Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (27 [11])

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Volume 27, Issue 11; November 1, 2007

Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis

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	Editorials
	Prevention of Tissue Death by Killer Cells?: The Role of the Immune System in Arteriogenesis Wolfgang Schaper Arterioscler Thromb Vasc Biol. 2007;27:2273-2274; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.153114 Extract \| Full Text \| PDF
	Brief Reviews
	Is Metabolic Syndrome the Main Threat to Human Health in the Twenty-First Century? Marja-Riitta Taskinen Arterioscler Thromb Vasc Biol. 2007;27:2275; published online before print September 27 2007, doi:10.1161/ATVBAHA.107.154195 Extract \| Full Text \| PDF
	Inflamed Adipose Tissue: A Culprit Underlying the Metabolic Syndrome and Atherosclerosis Birgit Gustafson, Ann Hammarstedt, Christian X. Andersson, and Ulf Smith Arterioscler Thromb Vasc Biol. 2007;27:2276-2283; published online before print September 6 2007, doi:10.1161/ATVBAHA.107.147835 Abstract \| Full Text \| PDF The Metabolic Syndrome is associated with a dysregulated adipose tissue attributable to inflammation with increased levels of several proinflammatory molecules. This alters the pattern of adipokines produced and prevents the differentiation of preadipocytes. Furthermore, insulin resistance is induced which enhances both lipolysis and the proinflammatory state because insulin has antiinflammatory effects.
	Links Between Adipose Tissue and Thrombosis in the Mouse Peter F. Bodary Arterioscler Thromb Vasc Biol. 2007;27:2284-2291; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.148221 Abstract \| Full Text \| PDF Obese individuals have an altered hemostatic profile which favors blood clot formation and thrombosis. To investigate the potential relationship between arterial thrombosis and adipose-derived proteins, mouse models of thrombosis have been used. This review examines the evidence that adipokines have a direct effect on arterial thrombosis.
	Vascular Adhesion Molecules in Atherosclerosis Elena Galkina and Klaus Ley Arterioscler Thromb Vasc Biol. 2007;27:2292-2301; published online before print August 2 2007, doi:10.1161/ATVBAHA.107.149179 Abstract \| Full Text \| PDF Leukocyte and endothelial adhesion molecules play key roles in the development and progression of atherosclerosis. In animal models, blocking or eliminating P-selectin, VCAM-1 or {alpha}4β1 integrin reduces atherosclerotic lesion formation by more than 50%. Smaller effects are seen by manipulating E-selectin, ICAM-1 or the JAM family of adhesion molecules.
	Osteopontin: A Multifunctional Molecule Regulating Chronic Inflammation and Vascular Disease Marta Scatena, Lucy Liaw, and Cecilia M. Giachelli Arterioscler Thromb Vasc Biol. 2007;27:2302-2309; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.144824 Abstract \| Full Text \| PDF \| Data Supplement Osteopontin OPN is expressed in chronic inflammatory diseases and regulates chemotaxis and cytokine production. Although OPN adhesive domains are characterized, signaling pathways mediating OPN effects on immune cells are not well established. OPN is cleaved by thrombin and matrix-metalloproteases to generate fragments with novel receptor binding sites and activity, suggesting that proteolysis is an important mechanism to regulate OPN function.
	Vascular Biology
	Natural Killer Cells and CD4⁺ T-Cells Modulate Collateral Artery Development V. van Weel, R.E.M. Toes, L. Seghers, M.M.L. Deckers, M.R. de Vries, P.H. Eilers, J. Sipkens, A. Schepers, D. Eefting, V.W.M. van Hinsbergh, J.H. van Bockel, and P.H.A. Quax Arterioscler Thromb Vasc Biol. 2007;27:2310-2318; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.151407 Abstract \| Full Text \| PDF \| Data Supplement The immune system is thought to play a crucial role in regulating collateral circulation (arteriogenesis). Here, we show that both natural killer cells and CD4+ T-cells modulate arteriogenesis. Promoting lymphocyte activation may represent a promising method to treat ischemic disease.
