print July 8 2004, doi:10.1161/01.ATV.0000138342.94314.64.
Abstract | Full Text | PDF | Data Supplement
MKP-1 is required for Ox-PAPC-mediated endothelial/monocyte interactions; however, an in vivo role of MKP-1 in atherogenesis has not been investigated. We now report that MKP-1 protein is expressed in the atherosclerotic lesions of mice and inhibition of tyrosine phosphatase activity and MKP-1 protein reduce atherosclerotic lesions in mouse models.  

Osamu Suda, Masato Tsutsui, Tsuyoshi Morishita, Hiromi Tasaki, Susumu Ueno, Sei Nakata, Takashi Tsujimoto, Yumiko Toyohira, Yoshiaki Hayashida, Yasuyuki Sasaguri, Yoichi Ueta, Yasuhide Nakashima, and Nobuyuki Yanagihara
Arterioscler Thromb Vasc Biol. 2004;24:1682-1688; published online before print June 24 2004, doi:10.1161/01.ATV.0000136656.26019.6e.
Abstract | Full Text | PDF | Data Supplement
This study demonstrates that asymmetrical dimethylarginine (ADMA) causes arteriosclerotic coronary lesions in mice in vivo through mechanisms other than simple inhibition of endothelial NO synthesis. Our findings should contribute to a better understanding of the pathophysiological role of ADMA in arteriosclerosis.  

Masaharu Hori, Maki Satoh, Kohichiro Furukawa, Yu-ichiro Sakamoto, Hideki Hakamata, Yoshihiro Komohara, Motohiro Takeya, Yutaka Sasaki, Akira Miyazaki, and Seikoh Horiuchi
Arterioscler Thromb Vasc Biol. 2004;24:1689-1695; published online before print July 8 2004, doi:10.1161/01.ATV.0000137976.88533.13.
Abstract | Full Text | PDF | Data Supplement
Diabetic rats exhibit dyslipidemia caused, in part, by elevated intestinal acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity. We determined which ACAT isozyme (ACAT-1 or ACAT-2) was involved in the elevated intestinal ACAT activity in diabetic rats. We demonstrated an important role of ACAT-2, implicating its involvement in dyslipidemia in diabetic patients.  

Helén L. Dichek, Kun Qian, and Nalini Agrawal
Arterioscler Thromb Vasc Biol. 2004;24:1696-1702; published online before print June 17 2004, doi:10.1161/01.ATV.0000135981.61827.9d.
Abstract | Full Text | PDF | Data Supplement
These studies demonstrate that high levels of catalytically active human hepatic lipase (HL) reduce atherosclerosis, whereas high levels of a catalytically inactive HL do not affect atherosclerosis in mice genetically deficient in low-density lipoprotein receptor and mouse HL.  

Francine K. Welty, Alice H. Lichtenstein, P. Hugh R. Barrett, Gregory G. Dolnikowski, and Ernst J. Schaefer
Arterioscler Thromb Vasc Biol. 2004;24:1703-1707; published online before print July 8 2004, doi:10.1161/01.ATV.0000137975.14996.df.
Abstract | Full Text | PDF
Using stable isotopes in humans, 2 links were observed between apoA-I and apoB kinetics: (1) when LDL apoB-100 PS is high, there is increased apoA-I PR; and (2) delayed chylomicron remnant clearance is associated with enhanced apoA-I FCR, indicating that alterations in intestinal lipoproteins may be more important in determining HDL-C levels than changes in liver lipoprotein particles.  

Nanette I. Steinle, Rasa Kazlauskaite, Ikhide G. Imumorin, Wen-Chi Hsueh, Toni I. Pollin, Jeffrey R. O’Connell, Braxton D. Mitchell, and Alan R. Shuldiner
Arterioscler Thromb Vasc Biol. 2004;24:1708-1713; published online before print June 17 2004, doi:10.1161/01.ATV.0000136384.53705.c9.
Abstract | Full Text | PDF | Data Supplement
To determine whether polymorphisms in LMNA influence susceptibility to metabolic syndrome and its constituent components, we performed DNA analysis of polymorphisms in LMNA. The H566H polymorphism was associated with metabolic syndrome and also higher mean fasting triglyceride and lower mean HDL-cholesterol concentrations in the Old Order Amish.  

