Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (29 [8])

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Volume 29, Issue 8; August 1, 2009

History of Discovery
Integrative Physiology/Experimental Medicine
Cell Biology/Signaling
Clinical and Population Studies
Recipients of the 2009 New Investigator Awards: Corrections
Corrections

Key: VB = Vascular Biology AL = Atherosclerosis/Lipoproteins TH = Thrombosis

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	History of Discovery
	The Tissue-Type Plasminogen Activator Story D. Collen and H.R. Lijnen Arterioscler Thromb Vasc Biol. 2009;29:1151-1155, doi:10.1161/ATVBAHA.108.179655 Abstract \| Full Text \| PDF
	How We Learned to Say NO Paul M. Vanhoutte Arterioscler Thromb Vasc Biol. 2009;29:1156-1160, doi:10.1161/ATVBAHA.109.190215 Extract \| Full Text \| PDF
	Integrative Physiology/Experimental Medicine
	Importance of Junctional Adhesion Molecule-C for Neointimal Hyperplasia and Monocyte Recruitment in Atherosclerosis-Prone Mice–Brief Report Erdenechimeg Shagdarsuren, Yassin Djalali-Talab, Michel Aurrand-Lions, Kiril Bidzhekov, Elisa A. Liehn, Beat A. Imhof, Christian Weber, and Alma Zernecke Arterioscler Thromb Vasc Biol. 2009;29:1161-1163; published online before print June 11 2009, doi:10.1161/ATVBAHA.109.187898 Abstract \| Full Text \| PDF \| Data Supplement We here show that junctional adhesion molecule (JAM)-C antibody blockade reduced neointimal hyperplasia after arterial injury and leukocyte adhesion to carotid arteries. Our data provide the first evidence for a crucial role of JAM-C in accelerated lesion formation and leukocyte recruitment in atherosclerosis-prone mice.
	Resveratrol Improves Endothelial Function: Role of TNF ${alpha}$ and Vascular Oxidative Stress Hanrui Zhang, Jing Zhang, Zoltan Ungvari, and Cuihua Zhang Arterioscler Thromb Vasc Biol. 2009;29:1164-1171; published online before print May 28 2009, doi:10.1161/ATVBAHA.109.187146 Abstract \| Full Text \| PDF We tested whether the naturally occurring polyphenol resveratrol protects against oxidative stress-induced endothelial dysfunction in type 2 diabetes. Our data demonstrate that resveratrol restored endothelial function in type 2 diabetic mice by inhibiting TNF{alpha}-induced activation of NAD(P)H oxidase and preserving eNOS (Ser1177) phosphorylation.
	Rapamycin Inhibition of the Akt/mTOR Pathway Blocks Select Stages of VEGF-A¹⁶⁴–Driven Angiogenesis, in Part by Blocking S6Kinase Qi Xue, Janice A. Nagy, Eleanor J. Manseau, Thuy L. Phung, Harold F. Dvorak, and Laura E. Benjamin Arterioscler Thromb Vasc Biol. 2009;29:1172-1178; published online before print May 14 2009, doi:10.1161/ATVBAHA.109.185918 Abstract \| Full Text \| PDF \| Data Supplement Rapamycin potently inhibited early and mid stages of VEGF-A164-driven angiogenesis, but not late-stage angiogenesis or lymphangiogenesis. Signaling events were consistent with inhibition of both TORC1 and TORC2. S6K1 signaling has an important role in pathological angiogenesis.
	Matrix Metalloproteinase-9 Is Essential for Ischemia-Induced Neovascularization by Modulating Bone Marrow–Derived Endothelial Progenitor Cells Po-Hsun Huang, Yung-Hsiang Chen, Chao-Hung Wang, Jia-Shiong Chen, Hsiao-Ya Tsai, Feng-Yen Lin, Wei-Yuh Lo, Tao-Cheng Wu, Masataka Sata, Jaw-Wen Chen, and Shing-Jong Lin Arterioscler Thromb Vasc Biol. 2009;29:1179-1184; published online before print May 21 2009, doi:10.1161/ATVBAHA.109.189175 Abstract \| Full Text \| PDF \| Data Supplement Considering the pivotal roles of matrix metalloproteinases (MMPs) and endothelial progenitor cells (EPCs) for vasculogenesis, we hypothesize that the expression of MMP-9 may not only contribute to matrix degradation but may also directly modulate the behaviors and functions of circulating EPCs. In this study, we show the influence of the targeted deletion of the MMP-9 gene on ischemia-induced neovascularization and address the potential mechanistic link between MMP-9 and EPCs.
	Inhibition of VEGF or TGF-β Signaling Activates Endothelium and Increases Leukocyte Rolling Tony E. Walshe, Vandana S. Dole, Arindel S.R. Maharaj, Ian S. Patten, Denisa D. Wagner, and Patricia A. D'Amore Arterioscler Thromb Vasc Biol. 2009;29:1185-1192; published online before print May 21 2009, doi:10.1161/ATVBAHA.109.186742 Abstract \| Full Text \| PDF \| Data Supplement VEGF or TGF-β neutralization resulted in increased leukocyte rolling along the mesenteric venules. VEGF and TGF-β signaling limits the expression of endothelial adhesion factors, such as P-selectin, and modulates the vasoactive response. Taken together, these findings indicate an essential role for VEGF and TGF-β in maintaining the endothelium in a noninflammatory state.