	Important Role of Nox4 Type NADPH Oxidase in Angiogenic Responses in Human Microvascular Endothelial Cells In Vitro Srinivasa Raju Datla, Hitesh Peshavariya, Gregory J. Dusting, Kalyankar Mahadev, Barry J. Goldstein, and Fan Jiang Arterioscler Thromb Vasc Biol. 2007;27:2319-2324; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.149450 Abstract \| Full Text \| PDF \| Data Supplement In vitro angiogenic responses were inhibited by Nox4 small interfering RNA or by dominant negative Nox4. Wild-type Nox4 overexpression enhanced VEGF-stimulated signaling, reduced apoptosis, and enhanced the angiogenic responses. Nox4-dependent redox signaling is an important positive modulator of angiogenic responses in human vascular endothelial cells.
	Nuclear Redox-Signaling Is Essential for Apoptosis Inhibition in Endothelial Cells—Important Role for Nuclear Thioredoxin-1 Peter Schroeder, Ruediger Popp, Barbara Wiegand, Joachim Altschmied, and Judith Haendeler Arterioscler Thromb Vasc Biol. 2007;27:2325-2331; published online before print September 6 2007, doi:10.1161/ATVBAHA.107.149419 Abstract \| Full Text \| PDF \| Data Supplement Physiological concentrations of ROS and NO activate signaling pathways. ROS induce karyopherin {alpha}-dependent nuclear import of Trx, which is enhanced by posttranslational modifications of Trx. Import of Trx modified antioxidant responsive element containing promoters and increased GST-P1 expression. Knocking down GST-P1 abolished the antiapoptotic properties of ROS. Nuclear Trx plays an important role in endothelial cell apoptosis.
	Involvement of Rho Kinase in Endothelial Barrier Maintenance G.P. van Nieuw Amerongen, C.M.L. Beckers, I.D. Achekar, S. Zeeman, R.J.P. Musters, and V.W.M. van Hinsbergh Arterioscler Thromb Vasc Biol. 2007;27:2332-2339; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.152322 Abstract \| Full Text \| PDF \| Data Supplement A well-known effect of activation of Rho kinase by vasoactive agents is disruption of endothelial barrier integrity. Here, we provide evidence for a role of basal Rho kinase activity in regulating proper expression of the junctional adhesion molecule VE-cadherin, opposite to the barrier-disruptive effects of Rho kinase.
	4-Hydroxy-2-Nonenal Increases Superoxide Anion Radical in Endothelial Cells via Stimulated GTP Cyclohydrolase Proteasomal Degradation Jennifer Whitsett, Matthew J. Picklo, Sr, and Jeannette Vasquez-Vivar Arterioscler Thromb Vasc Biol. 2007;27:2340-2347; published online before print September 13 2007, doi:10.1161/ATVBAHA.107.153742 Abstract \| Full Text \| PDF \| Data Supplement 4-Hydroxy-2-nonenal (4-HNE) mediates oxidative stress in the endothelium by controversial mechanisms. This study shows that 4-HNE uncouples eNOS by promoting GTPCH degradation by the proteasome. Sepiapterin and to a lesser extent ascorbate counteracted loss of NO and superoxide increase. Preventing eNOS uncoupling may be important in decreasing 4-HNE cytotoxicity.
	Adaptation of Vasomotor Function of Human Coronary Arterioles to the Simultaneous Presence of Obesity and Hypertension Tibor Fulop, Eva Jebelovszki, Nora Erdei, Tamas Szerafin, Tamas Forster, Istvan Edes, Akos Koller, and Zsolt Bagi Arterioscler Thromb Vasc Biol. 2007;27:2348-2354; published online before print September 6 2007, doi:10.1161/ATVBAHA.107.147991 Abstract \| Full Text \| PDF \| Data Supplement The present study shows enhanced dilations of coronary arterioles and brachial arteries in obese hypertensive patients, implying an important functional adaptation, such as an increased sensitivity to NO of coronary and peripheral arterial vessels, to the simultaneous presence of obesity and hypertension.
