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Volume 27, Issue 7; July 1, 2007
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
AHA News
AHA Meetings
AHA Fellows
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Editorials
Endothelial GTPCH in eNOS Uncoupling and Atherosclerosis
Tohru Fukai
Arterioscler Thromb Vasc Biol. 2007;27:1493-1495, doi:10.1161/ATVBAHA.107.148239
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Posttranslational Protein Palmitoylation: Promoting Platelet Purpose
Adam D. Munday and José A. López
Arterioscler Thromb Vasc Biol. 2007;27:1496-1499, doi:10.1161/ATVBAHA.106.136226
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Brief Reviews
Vascular Responses to Drug Eluting Stents: Importance of Delayed Healing
Aloke V. Finn, Gaku Nakazawa, Michael Joner, Frank D. Kolodgie, Erik K. Mont, Herman K. Gold, and Renu Virmani
Arterioscler Thromb Vasc Biol. 2007;27:1500-1510; published online before print May 17 2007, doi:10.1161/ATVBAHA.107.144220
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Late thrombosis after polymer-based sirolimus- (Cypher) and paclitaxel-eluting (Taxus) drug eluting stents has emerged as a major safety concern. This review will summarize our current understanding of the vascular response to these DES in both humans and animals, especially as it pertains to the issue of late DES thrombosis.
Platelet Receptor Proteolysis: A Mechanism for Downregulating Platelet Reactivity
Robert K. Andrews, Denuja Karunakaran, Elizabeth E. Gardiner, and Michael C. Berndt
Arterioscler Thromb Vasc Biol. 2007;27:1511-1520; published online before print April 26 2007, doi:10.1161/ATVBAHA.107.141390
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This review focuses on key proteolytic mechanisms regulating the surface expression, adheso-signaling function and plasma levels of platelet receptors involved in thrombosis, inflammation and other vascular processes, in particular using platelet collagen receptor, glycoprotein (GP)VI, shedding to illustrate the implications for normal physiology or future therapeutics.
Vascular Biology
Loss-of-Function Deletion of the Steroid Receptor Coactivator-1 Gene in Mice Reduces Estrogen Effect on the Vascular Injury Response
Yuhui Yuan and Jianming Xu
Arterioscler Thromb Vasc Biol. 2007;27:1521-1527; published online before print April 19 2007, doi:10.1161/ATVBAHA.107.144477
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Using SRC-1 knockout mice and a common carotid ligation model, we demonstrated that SRC-1 deficiency reduced the inhibitory effect of estrogen on the neointima formation and on the neointimal cell proliferation after a vascular injury. Our results indicate that SRC-1 dysfunction may result in partial impairment of the vasoprotective effect of estrogen.
Cooperation of SRC-1 and p300 With NF-
B and CREB in Angiotensin II-Induced IL-6 Expression in Vascular Smooth Muscle Cells
Saurabh Sahar, Marpadga A. Reddy, Cynthie Wong, Li Meng, Mei Wang, and Rama Natarajan
Arterioscler Thromb Vasc Biol. 2007;27:1528-1534; published online before print May 10 2007, doi:10.1161/ATVBAHA.107.145862
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In vascular smooth muscle cells Angiotensin II-induced IL-6 expression involves histone H3 lysine acetylation mediated by histone acetyl transferases p300 and SRC-1 and their cooperation with transcription factors NF-{kappa}B and CREB. ERK signaling plays a key role by regulating the activation of these transcription factors and histone acetyl transferases.
Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis
Nanae Kada, Toru Suzuki, Kenichi Aizawa, Takayoshi Matsumura, Naoto Ishibashi, Naomi Suzuki, Norifumi Takeda, Yoshiko Munemasa, Daigo Sawaki, Takashi Ishikawa, and Ryozo Nagai
Arterioscler Thromb Vasc Biol. 2007;27:1535-1541; published online before print May 3 2007, doi:10.1161/ATVBAHA.106.134114
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Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely neointima formation, effects of ACR on neointima formation and the involved mechanisms were investigated.
CYP26 Inhibitor R115866 Increases Retinoid Signaling in Intimal Smooth Muscle Cells
Pauline Ocaya, Andreas C. Gidlöf, Peder S. Olofsson, Hans Törmä, and Allan Sirsjö
Arterioscler Thromb Vasc Biol. 2007;27:1542-1548; published online before print May 17 2007, doi:10.1161/ATVBAHA.106.138602
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atRA regulates proliferation and differentiation of various cell types. We show that inhibition of CYP26 by R115866 in intimal SMCs results in increased cellular retinoids and retinoidal effects, ie, inhibition of DNA synthesis and alteration of cell morphology. Therefore, CYP26 inibitors offer a potential new therapeutic approach to vascular proliferative disorders.
