Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (24 [7])

About This Cover

Volume 24, Issue 7; July 1, 2004

In Memoriam
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
Corrections

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

	In Memoriam
	Gardner Craddock McMillan Momtaz Wassef Arterioscler Thromb Vasc Biol. 2004;24:1326-1327, doi:10.1161/01.ATV.0000134967.87210.a2. Full Text \| PDF
	Editorials
	Myeloperoxidase and Plaque Vulnerability Stanley L. Hazen Arterioscler Thromb Vasc Biol. 2004;24:1143-1146, doi:10.1161/01.ATV.0000135267.82813.52. Full Text \| PDF
	Origin of Neointimal Cells in Autologous Vein Graft Masataka Sata and Ryozo Nagai Arterioscler Thromb Vasc Biol. 2004;24:1147-1149, doi:10.1161/01.ATV.0000134296.22448.eb. Full Text \| PDF
	Brief Reviews
	Intracellular Cholesterol Transport Raymond E. Soccio and Jan L. Breslow Arterioscler Thromb Vasc Biol. 2004;24:1150-1160; published online before print May 6 2004, doi:10.1161/01.ATV.0000131264.66417.d5. Abstract \| Full Text \| PDF Intracellular cholesterol transport is essential for the maintenance of cholesterol homeostasis. Many aspects of cholesterol metabolism are well-known, including its synthesis in the endoplasmic reticulum, its extracellular transport in plasma lipoproteins, its uptake by the low-density lipoprotein receptor, and its regulation of SREBP and LXR transcription factors. In this review, we discuss cholesterol transport among specific intracellular compartments, emphasizing the relevance of these pathways to cholesterol homeostasis.
	Vascular Calcification: Mechanisms and Clinical Ramifications Moeen Abedin, Yin Tintut, and Linda L. Demer Arterioscler Thromb Vasc Biol. 2004;24:1161-1170; published online before print May 20 2004, doi:10.1161/01.ATV.0000133194.94939.42. Abstract \| Full Text \| PDF Vascular calcification involves a complex biomineralization process that resembles osteogenesis. It is regulated by bone proteins and osteoblast-like cells found in the artery wall. Understanding its mechanism has implications for management of vascular disease, particularly in the context of bone disease.
	Should Progestins Be Blamed for the Failure of Hormone Replacement Therapy to Reduce Cardiovascular Events in Randomized Controlled Trials? Kwang Kon Koh and Ichiro Sakuma Arterioscler Thromb Vasc Biol. 2004;24:1171-1179; published online before print May 6 2004, doi:10.1161/01.ATV.0000131262.98040.65. Abstract \| Full Text \| PDF Recent randomized controlled trials have caused many people to suggest that the inclusion of the progestin in the HRT portion of this study is responsible for the adverse cardiovascular outcomes observed. Discussion of this issue is the focus of this review article.
	Vascular Biology
	Murine Model of Neointimal Formation and Stenosis in Vein Grafts Brian C. Cooley Arterioscler Thromb Vasc Biol. 2004;24:1180-1185; published online before print April 22 2004, doi:10.1161/01.ATV.0000129330.19057.9f. Abstract \| Full Text \| PDF \| Data Supplement Vein grafting between Rosa26 (constitutive marker gene expression) and wild-type mice demonstrated that neointimal cells originate predominantly from the vein graft. Neointimal proliferation appeared early and adjacent to the graft-preserved endothelium. Neointimal thickening was progressive with time and was greater at the proximal and distal ends of the graft.