	Angiotensin II Stimulates Protein Kinase D-Dependent Histone Deacetylase 5 Phosphorylation and Nuclear Export Leading to Vascular Smooth Muscle Cell Hypertrophy Xiangbin Xu, Chang-Hoon Ha, Chelsea Wong, Weiye Wang, Angelika Hausser, Klaus Pfizenmaier, Eric N. Olson, Timothy A. McKinsey, and Zheng-Gen Jin Arterioscler Thromb Vasc Biol. 2007;27:2355-2362; published online before print September 6 2007, doi:10.1161/ATVBAHA.107.151704 Abstract \| Full Text \| PDF \| Data Supplement Angiotensin II is implicated in the pathological vascular remodeling. In this study we demonstrate a critical role of protein kinase D and histone deacetylases 5 in Angiotensin II-induced VSMC hypertrophy, and reveal a new signal pathway for the pathological vascular effects of Angiotensin II.
	Angiotensin II Receptor Blocker Inhibits Neointimal Hyperplasia Through Regulation of Smooth Muscle–Like Progenitor Cells Takaaki Yamada, Takahisa Kondo, Yasushi Numaguchi, Michitaka Tsuzuki, Tatsuaki Matsubara, Ichiro Manabe, Masataka Sata, Ryozo Nagai, and Toyoaki Murohara Arterioscler Thromb Vasc Biol. 2007;27:2363-2369; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.147124 Abstract \| Full Text \| PDF \| Data Supplement Bone marrow (BM)-derived cells differentiate into smooth muscle-like cells at injured arteries and contribute to neointimal formation. However, role of angiotensin II (ATII) in this process was unknown. Here we show that ATII accelerated whereas AT1 receptor blocker (ARB) suppressed this process. These are new aspects of ARB-mediated inhibition of atherosclerotic disease.
	CXCR2 Blockade Impairs Angiotensin II–Induced CC Chemokine Synthesis and Mononuclear Leukocyte Infiltration Yafa Naim Abu Nabah, Mercedes Losada, Rossana Estellés, Teresa Mateo, Chantal Company, Laura Piqueras, Concha Lopez-Gines, Henry Sarau, Julio Cortijo, Esteban J. Morcillo, Peter J. Jose, and Maria-Jesus Sanz Arterioscler Thromb Vasc Biol. 2007;27:2370-2376; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.147009 Abstract \| Full Text \| PDF \| Data Supplement The effect of a CXCR2 antagonist, SB-517785-M, on angiotensin-II (Ang-II) vascular inflammation was investigated. SB-517785-M reduced Ang-II-induced release of CC chemokines, arteriolar adhesion, and recruitment of mononuclear cells in rats. Therefore CXCR2 antagonists may help to prevent mononuclear cell infiltration and the progression of the atherogenic process.
	Multiple Effects of High Mobility Group Box Protein 1 in Skeletal Muscle Regeneration Roberta De Mori, Stefania Straino, Anna Di Carlo, Antonella Mangoni, Giulio Pompilio, Roberta Palumbo, Marco E. Bianchi, Maurizio C. Capogrossi, and Antonia Germani Arterioscler Thromb Vasc Biol. 2007;27:2377-2383; published online before print September 13 2007, doi:10.1161/ATVBAHA.107.153429 Abstract \| Full Text \| PDF \| Data Supplement In this study we provide evidence of the involvement of HMGB1 in skeletal muscle regeneration. Endogenous HMGB1 blockade or HMGB1 administration, in a mouse model of hindlimb ischemia, affect myoblast function and neovascularization. HMGB1 induces myoblast migration and modulates endothelial cell functions in vitro, activating JNK and ERK signaling pathways.
	Atherosclerosis and Lipoproteins