Inducible cAMP Early Repressor Inhibits Growth of Vascular Smooth Muscle Cell
Hideki Ohtsubo, Toshihiro Ichiki, Ryohei Miyazaki, Keita Inanaga, Ikuyo Imayama, Yasuko Hashiguchi, Junichi Sadoshima, and Kenji Sunagawa
Arterioscler Thromb Vasc Biol. 2007;27:1549-1555; published online before print April 26 2007, doi:10.1161/ATVBAHA.107.145011
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Inducible cAMP early repressor (ICER) is involved in beraprost-induced growth inhibition of vascular smooth muscle cells. Overexpression of ICER suppressed neointimal formation in balloon-injured artery, suggesting that ICER may be an important negative regulator of the vascular remodeling process and an effective therapeutic tool to treat vascular proliferative disease.
Histamine Upregulates the Expression of Inducible Nitric Oxide Synthase in Human Intimal Smooth Muscle Cells via Histamine H1 Receptor and NF-
B Signaling Pathway
Akihide Tanimoto, Ke-Yong Wang, Yoshitaka Murata, Satoshi Kimura, Masako Nomaguchi, Sei Nakata, Masato Tsutsui, and Yasuyuki Sasaguri
Arterioscler Thromb Vasc Biol. 2007;27:1556-1561; published online before print May 3 2007, doi:10.1161/ATVBAHA.106.139089
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Histamine increases endothelial nitric oxide (NO) production as an endothelium-dependent vasodilator, which acts as a vasoconstrictor in atherosclerotic coronary arteries. To investigate the relation between histamine and NO production in intimal smooth muscle cells (SMCs), we studied the effect of histamine on inducible NO synthase (iNOS) expression in the SMCs.
Venous Identity Is Lost but Arterial Identity Is Not Gained During Vein Graft Adaptation
Fabio A. Kudo, Akihito Muto, Stephen P. Maloney, Jose M. Pimiento, Sonia Bergaya, Tamara N. Fitzgerald, Tormod S. Westvik, Jared C. Frattini, Christopher K. Breuer, Charles H. Cha, Toshiya Nishibe, George Tellides, William C. Sessa, and Alan Dardik
Arterioscler Thromb Vasc Biol. 2007;27:1562-1571; published online before print April 26 2007, doi:10.1161/ATVBAHA.107.143032
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In human and aged rat vein graft adaptation, Eph-B4, a marker of venous identity, is downregulated, whereas markers of arterial identity such as Ephrin-B2 are not induced. These results suggest that markers of vessel identity that are developmentally regulated are plastic in adults.
Endothelial Outgrowth Cells Are Not Derived From CD133
+
Cells or CD45
+
Hematopoietic Precursors
Frank Timmermans, Filip Van Hauwermeiren, Magda De Smedt, Robrecht Raedt, Frank Plasschaert, Marc L. De Buyzere, Thierry C. Gillebert, Jean Plum, and Bart Vandekerckhove
Arterioscler Thromb Vasc Biol. 2007;27:1572-1579; published online before print May 10 2007, doi:10.1161/ATVBAHA.107.144972
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Two types of endothelial progenitor cells (EPCs) were previously described. In the present article, we dissect the relation of the cell surface markers CD34, CD133, VEGFR2, and CD45 on fresh isolated human cells with respect to both in vitro generated EPC populations.
Removal of Fkbp12/12.6 From Endothelial Ryanodine Receptors Leads to an Intracellular Calcium Leak and Endothelial Dysfunction
Cheng Long, Leslie G. Cook, Gang-Yi Wu, and Brett M. Mitchell
Arterioscler Thromb Vasc Biol. 2007;27:1580-1586; published online before print May 3 2007, doi:10.1161/ATVBAHA.107.144808
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We tested whether rapamycin or FK506 alters intracellular Ca2+ in endothelial cells and whether this affects endothelial function and blood pressure regulation. Complete removal of FKBP12 and 12.6 from endothelial RyRs induced an intracellular Ca2+ leak which may contribute to the pathogenesis of rapamycin/FK506-induced endothelial dysfunction and hypertension.
Vascular Endothelial Growth Factor Is Induced by the Inflammatory Cytokines Interleukin-6 and Oncostatin M in Human Adipose Tissue In Vitro and in Murine Adipose Tissue In Vivo
G. Rega, C. Kaun, S. Demyanets, S. Pfaffenberger, K. Rychli, P.J. Hohensinner, S.P. Kastl, W.S. Speidl, T.W. Weiss, J.M. Breuss, A. Furnkranz, P. Uhrin, J. Zaujec, V. Zilberfarb, M. Frey, R. Roehle, G. Maurer, K. Huber, and J. Wojta
Arterioscler Thromb Vasc Biol. 2007;27:1587-1595; published online before print May 24 2007, doi:10.1161/ATVBAHA.107.143081
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Recent studies found that adipose tissue mass could be regulated through the vasculature. We show that the inflammatory cytokines IL-6 and OSM upregulate VEGF in human adipose tissue via JAK/STAT. We hypothesize that a link between adipokines, vascularization, adipose tissue growth, and thus possibly also cardiovascular diseases could exist.