	Cyclophilin A Is a Proinflammatory Cytokine that Activates Endothelial Cells Zheng-Gen Jin, Andreea O. Lungu, Liang Xie, Meng Wang, Chelsea Wong, and Bradford C. Berk Arterioscler Thromb Vasc Biol. 2004;24:1186-1191; published online before print May 6 2004, doi:10.1161/01.ATV.0000130664.51010.28. Abstract \| Full Text \| PDF This work defines a new role of cyclophilin A (CyPA) in endothelial cells as pro-inflammatory cytokine. We showed that CyPA was highly expressed in atherosclerotic plaques, and CyPA stimulated endothelial activation, induced expression of adhesion molecules and induced apoptosis, suggesting a potential role of CyPA in the pathogenesis of atherosclerosis.
	Deciphering Regulatory Patterns of Inflammatory Gene Expression From Interleukin-1—Stimulated Human Endothelial Cells Herbert Mayer, Martin Bilban, Vladislav Kurtev, Florian Gruber, Oswald Wagner, Bernd R. Binder, and Rainer de Martin Arterioscler Thromb Vasc Biol. 2004;24:1192-1198; published online before print May 6 2004, doi:10.1161/01.ATV.0000131263.06296.77. Abstract \| Full Text \| PDF \| Data Supplement We analyzed the early gene expression program of IL-1-stimulated ECs using microarray technology, particularly focusing on TF profiles. Furthermore, large-scale bioinformatic comparisons of promoter sequence sets led to the identification of a novel DNA binding site that was shown to specifically bind an IL-1-inducible protein.
	Angiotensin II Stimulates the Release of Interleukin-6 and Interleukin-8 From Cultured Human Adipocytes by Activation of NF- ${kappa}$ B Thomas Skurk, Vanessa van Harmelen, and Hans Hauner Arterioscler Thromb Vasc Biol. 2004;24:1199-1203; published online before print May 6 2004, doi:10.1161/01.ATV.0000131266.38312.2e. Abstract \| Full Text \| PDF \| Data Supplement The effect of angiotensin (Ang) II on the production of IL-6 and IL-8 in in vitro differentiated human adipocytes was studied. Ang II-stimulated IL-6 and IL-8 production by a NF-{kappa}B-dependent pathway. This proinflammatory action of Ang II was mediated by the AT1 and less by the AT2 receptor.
	R-Cadherin:ß-Catenin Complex and Its Association With Vascular Smooth Muscle Cell Proliferation Sadie C. Slater, Evgenia Koutsouki, Christopher L. Jackson, Raymond C. Bush, Gianni D. Angelini, Andrew C. Newby, and Sarah J. George Arterioscler Thromb Vasc Biol. 2004;24:1204-1210; published online before print April 29 2004, doi:10.1161/01.ATV.0000130464.24599.e0. Abstract \| Full Text \| PDF \| Data Supplement Human VSMCs that overexpress AIF-1 grow more rapidly and express G-CSF. G-CSF is capable of promoting VSMC proliferation, and AIF-1-transduced VSMCs are chemotactic for monocytes. This study indicates that AIF-1 enhances VSMC growth by autocrine production of G-CSF, and AIF-1 expression may influence VSMC-inflammatory cell communication.
	CCL11 (Eotaxin) Induces CCR3-Dependent Smooth Muscle Cell Migration Ravindra B. Kodali, William J.H. Kim, Irfan I. Galaria, Christine Miller, Alison D. Schecter, Sergio A. Lira, and Mark B. Taubman Arterioscler Thromb Vasc Biol. 2004;24:1211-1216; published online before print May 6 2004, doi:10.1161/01.ATV.0000131654.90788.f5. Abstract \| Full Text \| PDF CCL11 (Eotaxin) is an eosinophil chemoattractant that is abundant in atheromatous plaques. Mouse aortic smooth muscle cells (SMCs) possessed mRNA and protein for CCR3, the major CCL11 receptor. CCL11 induced CCR3-dependent SMC chemotaxis, but not proliferation. CCR3 and CCR11 were also markedly induced in arterial SMCs 5 and 28 days after femoral arterial injury.