	Local Overexpression of Toll-Like Receptors at the Vessel Wall Induces Atherosclerotic Lesion Formation: Synergism of TLR2 and TLR4 Masakazu Shinohara, Ken-ichi Hirata, Tomoya Yamashita, Tomofumi Takaya, Naoto Sasaki, Rio Shiraki, Tomomi Ueyama, Noriaki Emoto, Nobutaka Inoue, Mitsuhiro Yokoyama, and Seinosuke Kawashima Arterioscler Thromb Vasc Biol. 2007;27:2384-2391; published online before print September 13 2007, doi:10.1161/ATVBAHA.106.139253 Abstract \| Full Text \| PDF \| Data Supplement Local cotransfection of TLR2 and TLR4 at the vessel wall synergistically accelerated atherosclerosis in carotid arteries of rabbits fed a high-cholesterol diet. The synergistic augmentation was likely related to the marked activation of NF-{kappa}B, leading to augmented expressions of ICAM-1, VCAM-1, and MCP-1, at the vessel wall.
	Sphingosine-1-Phosphate Analogue FTY720 Causes Lymphocyte Redistribution and Hypercholesterolemia in ApoE-Deficient Mice Roland Klingenberg, Jerzy-Roch Nofer, Mats Rudling, Florian Bea, Erwin Blessing, Michael Preusch, Hermann J. Grone, Hugo A. Katus, Göran K. Hansson, and Thomas J. Dengler Arterioscler Thromb Vasc Biol. 2007;27:2392-2399; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.149476 Abstract \| Full Text \| PDF \| Data Supplement Administration of the sphingolipid analogue FTY720 to ApoE-/- mice on normal laboratory diet altered lipid metabolism yielding pronounced hypercholesterolemia. Despite lymphocyte depletion and retrafficking the overall balance of pro- and antiatherogenic lymphocyte populations was not changed. Hypercholesterolemia appears to have counteracted the otherwise beneficial effect on atherogenesis.
	Esculeogenin A, a New Tomato Sapogenol, Ameliorates Hyperlipidemia and Atherosclerosis in ApoE-Deficient Mice by Inhibiting ACAT Yukio Fujiwara, Naoko Kiyota, Masaharu Hori, Sayaka Matsushita, Yoko Iijima, Koh Aoki, Daisuke Shibata, Motohiro Takeya, Tsuyoshi Ikeda, Toshihiro Nohara, and Ryoji Nagai Arterioscler Thromb Vasc Biol. 2007;27:2400-2406; published online before print September 13 2007, doi:10.1161/ATVBAHA.107.147405 Abstract \| Full Text \| PDF \| Data Supplement Esculeogenin A, a new aglycon of esculeoside A isolated from tomato, significantly inhibited the accumulation of cholesterol ester in macrophages by inhibiting acyl-CoA: cholesterol acyl-transferase (ACAT). Oral administration of esculeoside A to apoE-deficient mice significantly reduced the levels of serum cholesterol and the areas of atherosclerotic lesions.
	Cholesterol Accumulation Is Increased in Macrophages of Phospholipid Transfer Protein-Deficient Mice: Normalization by Dietary Alpha-Tocopherol Supplementation Nicolas Ogier, Alexis Klein, Valérie Deckert, Anne Athias, Ginette Bessède, Naig Le Guern, Laurent Lagrost, and Catherine Desrumaux Arterioscler Thromb Vasc Biol. 2007;27:2407-2412; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.151753 Abstract \| Full Text \| PDF \| Data Supplement Although systemic PLTP is proatherogenic, recent findings suggested that macrophage-derived PLTP could be antiatherogenic. This study shows that the reduced {alpha}-tocopherol content of isolated macrophages from PLTP-deficient mice is associated with increased cholesterol accumulation in these cells. Cholesterol parameters in the macrophages of PLTP-deficient mice were normalized by dietary supplementation with {alpha}-tocopherol.
	Increased Oxidative Stress in Scavenger Receptor BI Knockout Mice With Dysfunctional HDL Miranda Van Eck, Menno Hoekstra, Reeni B. Hildebrand, Yuemang Yaong, Dominique Stengel, J. Kar Kruijt, Wolfgang Sattler, Uwe J.F. Tietge, Ewa Ninio, Theo J.C. Van Berkel, and Domenico Praticò Arterioscler Thromb Vasc Biol. 2007;27:2413-2419; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.145474 Abstract \| Full Text \| PDF \| Data Supplement HDL reduces atherosclerosis by its antioxidant properties. In the current study we show that disruption of SR-BI, a prominent regulator of HDL metabolism, decreases the activity of the HDL-associated antioxidant enzyme paraoxonase 1 and leads to increased oxidative stress, potentially contributing to the proatherogenic effect of SR-BI deficiency.