Atherosclerosis and Lipoproteins
Elevated Cholesterol Levels in the Plasma Membranes of Macrophages Inhibit Migration by Disrupting RhoA Regulation
Tomokazu Nagao, Chunbo Qin, Inna Grosheva, Frederick R. Maxfield, and Lynda M. Pierini
Arterioscler Thromb Vasc Biol. 2007;27:1596-1602; published online before print May 10 2007, doi:10.1161/ATVBAHA.107.145086
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We tested the hypothesis that elevated membrane cholesterol levels affect macrophage migration. The results suggest that increases in cholesterol levels interfere with RhoA activation, resulting in inhibition of migration attributable to reduced contractile force generation. These findings provide one possible explanation for the retention of foam cells in atherosclerotic lesions.
ABCA1-Induced Cell Surface Binding Sites for ApoA-I
Charulatha Vedhachalam, Amy B. Ghering, W. Sean Davidson, Sissel Lund-Katz, George H. Rothblat, and Michael C. Phillips
Arterioscler Thromb Vasc Biol. 2007;27:1603-1609; published online before print May 3 2007, doi:10.1161/ATVBAHA.107.145789
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15-LO-I is expressed in rabbit aorta. 15-LO regulates vasodilatory eicosanoid synthesis and vascular tone. The current study demonstrates that ABCA1 activity creates 2 types of high affinity apoA-I binding sites at the cell surface. The low capacity site formed by direct apoA-I/ABCA1 interaction functions in a regulatory role, whereas the much higher capacity site generated by apoA-I/lipid interactions functions in the assembly of nascent HDL particles.
Apolipoprotein E Interrupts Interleukin-1ß Signaling in Vascular Smooth Muscle Cells
Akira Kawamura, Daniel Baitsch, Ralph Telgmann, Renata Feuerborn, Gabriele Weissen-Plenz, Claudia Hagedorn, Keijiro Saku, Stefan-Martin Brand-Herrmann, Arnold von Eckardstein, Gerd Assmann, and Jerzy-Roch Nofer
Arterioscler Thromb Vasc Biol. 2007;27:1610-1617; published online before print May 17 2007, doi:10.1161/ATVBAHA.106.129957
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Apolipoprotein E (apoE) exerts antiatherogenic effects, but precise mechanisms remain unclear. The present study demonstrates that apoE suppress IL-1ß-induced inflammatory activation of vascular smooth muscle cells by targeting IL receptor-associated kinase-1 (IRAK-1) and transcription factors NF-{kappa}B and AP-1 in a process dependent on protein kinase A (PKA).
Expression of Human OSBP-Related Protein 1L in Macrophages Enhances Atherosclerotic Lesion Development in LDL ReceptorDeficient Mice
Daoguang Yan, Matti Jauhiainen, Reeni B. Hildebrand, Ko Willems van Dijk, Theo J.C. Van Berkel, Christian Ehnholm, Miranda Van Eck, and Vesa M. Olkkonen
Arterioscler Thromb Vasc Biol. 2007;27:1618-1624; published online before print May 3 2007, doi:10.1161/ATVBAHA.107.144121
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LDLr-/- animals that received bone marrow of mice expressing human ORP1L in macrophages displayed a 2.1-fold increase in aortic root lesion size relative to controls. Decreased macrophage ABCG1 and apoE expression and cholesterol efflux to HDL2, as well as increased PLTP expression, provide plausible explanations for the increased lesion size.
Enhanced Immune System Activation and Arterial Inflammation Accelerates Atherosclerosis in Lupus-Prone Mice
Emmanuel L. Gautier, Thierry Huby, Betty Ouzilleau, Chantal Doucet, Flora Saint-Charles, Guilaine Gremy, M. John Chapman, and Philippe Lesnik
Arterioscler Thromb Vasc Biol. 2007;27:1625-1631; published online before print April 19 2007, doi:10.1161/ATVBAHA.107.142430
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Premature atherosclerosis is a feature of autoimmune disease but the mechanisms that underlie such accelerated atherosclerosis are indeterminate. Our experimental findings highlight enhanced immune system activation, aortic inflammation, and lesional accumulation of apoptotic cells, macrophages, and CD4 T cells as central mechanisms in the progression of atherosclerosis in autoimmune mice.