	Monocytes and Neutrophils Exhibit Both Distinct and Common Mechanisms in Penetrating the Vascular Basement Membrane In Vivo Mathieu-Benoît Voisin, Abigail Woodfin, and Sussan Nourshargh Arterioscler Thromb Vasc Biol. 2009;29:1193-1199; published online before print June 4 2009, doi:10.1161/ATVBAHA.109.187450 Abstract \| Full Text \| PDF Detailed analysis of inflamed tissues by immunofluorescent staining and confocal microscopy demonstrated distinct mechanisms used by neutrophils and monocytes in penetrating the vascular basement membrane. Collectively, neutrophil but not monocyte transmigration led to remodeling of the vascular BM with monocytes exhibiting a greater level of deformability in penetrating this barrier.
	Cell Biology/Signaling
	JAM-C Induces Endothelial Cell Permeability Through Its Association and Regulation of β₃ Integrins Xiaochun Li, Milena Stankovic, Boris P.-L. Lee, Michel Aurrand-Lions, Chris N. Hahn, Ying Lu, Beat A. Imhof, Mathew A. Vadas, and Jennifer R. Gamble Arterioscler Thromb Vasc Biol. 2009;29:1200-1206; published online before print May 21 2009, doi:10.1161/ATVBAHA.109.189217 Abstract \| Full Text \| PDF \| Data Supplement
	Cross-Talk Between PKA and Akt Protects Endothelial Cells From Apoptosis in the Late Ischemic Preconditioning Alessandro Bellis, Diletta Castaldo, Valentina Trimarco, Maria Gaia Monti, Pierpaolo Chivasso, Junichi Sadoshima, Bruno Trimarco, and Carmine Morisco Arterioscler Thromb Vasc Biol. 2009;29:1207-1212; published online before print May 21 2009, doi:10.1161/ATVBAHA.109.184135 Abstract \| Full Text \| PDF \| Data Supplement We explored the molecular mechanisms involved in late preconditioning (PC)-induced protection of endothelial cells. Late PC protects endothelial cells from hypoxia-induced cell death through protein kinase A- and phosphatidyl-inositol-3-kinase-dependent mechanisms. Both pathways account for late PC-induced activation of Akt, which plays a critical role in PC-mediated cytoprotection.
	Cardiovascular Inflammation and Lesion Cell Apoptosis: A Novel Connection via the Interferon-Inducible Immunoproteasome Zhaoqing Yang, Dmitry Gagarin, Georges St. Laurent, III, Neil Hammell, Ian Toma, Chien-an Hu, Ayaka Iwasa, and Timothy A. McCaffrey Arterioscler Thromb Vasc Biol. 2009;29:1213-1219; published online before print May 14 2009, doi:10.1161/ATVBAHA.109.189407 Abstract \| Full Text \| PDF \| Data Supplement Cells from human atherosclerotic lesions are sensitized by IFN{gamma} to Fas-induced apoptosis. Microarrays identified 72 IFN{gamma}-induced transcripts relevant to apoptosis. siRNA knockdown of PSMB8 (LMP7), an "immunoproteasome" component, reversed IFN{gamma}-induced sensitivity and prevented degradation of Mcl-1, a potent survival factor. The immunoproteasome may link inflammation to vascular cell apoptosis.
	Clinical and Population Studies
	High Levels of Myeloid-Related Protein 14 in Human Atherosclerotic Plaques Correlate With the Characteristics of Rupture-Prone Lesions Mihaela G. Ionita, Aryan Vink, I. Esmé Dijke, Jon D. Laman, Wouter Peeters, Petra Homoet van der Kraak, Frans L. Moll, Jean-Paul P.M. de Vries, Gerard Pasterkamp, and Dominique P.V. de Kleijn Arterioscler Thromb Vasc Biol. 2009;29:1220-1227; published online before print June 11 2009, doi:10.1161/ATVBAHA.109.190314 Abstract \| Full Text \| PDF \| Data Supplement
	Dickkopf-1 Enhances Inflammatory Interaction Between Platelets and Endothelial Cells and Shows Increased Expression in Atherosclerosis Thor Ueland, Kari Otterdal, Tove Lekva, Bente Halvorsen, Anders Gabrielsen, Wiggo J. Sandberg, Gabrielle Paulsson-Berne, Turid M. Pedersen, Lasse Folkersen, Lars Gullestad, Erik Øie, Göran K. Hansson, and Pål Aukrust Arterioscler Thromb Vasc Biol. 2009;29:1228-1234; published online before print June 4 2009, doi:10.1161/ATVBAHA.109.189761 Abstract \| Full Text \| PDF \| Data Supplement We report increased levels of Dickkopf-1, a regulatory molecule of the wingless pathway, in experimental and clinical atherosclerosis, both systemically and within the plaques. Both endothelial- and platelet-derived Dickkopf-1 enhanced the inflammatory interaction between platelets and endothelial cells, potentially representing a self-perpetuating pathogenic mechanism in atherogenesis and plaque destabilization.
	Control of ACAT2 Liver Expression by HNF4 ${alpha}$ : Lesson From MODY1 Patients C. Pramfalk, E. Karlsson, L. Groop, L.L. Rudel, B. Angelin, M. Eriksson, and P. Parini Arterioscler Thromb Vasc Biol. 2009;29:1235-1241; published online before print May 28 2009, doi:10.1161/ATVBAHA.109.188581 Abstract \| Full Text \| PDF HNF1{alpha} is an important regulator of human ACAT2. MODY3 and MODY1 subjects may thus have lower VLDL esterified cholesterol, which, however, was only seen in MODY1 subjects. In vitro and in vivo experiments identified HNF4{alpha} as an important regulator of the hepatocyte-specific expression of the human ACAT2 promoter.
	Recipients of the 2009 New Investigator Awards: Corrections
	Correction Arterioscler Thromb Vasc Biol. 2009;29:1242, doi:10.1161/ATV.0b013e3181a4cec9 Extract \| Full Text \| PDF
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2009;29:e131, doi:10.1161/ATV.0b013e3181b32773 Extract \| Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 29, Issue 8; August 1, 2009