	Angptl4 Upregulates Cholesterol Synthesis in Liver via Inhibition of LPL- and HL-Dependent Hepatic Cholesterol Uptake Laeticia Lichtenstein, Jimmy F.P. Berbée, Susan J. van Dijk, Ko Willems van Dijk, André Bensadoun, Ido P. Kema, Peter J. Voshol, Michael Müller, Patrick C.N. Rensen, and Sander Kersten Arterioscler Thromb Vasc Biol. 2007;27:2420-2427; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.151894 Abstract \| Full Text \| PDF \| Data Supplement The present study exploits the fasting-dependent phenotype of Angptl4-transgenic mice to characterize the function of Angptl4. We conclude that: (1) Angptl4 causes hypertriglyceridemia by inhibiting LPL-dependent VLDL lipolysis by converting LPL dimers to monomers, and (2) Angptl4 upregulates hepatic cholesterol synthesis secondary to inhibition of LPL- and HL-dependent hepatic cholesterol uptake.
	Pioglitazone Stimulates Apolipoprotein A-I Production Without Affecting HDL Removal in HepG2 Cells: Involvement of PPAR- ${alpha}$ Shucun Qin, Tianjiao Liu, Vaijinath S. Kamanna, and Moti L. Kashyap Arterioscler Thromb Vasc Biol. 2007;27:2428-2434; published online before print September 13 2007, doi:10.1161/ATVBAHA.107.150193 Abstract \| Full Text \| PDF This study examined the mechanism by which pioglitazone increases apoA-I/A-II and HDL. Pioglitazone, by PPAR-{alpha}-mediated events increased the synthesis of apoA-I and apoA-II without affecting the uptake of HDL. Hepatic activation of PPAR-{alpha} may be involved in the effect of pioglitazone to raise apoA-I and HDL.
	Small Concentrations of oxLDL Induce Capillary Tube Formation From Endothelial Cells via LOX-1–Dependent Redox-Sensitive Pathway Abhijit Dandapat, Changping Hu, Liuqin Sun, and Jawahar L. Mehta Arterioscler Thromb Vasc Biol. 2007;27:2435-2442; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.152272 Abstract \| Full Text \| PDF \| Data Supplement Low levels of reactive oxygen species function as signaling molecules for angiogenesis. In keeping with this concept, we postulated and found that oxLDL (0.1 to 5 {micro}g/mL) promoted capillary tube formation by inducing the expression of VEGF via LOX-1-mediated activation of NADPH oxidase-MAPKs-NF-{kappa}B pathway.
	Genomic Changes in Regenerated Porcine Coronary Arterial Endothelial Cells Mary Y.K. Lee, Hung-Fat Tse, Chung-Wah Siu, Shu-Guang Zhu, Ricky Y.K. Man, and Paul M. Vanhoutte Arterioscler Thromb Vasc Biol. 2007;27:2443-2449, doi:10.1161/ATVBAHA.107.141705 Abstract \| Full Text \| PDF \| Data Supplement Genomic changes were determined in cultured regenerated endothelial cells. cGMP production was reduced. Changes in mRNA expression related to vasomotor control, coagulation, oxidative stress, extracellular matrix, and lipid were confirmed by Western blotting for eNOS, F2, Mn SOD, matrix metalloproteinase 7, and TR. These findings reveal linkages between regeneration and endothelial dysfunction.
	Resequencing Genomic DNA of Patients With Severe Hypertriglyceridemia (MIM 144650) Jian Wang, Henian Cao, Matthew R. Ban, Brooke A. Kennedy, Siqi Zhu, Sonia Anand, Salim Yusuf, Rebecca L. Pollex, and Robert A. Hegele Arterioscler Thromb Vasc Biol. 2007;27:2450-2455; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.150680 Abstract \| Full Text \| PDF Severe hypertriglyceridemia has been presumed to have a genetic basis, but this has never been quantified. With resequencing, we now document a range of DNA variants in LPL, APOC2, and APOA5 genes which together were found in 41.8% of patients with severe HTG compared with 8.9% of control subjects (P<10-13).