	AIF-1 Expression Modulates Proliferation of Human Vascular Smooth Muscle Cells by Autocrine Expression of G-CSF Xing Chen, Sheri E. Kelemen, and Michael V. Autieri Arterioscler Thromb Vasc Biol. 2004;24:1217-1222; published online before print April 29 2004, doi:10.1161/01.ATV.0000130024.50058.de. Abstract \| Full Text \| PDF \| Data Supplement Human VSMCs that overexpress AIF-1 grow more rapidly and express G-CSF. G-CSF is capable of promoting VSMC proliferation, and AIF-1-transduced VSMCs are chemotactic for monocytes. This study indicates that AIF-1 enhances VSMC growth by autocrine production of G-CSF, and AIF-1 expression may influence VSMC-inflammatory cell communication.
	Microtubules Regulate Angiotensin II Type 1 Receptor and Rac1 Localization in Caveolae/Lipid Rafts: Role in Redox Signaling Lian Zuo, Masuko Ushio-Fukai, Lula L. Hilenski, and R. Wayne Alexander Arterioscler Thromb Vasc Biol. 2004;24:1223-1228; published online before print May 13 2004, doi:10.1161/01.ATV.0000132400.25045.2a. Abstract \| Full Text \| PDF \| Data Supplement The role of microtubules in angiotensin II (Ang II) signaling remains unknown. We demonstrate that Ang II promotes Rac1 and Ang II type 1 receptor trafficking into the caveolae/lipid rafts, which requires the integrity of microtubules. We also found that intact microtubules mediate Ang II-stimulated H2O2 production, its downstream EGF-R transactivation, Akt phosphorylation, and vascular hypertrophy.
	Basic Fibroblast Growth Factor–Induced Endothelial Proliferation and NO Synthesis Involves Inward Rectifier K⁺ Current Wolfram Scharbrodt, Christoph Rüdiger Wolfram Kuhlmann, Yongijan Wu, Christian Alexander Schaefer, Astrid Kerstin Most, Ulrich Backenköhler, Thomas Neumann, Harald Tillmanns, Bernd Waldecker, Ali Erdogan, and Johannes Wiecha Arterioscler Thromb Vasc Biol. 2004;24:1229-1233; published online before print May 6 2004, doi:10.1161/01.ATV.0000130663.37663.6a. Abstract \| Full Text \| PDF The effect of bFGF on inward rectifier K+ currents (Kir) was analyzed in HUVEC. bFGF caused an increase of Kir, which was blocked by barium. Endothelial proliferation and NO production induced by bFGF were inhibited by reducing Kir activity with barium.
	DC Electric Fields Induce Distinct Preangiogenic Responses in Microvascular and Macrovascular Cells Huai Bai, Colin D. McCaig, John V. Forrester, and Min Zhao Arterioscler Thromb Vasc Biol. 2004;24:1234-1239; published online before print May 6 2004, doi:10.1161/01.ATV.0000131265.76828.8a. Abstract \| Full Text \| PDF \| Data Supplement Electrical stimulation of 150 to 400 mV/mm induces distinctive preangiogenesis responses by directing microvascular endothelial cells to migrate toward the cathode, whereas macrovascular endothelial cells, fibroblasts, and smooth muscle cells migrate to the anode. The cell type-specific responses suggest that electrical stimulation may play a spatial organizing role in angiogenesis.
	Enhanced P2X₇ Activity in Human Fibroblasts From Diabetic Patients: A Possible Pathogenetic Mechanism for Vascular Damage in Diabetes Anna Solini, Paola Chiozzi, Anna Morelli, Elena Adinolfi, Roberta Rizzo, Olavio R. Baricordi, and Francesco Di Virgilio Arterioscler Thromb Vasc Biol. 2004;24:1240-1245; published online before print May 20 2004, doi:10.1161/01.ATV.0000133193.11078.c0. Abstract \| Full Text \| PDF \| Data Supplement Fibroblasts from type 2 diabetic subjects exhibit a higher level of P2X7 receptor activity compared with fibroblasts from healthy subjects, as witnessed by a larger ATP-dependent release of IL-6 and fibronectin and a higher susceptibility to ATP-dependent cytotoxicity. In addition, fibroblasts from diabetic subjects also secrete a larger amount of ATP compared with controls.