A Specific Role for eNOS-Derived Reactive Oxygen Species in Atherosclerosis Progression
Tomofumi Takaya, Ken-ichi Hirata, Tomoya Yamashita, Masakazu Shinohara, Naoto Sasaki, Nobutaka Inoue, Toyotaka Yada, Masami Goto, Akiko Fukatsu, Toshio Hayashi, Nicholas J. Alp, Keith M. Channon, Mitsuhiro Yokoyama, and Seinosuke Kawashima
Arterioscler Thromb Vasc Biol. 2007;27:1632-1637; published online before print April 26 2007, doi:10.1161/ATVBAHA.107.142182
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In apolipoprotein E-deficient mice overexpressing eNOS in the endothelium, augmenting BH4 levels in the endothelium by GTP-cyclohydrolase I overexpression was more efficient to reduce the accelerated atherosclerotic lesion formation and superoxide production from uncoupled eNOS compared with chronic vitamin C treatment.
Type A Eagerness-Energy Across Developmental Periods Predicts Adulthood Carotid Intima-Media Thickness: The Cardiovascular Risk in Young Finns Study
Liisa Keltikangas-Järvinen, Taina Hintsa, Mika Kivimäki, Sampsa Puttonen, Markus Juonala, Jorma S.A. Viikari, and Olli T. Raitakari
Arterioscler Thromb Vasc Biol. 2007;27:1638-1644; published online before print May 10 2007, doi:10.1161/ATVBAHA.107.145524
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Type A behavior as a predictor of adult carotid artery intima-media thickness (IMT) was examined in a population-based sample of 408 men and 606 women. It was shown that eagerness-energy component of Type A behavior over different developmental transitions seems to be a robust predictor of IMT in men.
Thrombosis
Impact of Serum Amyloid A on Tissue Factor and Tissue Factor Pathway Inhibitor Expression and Activity in Endothelial Cells
Yulan Zhao, Shuli Zhou, and Chew-Kiat Heng
Arterioscler Thromb Vasc Biol. 2007;27:1645-1650; published online before print April 26 2007, doi:10.1161/ATVBAHA.106.137455
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This study investigates the impact of SAA on the expression and activity of TF and TFPI in endothelial cells. The stimulating effect of SAA was faster-acting on TF and the inhibitory effect was slower-acting on TFPI. The effects are mediated through FPRL1, MAP kinases and NF{kappa}B.
Endothelial Fibrinolytic Capacity Predicts Future Adverse Cardiovascular Events in Patients With Coronary Heart Disease
Simon D. Robinson, Christopher A. Ludlam, Nicholas A. Boon, and David E. Newby
Arterioscler Thromb Vasc Biol. 2007;27:1651-1656; published online before print April 26 2007, doi:10.1161/ATVBAHA.107.143248
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We show that endothelial tissue plasminogen activator (t-PA) release is a distinct marker of endothelial function and that in patients with stable coronary heart disease acute t-PA release predicts an increased risk of future adverse cardiovascular events.
Activation of Human Platelets by Misfolded Proteins
Eszter Herczenik, Barend Bouma, Suzanne J.A. Korporaal, Remo Strangi, Qinghong Zeng, Piet Gros, Miranda Van Eck, Theo J.C. Van Berkel, Martijn F.B.G. Gebbink, and Jan-Willem N. Akkerman
Arterioscler Thromb Vasc Biol. 2007;27:1657-1665; published online before print May 17 2007, doi:10.1161/ATVBAHA.107.143479
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Protein misfolding is a common feature in Alzheimer disease, atherosclerosis, diabetes mellitus, and systemic amyloidosis. These diseases are associated with platelet hyperactivity. This study demonstrates that amyloid properties in proteins represent a novel platelet activating property. These properties explain the increased platelet activation in many diseases with appearance of misfolded proteins.
Letters to the Editor
Elevated Endothelial Microparticles in Fabry Children Decreased After Enzyme Replacement Therapy
Monique P. Gelderman, Raphael Schiffmann, and Jan Simak
Arterioscler Thromb Vasc Biol. 2007;27:e138-e139, doi:10.1161/ATVBAHA.107.143511
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Animal Models and Virtual Histology
Renu Virmani and Gaku Nakazawa
Arterioscler Thromb Vasc Biol. 2007;27:1666, doi:10.1161/ATVBAHA.107.143198
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Animal Models and Virtual Histology
Juan F. Granada, Albert E. Raizner, and Greg L. Kaluza
Arterioscler Thromb Vasc Biol. 2007;27:1667-1668, doi:10.1161/ATVBAHA.107.146837
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AHA News
AHA News
Arterioscler Thromb Vasc Biol. 2007;27:B1-B2, doi:10.1161/01.ATVBAHA.0000278629.94381.91
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AHA Meetings
AHA Meetings
Arterioscler Thromb Vasc Biol. 2007;27:B3-B4, doi:10.1161/01.ATVBAHA.0000278630.02005.0f
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AHA Fellows
AHA Fellows
Arterioscler Thromb Vasc Biol. 2007;27:B5-B6, doi:10.1161/01.ATVBAHA.0000278631.79134.0d
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