	Nateglinide Reduces Carotid Intima-Media Thickening in Type 2 Diabetic Patients Under Good Glycemic Control Tomoya Mita, Hirotaka Watada, Tomoaki Shimizu, Yoshifumi Tamura, Fumihiko Sato, Takahiro Watanabe, Jong Bock Choi, Takahisa Hirose, Yasushi Tanaka, and Ryuzo Kawamori Arterioscler Thromb Vasc Biol. 2007;27:2456-2462; published online before print September 13 2007, doi:10.1161/ATVBAHA.107.152835 Abstract \| Full Text \| PDF \| Data Supplement To investigate the effect of nateglinide on atherosclerosis, we performed an open labeled randomized prospective trial on drug-naive type 2 diabetic patients whose HbA1c was less than 6.5%. The carotid intima-media thickness at the end of 1-year follow-up period was significantly decreased in the nateglinide group compared with the untreated group. In type 2 diabetic patients under good glycemic control, further strict glycemic control by nateglinide results in regression of carotid intima-media thickness.
	Prognostic Utility of Lipoprotein-Associated Phospholipase A₂ for Cardiovascular Outcomes in Patients With Stable Coronary Artery Disease Marc S. Sabatine, David A. Morrow, Michelle O’Donoghue, Kathleen A. Jablonksi, Madeline Murguia Rice, Scott Solomon, Yves Rosenberg, Michael J. Domanski, Judith Hsia for the PEACE Investigators Arterioscler Thromb Vasc Biol. 2007;27:2463-2469; published online before print August 31 2007, doi:10.1161/ATVBAHA.107.151670 Abstract \| Full Text \| PDF In 3766 patients with stable CAD, an elevated level of Lp-PLA2 was a significant predictor of adverse cardiovascular outcomes independent of traditional clinical risk factors. When analyzed together, both hs-CRP and Lp-PLA2 were highly significant predictors of ACS, whereas only Lp-PLA2 was a significant predictor of revascularization.
	Thrombosis
	The PI3K/Akt Pathway Mediates the Neuroprotective Effect of Atorvastatin in Extending Thrombolytic Therapy After Embolic Stroke in the Rat Li Zhang, Zheng Gang Zhang, Xian Shuang Liu, Ann Hozeska-Solgot, and Michael Chopp Arterioscler Thromb Vasc Biol. 2007;27:2470-2475; published online before print August 23 2007, doi:10.1161/ATVBAHA.107.150748 Abstract \| Full Text \| PDF Combination treatment with atorvastatin and tPA 4h after embolic stroke substantially reduced infarct volume and activated Akt. Blockage of the PI3K/Akt pathway with wortmannin completely abolished the neuroprotective effect of the combination therapy. These data indicate that the PI3K/Akt pathway mediates the neuroprotective effects of atorvastatin.
	Platelet Activation by Oxidized Low Density Lipoprotein Is Mediated by Cd36 and Scavenger Receptor-A Suzanne J.A. Korporaal, Miranda Van Eck, Jelle Adelmeijer, Martin Ijsseldijk, Ruud Out, Ton Lisman, Peter J. Lenting, Theo J.C. Van Berkel, and Jan-Willem N. Akkerman Arterioscler Thromb Vasc Biol. 2007;27:2476-2483; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.150698 Abstract \| Full Text \| PDF \| Data Supplement Platelets are activated by nLDL through binding to apoER2', which signals to p38MAPK. Oxidation induces more p38MAPK activation through loss of apoER2' binding thereby initiating the combined activity of CD36 and SR-A.
	Segregation of Platelet Aggregatory and Procoagulant Microdomains in Thrombus Formation: Regulation by Transient Integrin Activation Imke C.A. Munnix, Marijke J.E. Kuijpers, Jocelyn Auger, Christella M.L.G.D. Thomassen, Peter Panizzi, Marc A.M. van Zandvoort, Jan Rosing, Paul E. Bock, Steve P. Watson, and Johan W.M. Heemskerk Arterioscler Thromb Vasc Biol. 2007;27:2484-2490; published online before print August 30 2007, doi:10.1161/ATVBAHA.107.151100 Abstract \| Full Text \| PDF \| Data Supplement The organization and integration of 2 key functions of platelets, aggregation and procoagulant activity, is investigated. During thrombus formation under flow, platelets in aggregates segregate from patches of coagulation-active platelets with low integrin activation. The inactivation of integrins in procoagulant platelets is triggered by tyrosine kinase activity.