	Decreased Number and Impaired Angiogenic Function of Endothelial Progenitor Cells in Patients With Chronic Renal Failure Jin-Ho Choi, Koung Li Kim, Wooseong Huh, Beom Kim, Jonghoe Byun, Wonhee Suh, Jidong Sung, Eun-Seok Jeon, Ha-Young Oh, and Duk-Kyung Kim Arterioscler Thromb Vasc Biol. 2004;24:1246-1252; published online before print May 20 2004, doi:10.1161/01.ATV.0000133488.56221.4a. Abstract \| Full Text \| PDF \| Data Supplement Our study shows that EPC is numerically and functionally impaired in CRF. This may contribute to the accelerated atherosclerosis and impaired angiogenesis observed in patients with CRF. Altered biology of EPC may therefore account for the increased cardiovascular disease risk in CRF.
	Muscarinic (M) Receptors in Coronary Circulation: Gene-Targeted Mice Define the Role of M₂ and M₃ Receptors in Response to Acetylcholine Kathryn G. Lamping, Jürgen Wess, Yinghong Cui, Daniel W. Nuno, and Frank M. Faraci Arterioscler Thromb Vasc Biol. 2004;24:1253-1258; published online before print May 6 2004, doi:10.1161/01.ATV.0000130661.82773.ca. Abstract \| Full Text \| PDF This study examined the M receptor subtype (M2 versus M3 receptors) involved in the response of coronary circulation to ACh using mice deficient in the genes for M2 and M3 receptors. M3 receptor activation and not M2 receptors primarily mediates responses to ACh in the coronary circulation.
	Atherosclerosis and Lipoproteins
	Balance Between PGD Synthase and PGE Synthase Is a Major Determinant of Atherosclerotic Plaque Instability in Humans Francesco Cipollone, Maria Fazia, Annalisa Iezzi, Giovanni Ciabattoni, Barbara Pini, Chiara Cuccurullo, Sante Ucchino, Francesco Spigonardo, Mariella De Luca, Cesaria Prontera, Francesco Chiarelli, Franco Cuccurullo, and Andrea Mezzetti Arterioscler Thromb Vasc Biol. 2004;24:1259-1265; published online before print May 20 2004, doi:10.1161/01.ATV.0000133192.39901.be. Abstract \| Full Text \| PDF \| Data Supplement The aim of this study was to investigate whether the balance between PGD synthase and PGE synthase activity in macrophages could influence the evolution of human atherosclerotic plaque toward instability. Results clearly demonstrate that COX-2 may have proinflammatory or antiinflammatory properties as a function of downstream PGH2 isomerases expression.
	Morphologic Findings of Coronary Atherosclerotic Plaques in Diabetics: A Postmortem Study Allen P. Burke, Frank D. Kolodgie, Arthur Zieske, David R. Fowler, Deena K. Weber, P. Jacob Varghese, Andrew Farb, and Renu Virmani Arterioscler Thromb Vasc Biol. 2004;24:1266-1271; published online before print May 13 2004, doi:10.1161/01.ATV.0000131783.74034.97. Abstract \| Full Text \| PDF \| Data Supplement In sudden coronary death, there is a prominent role of plaque-infiltrating macrophages and T cells in the progression of atherosclerosis in diabetic subjects. The expression of RAGE (receptor for advanced glycation end products) and the binding protein (S100 A12, EN-RAGE) may further compromise cell survival and promote plaque destabilization.
	Progression of Coronary Artery Calcium and Risk of First Myocardial Infarction in Patients Receiving Cholesterol-Lowering Therapy Paolo Raggi, Tracy Q. Callister, and Leslee J. Shaw Arterioscler Thromb Vasc Biol. 2004;24:1272-1277; published online before print April 1 2004, doi:10.1161/01.ATV.0000127024.40516.ef. Abstract \| Full Text \| PDF Statins reduce risk by only 30%, and a direct measurement of change in atherosclerosis burden may provide a clue to the persistent risk measured in subjects at risk. On sequential computed tomography scans, the progression of coronary calcification was significantly greater in patients who had an event compared with event-free subjects despite similar low-density lipoprotein control.