Key: VB = Vascular Biology AL = Atherosclerosis/Lipoproteins TH = Thrombosis

History of Discovery

The Tissue-Type Plasminogen Activator Story

How We Learned to Say NO

Integrative Physiology/Experimental Medicine

Importance of Junctional Adhesion Molecule-C for Neointimal Hyperplasia and Monocyte Recruitment in Atherosclerosis-Prone Mice–Brief Report

Resveratrol Improves Endothelial Function: Role of TNF and Vascular Oxidative Stress

Rapamycin Inhibition of the Akt/mTOR Pathway Blocks Select Stages of VEGF-A164–Driven Angiogenesis, in Part by Blocking S6Kinase

Matrix Metalloproteinase-9 Is Essential for Ischemia-Induced Neovascularization by Modulating Bone Marrow–Derived Endothelial Progenitor Cells

Inhibition of VEGF or TGF-β Signaling Activates Endothelium and Increases Leukocyte Rolling

Monocytes and Neutrophils Exhibit Both Distinct and Common Mechanisms in Penetrating the Vascular Basement Membrane In Vivo

Cell Biology/Signaling

JAM-C Induces Endothelial Cell Permeability Through Its Association and Regulation of β3 Integrins

Cross-Talk Between PKA and Akt Protects Endothelial Cells From Apoptosis in the Late Ischemic Preconditioning

Cardiovascular Inflammation and Lesion Cell Apoptosis: A Novel Connection via the Interferon-Inducible Immunoproteasome

Clinical and Population Studies

High Levels of Myeloid-Related Protein 14 in Human Atherosclerotic Plaques Correlate With the Characteristics of Rupture-Prone Lesions

Dickkopf-1 Enhances Inflammatory Interaction Between Platelets and Endothelial Cells and Shows Increased Expression in Atherosclerosis

Control of ACAT2 Liver Expression by HNF4: Lesson From MODY1 Patients

Recipients of the 2009 New Investigator Awards: Corrections

Correction

Corrections

Correction

Spotlight

Resveratrol Improves Endothelial Function: Role of TNF ${alpha}$ and Vascular Oxidative Stress

Rapamycin Inhibition of the Akt/mTOR Pathway Blocks Select Stages of VEGF-A¹⁶⁴–Driven Angiogenesis, in Part by Blocking S6Kinase

JAM-C Induces Endothelial Cell Permeability Through Its Association and Regulation of β₃ Integrins

Control of ACAT2 Liver Expression by HNF4 ${alpha}$ : Lesson From MODY1 Patients