Spotlight

TOC Spotlight File

Volume 27, Issue 11; November 1, 2007

Editorials

Prevention of Tissue Death by Killer Cells?: The Role of the Immune System in Arteriogenesis

Brief Reviews

Is Metabolic Syndrome the Main Threat to Human Health in the Twenty-First Century?

Inflamed Adipose Tissue: A Culprit Underlying the Metabolic Syndrome and Atherosclerosis

Links Between Adipose Tissue and Thrombosis in the Mouse

Vascular Adhesion Molecules in Atherosclerosis

Osteopontin: A Multifunctional Molecule Regulating Chronic Inflammation and Vascular Disease

Vascular Biology

Natural Killer Cells and CD4+ T-Cells Modulate Collateral Artery Development

Important Role of Nox4 Type NADPH Oxidase in Angiogenic Responses in Human Microvascular Endothelial Cells In Vitro

Nuclear Redox-Signaling Is Essential for Apoptosis Inhibition in Endothelial Cells—Important Role for Nuclear Thioredoxin-1

Involvement of Rho Kinase in Endothelial Barrier Maintenance

4-Hydroxy-2-Nonenal Increases Superoxide Anion Radical in Endothelial Cells via Stimulated GTP Cyclohydrolase Proteasomal Degradation

Adaptation of Vasomotor Function of Human Coronary Arterioles to the Simultaneous Presence of Obesity and Hypertension

Angiotensin II Stimulates Protein Kinase D-Dependent Histone Deacetylase 5 Phosphorylation and Nuclear Export Leading to Vascular Smooth Muscle Cell Hypertrophy

Angiotensin II Receptor Blocker Inhibits Neointimal Hyperplasia Through Regulation of Smooth Muscle–Like Progenitor Cells

CXCR2 Blockade Impairs Angiotensin II–Induced CC Chemokine Synthesis and Mononuclear Leukocyte Infiltration

Multiple Effects of High Mobility Group Box Protein 1 in Skeletal Muscle Regeneration

Atherosclerosis and Lipoproteins

Local Overexpression of Toll-Like Receptors at the Vessel Wall Induces Atherosclerotic Lesion Formation: Synergism of TLR2 and TLR4

Sphingosine-1-Phosphate Analogue FTY720 Causes Lymphocyte Redistribution and Hypercholesterolemia in ApoE-Deficient Mice

Esculeogenin A, a New Tomato Sapogenol, Ameliorates Hyperlipidemia and Atherosclerosis in ApoE-Deficient Mice by Inhibiting ACAT

Cholesterol Accumulation Is Increased in Macrophages of Phospholipid Transfer Protein-Deficient Mice: Normalization by Dietary Alpha-Tocopherol Supplementation

Increased Oxidative Stress in Scavenger Receptor BI Knockout Mice With Dysfunctional HDL

Angptl4 Upregulates Cholesterol Synthesis in Liver via Inhibition of LPL- and HL-Dependent Hepatic Cholesterol Uptake

Pioglitazone Stimulates Apolipoprotein A-I Production Without Affecting HDL Removal in HepG2 Cells: Involvement of PPAR-

Small Concentrations of oxLDL Induce Capillary Tube Formation From Endothelial Cells via LOX-1–Dependent Redox-Sensitive Pathway

Genomic Changes in Regenerated Porcine Coronary Arterial Endothelial Cells

Resequencing Genomic DNA of Patients With Severe Hypertriglyceridemia (MIM 144650)

Nateglinide Reduces Carotid Intima-Media Thickening in Type 2 Diabetic Patients Under Good Glycemic Control

Prognostic Utility of Lipoprotein-Associated Phospholipase A2 for Cardiovascular Outcomes in Patients With Stable Coronary Artery Disease

Thrombosis

The PI3K/Akt Pathway Mediates the Neuroprotective Effect of Atorvastatin in Extending Thrombolytic Therapy After Embolic Stroke in the Rat

Platelet Activation by Oxidized Low Density Lipoprotein Is Mediated by Cd36 and Scavenger Receptor-A

Segregation of Platelet Aggregatory and Procoagulant Microdomains in Thrombus Formation: Regulation by Transient Integrin Activation

Spotlight

Natural Killer Cells and CD4⁺ T-Cells Modulate Collateral Artery Development

Pioglitazone Stimulates Apolipoprotein A-I Production Without Affecting HDL Removal in HepG2 Cells: Involvement of PPAR- ${alpha}$

Prognostic Utility of Lipoprotein-Associated Phospholipase A₂ for Cardiovascular Outcomes in Patients With Stable Coronary Artery Disease