	Infrarenal Aortic Diameter Predicts All-Cause Mortality Paul Norman, Max Le, Carole Pearce, and Konrad Jamrozik Arterioscler Thromb Vasc Biol. 2004;24:1278-1282; published online before print May 6 2004, doi:10.1161/01.ATV.0000131261.12051.7f. Abstract \| Full Text \| PDF Infrarenal aortic diameter was measured in 12 203 men. Cumulative mortality increased in a graded fashion with increasing aortic diameter. Using the interval 19 to 22 mm as the reference, the hazard ratio for all-cause mortality increased from 1.26 for aortic diameters of 23 to 26 mm to 2.38 for aortic diameters of 47 to 50 mm.
	Atherosclerotic Plaque Smooth Muscle Cells Have a Distinct Phenotype Eileen R. Mulvihill, Jochen Jaeger, Rimli Sengupta, Walter L. Ruzzo, Cecile Reimer, Sheila Lukito, and Stephen M. Schwartz Arterioscler Thromb Vasc Biol. 2004;24:1283-1289; published online before print May 13 2004, doi:10.1161/01.ATV.0000132401.12275.0c. Abstract \| Full Text \| PDF \| Data Supplement We characterized gene expression in plaque and medial SMC cultures developed from human carotid endarterectomy specimens. These cells were nearly indistinguishable by morphological features, population doubling time, and sensitivity to cell death induced by Fas cross-linking. Surprisingly, array expression analysis identified differences so extensive that we conclude that plaque and medial SMC are distinctly different SMC cell types.
	Human Smooth Muscle Cell Subpopulations Differentially Accumulate Cholesteryl Ester When Exposed to Native and Oxidized Lipoproteins Carmen A. Argmann, Cynthia G. Sawyez, Shaohua Li, Zengxuan Nong, Robert A. Hegele, J. Geoffrey Pickering, and Murray W. Huff Arterioscler Thromb Vasc Biol. 2004;24:1290-1296; published online before print May 6 2004, doi:10.1161/01.ATV.0000131260.80316.37. Abstract \| Full Text \| PDF \| Data Supplement We tested whether epithelioid and spindle-shaped human SMCs differentially accumulated lipid on exposure to native and oxidized lipoproteins. Spindle-shaped HITB5 cells preferentially accumulated cholesteryl ester and triglyceride, whereas the epithelioid-like HITA2 SMCs required exogenous LPL to accumulate lipid in the presence of lipoproteins. Therefore, SMC subtypes are differentially predisposed to a lipid-accumulating phenotype.
	Analysis of Apolipoprotein A5, C3, and Plasma Triglyceride Concentrations in Genetically Engineered Mice Nadine Baroukh, Eric Bauge, Jennifer Akiyama, Jessie Chang, Veena Afzal, Jean-Charles Fruchart, Edward M. Rubin, Jamila Fruchart-Najib, and Len A. Pennacchio Arterioscler Thromb Vasc Biol. 2004;24:1297-1302; published online before print April 29 2004, doi:10.1161/01.ATV.0000130463.68272.1d. Abstract \| Full Text \| PDF \| Data Supplement To address the relationship between the apolipoprotein A5 and C3 genes, we generated independent lines of mice that either overexpressed or completely lacked both genes. We report both lines display normal triglyceride concentrations compared with overexpression or deletion of either gene alone. Together, these data support that APOA5 and APOC3 independently influence plasma triglyceride concentrations but in an opposing manner.