Eugene Trogan, Zahi A. Fayad, Vitalii V. Itskovich, Juan-Gilberto S. Aguinaldo, Venkatesh Mani, John T. Fallon, Igor Chereshnev, and Edward A. Fisher
Arterioscler Thromb Vasc Biol. 2004;24:1714-1719; published online before print July 15 2004, doi:10.1161/01.ATV.0000139313.69015.1c.
Abstract | Full Text | PDF | Data Supplement
Serial in vivo MRI of mouse arterial plaque after correction of dyslipidemia revealed a monotonic decrease in lesion size (regression) and changes in lesion composition consistent with a stable plaque phenotype. Serial in vivo MRI will enhance studies of plaque regression in animal models in response to therapeutic interventions.  

 

ThrombosisBack

Andreas Schäfer, Nicholas J. Alp, Shije Cai, Craig A. Lygate, Stefan Neubauer, Martin Eigenthaler, Johann Bauersachs, and Keith M. Channon
Arterioscler Thromb Vasc Biol. 2004;24:1720-1726; published online before print July 8 2004, doi:10.1161/01.ATV.0000138072.76902.dd.
Abstract | Full Text | PDF
Endothelial dysfunction caused by uncoupling of endothelial NO synthase is well described in diabetes mellitus and may lead to platelet activation. Acute loss of systemic NO bioavailability causes platelet activation. eNOS uncoupling prevention in diabetes preserved systemic NO bioavailability and maintained a physiological platelet state without activation in vivo.  

Christelle Lecut, Anne Schoolmeester, Marijke J.E. Kuijpers, Jos L.V. Broers, Marc A.M.J. van Zandvoort, Karen Vanhoorelbeke, Hans Deckmyn, Martine Jandrot-Perrus, and Johan W.M. Heemskerk
Arterioscler Thromb Vasc Biol. 2004;24:1727-1733; published online before print July 1 2004, doi:10.1161/01.ATV.0000137974.85068.93.
Abstract | Full Text | PDF | Data Supplement
Integrin activation during thrombus formation on collagen was studied using fluorescent-labeled antibodies IAC-1 and PAC1 directed against activation-dependent epitopes of {alpha}2ß1 and {alpha}IIbß3 integrin, respectively. Glycoprotein VI blockade by 9O12 antibody or P2Y ADP receptors reduced integrin activation along with aggregate formation and fibrinogen binding but not {alpha}2ß1-dependent adhesion.  

Kristof Vanschoonbeek, Marion A.H. Feijge, Martine Paquay, Jan Rosing, Wim Saris, Cornelis Kluft, Peter L.A. Giesen, Moniek P.M. de Maat, and Johan W.M. Heemskerk
Arterioscler Thromb Vasc Biol. 2004;24:1734-1740; published online before print June 24 2004, doi:10.1161/01.ATV.0000137119.28893.0b.
Abstract | Full Text | PDF | Data Supplement
Intake of fish oil reduced fibrinogen and factor V levels as well as thrombin generation in plasma. The effects on thrombin generation and fibrinogen clustered around subjects with high fibrinogen carrying {alpha}-chain fibrinogen polymorphism. Thus, dietary fish oil can provoke a hypocoagulant effect depending on the fibrinogen level.  

 

Letters to the EditorBack

CD40L-Positive Platelets Induce CD40L Expression De Novo in Endothelial Cells: Adding a Loop to Microvascular Inflammation

Silvio Danese, Franco Scaldaferri, Alfredo Papa, Roberto Pola, Antonio Gasbarrini, Allesandro Sgambato, and Achille Cittadini
Arterioscler Thromb Vasc Biol. 2004;24:e162, doi:10.1161/01.ATV.0000138073.91195.70.
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Subantimicrobial Doses of Tetracycline

Thomas Pallasch, David L. Brown, Lorne M. Golub, and John G. Thomas
Arterioscler Thromb Vasc Biol. 2004;24:e163, doi:10.1161/01.ATV.0000138071.21565.7e.
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