	Effect of Pravastatin on Low-Density Lipoprotein Oxidation and Myocardial Perfusion in Young Adults With Type 1 Diabetes Tuula Janatuinen, Juhani Knuuti, Jyri O. Toikka, Markku Ahotupa, Pirjo Nuutila, Tapani Rönnemaa, and Olli T. Raitakari Arterioscler Thromb Vasc Biol. 2004;24:1303-1308; published online before print May 13 2004, doi:10.1161/01.ATV.0000132409.87124.60. Abstract \| Full Text \| PDF In this randomized, double-blind study, low-density lipoprotein (LDL) oxidation and myocardial perfusion were measured in 42 normocholesterolemic patients with type 1 diabetes before and after 4-month treatment with pravastatin or placebo. Pravastatin decreased LDL oxidation; however, this was not associated with improvement in myocardial perfusion reserve measured by positron emission tomography.
	Thrombosis
	Hypochlorous Acid, a Macrophage Product, Induces Endothelial Apoptosis and Tissue Factor Expression: Involvement of Myeloperoxidase-Mediated Oxidant in Plaque Erosion and Thrombogenesis Seigo Sugiyama, Kiyotaka Kugiyama, Masanori Aikawa, Shinichi Nakamura, Hisao Ogawa, and Peter Libby Arterioscler Thromb Vasc Biol. 2004;24:1309-1314; published online before print May 13 2004, doi:10.1161/01.ATV.0000131784.50633.4f. Abstract \| Full Text \| PDF \| Data Supplement Coronary erosion causes acute coronary syndromes (ACS). Macrophages at sites of ulceration in human atheromata can contain myeloperoxidase (MPO) that generates hypochlorous acid (HOCl). HOCl provokes endothelial cell death by either apoptosis or oncosis and increases tissue factor. MPO-positive macrophage-derived HOCl may participate in ACS by promoting erosion and increasing thrombogenicity.
	Small GTP-Binding Protein Ral Is Involved in cAMP-Mediated Release of von Willebrand Factor From Endothelial Cells Mariska G. Rondaij, Erica Sellink, Karina A. Gijzen, Jean Paul ten Klooster, Peter L. Hordijk, Jan A. van Mourik, and Jan Voorberg Arterioscler Thromb Vasc Biol. 2004;24:1315-1320; published online before print May 6 2004, doi:10.1161/01.ATV.0000131267.13425.45. Abstract \| Full Text \| PDF \| Data Supplement Epinephrine, a cAMP-raising agonist of WPB exocytosis, activates the small GTPase Ral in a PKA-dependent manner. Furthermore, a cell-permeable, Ral-derived peptide inhibited epinephrine-induced and thrombin-induced vWF secretion. These results suggest that Ral is a crucial component of cAMP-dependent and Ca2+-dependent signaling pathways that mediate WPB exocytosis.
	Protein C Levels Are Regulated by a Quantitative Trait Locus on Chromosome 16: Results from the Genetic Analysis of Idiopathic Thrombophilia (GAIT) Project Alfonso Buil, José Manuel Soria, Juan Carlos Souto, Laura Almasy, Mark Lathrop, John Blangero, and Jordi Fontcuberta Arterioscler Thromb Vasc Biol. 2004;24:1321-1325; published online before print May 13 2004, doi:10.1161/01.ATV.0000132408.13064.09. Abstract \| Full Text \| PDF As part of the Genetic Analysis of Idiopathic Thrombophilia (GAIT) Project, we conducted a genome-wide linkage scan to localize genes influencing variation in PC plasma levels. Our results provide strong evidence for a locus (QTL) on chromosome 16. This locus is likely the NQO1 gene that influences PC levels.
	Letters to the Editor
	Vitamin E Is Not Deficient in Human Atherosclerotic Plaques Anatol Kontush, M. John Chapman, and Roland Stocker Arterioscler Thromb Vasc Biol. 2004;24:e139-e140, doi:10.1161/01.ATV.0000131259.97572.99. Full Text \| PDF
	Supplemented ${alpha}$ -Tocopherol Apparently Does Not Enter the Plaque Compartment Fausta Micheletta, Silvia Natoli, and Luigi Iuliano Arterioscler Thromb Vasc Biol. 2004;24:e141-e142, doi:10.1161/01.ATV.0000133190.17531.ec. Full Text \| PDF
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2004;24:1328. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 24, Issue 7; July 1, 2004

In Memoriam

Gardner Craddock McMillan

Editorials

Myeloperoxidase and Plaque Vulnerability

Origin of Neointimal Cells in Autologous Vein Graft

Brief Reviews

Intracellular Cholesterol Transport

Vascular Calcification: Mechanisms and Clinical Ramifications

Should Progestins Be Blamed for the Failure of Hormone Replacement Therapy to Reduce Cardiovascular Events in Randomized Controlled Trials?

Vascular Biology

Murine Model of Neointimal Formation and Stenosis in Vein Grafts

Cyclophilin A Is a Proinflammatory Cytokine that Activates Endothelial Cells

Deciphering Regulatory Patterns of Inflammatory Gene Expression From Interleukin-1—Stimulated Human Endothelial Cells

Angiotensin II Stimulates the Release of Interleukin-6 and Interleukin-8 From Cultured Human Adipocytes by Activation of NF-B

R-Cadherin:ß-Catenin Complex and Its Association With Vascular Smooth Muscle Cell Proliferation

CCL11 (Eotaxin) Induces CCR3-Dependent Smooth Muscle Cell Migration

AIF-1 Expression Modulates Proliferation of Human Vascular Smooth Muscle Cells by Autocrine Expression of G-CSF

Microtubules Regulate Angiotensin II Type 1 Receptor and Rac1 Localization in Caveolae/Lipid Rafts: Role in Redox Signaling

Basic Fibroblast Growth Factor–Induced Endothelial Proliferation and NO Synthesis Involves Inward Rectifier K+ Current

DC Electric Fields Induce Distinct Preangiogenic Responses in Microvascular and Macrovascular Cells

Enhanced P2X7 Activity in Human Fibroblasts From Diabetic Patients: A Possible Pathogenetic Mechanism for Vascular Damage in Diabetes

Decreased Number and Impaired Angiogenic Function of Endothelial Progenitor Cells in Patients With Chronic Renal Failure

Muscarinic (M) Receptors in Coronary Circulation: Gene-Targeted Mice Define the Role of M2 and M3 Receptors in Response to Acetylcholine

Atherosclerosis and Lipoproteins

Balance Between PGD Synthase and PGE Synthase Is a Major Determinant of Atherosclerotic Plaque Instability in Humans

Morphologic Findings of Coronary Atherosclerotic Plaques in Diabetics: A Postmortem Study

Progression of Coronary Artery Calcium and Risk of First Myocardial Infarction in Patients Receiving Cholesterol-Lowering Therapy

Infrarenal Aortic Diameter Predicts All-Cause Mortality

Atherosclerotic Plaque Smooth Muscle Cells Have a Distinct Phenotype

Human Smooth Muscle Cell Subpopulations Differentially Accumulate Cholesteryl Ester When Exposed to Native and Oxidized Lipoproteins

Analysis of Apolipoprotein A5, C3, and Plasma Triglyceride Concentrations in Genetically Engineered Mice

Effect of Pravastatin on Low-Density Lipoprotein Oxidation and Myocardial Perfusion in Young Adults With Type 1 Diabetes

Thrombosis

Hypochlorous Acid, a Macrophage Product, Induces Endothelial Apoptosis and Tissue Factor Expression: Involvement of Myeloperoxidase-Mediated Oxidant in Plaque Erosion and Thrombogenesis

Small GTP-Binding Protein Ral Is Involved in cAMP-Mediated Release of von Willebrand Factor From Endothelial Cells

Protein C Levels Are Regulated by a Quantitative Trait Locus on Chromosome 16: Results from the Genetic Analysis of Idiopathic Thrombophilia (GAIT) Project

Letters to the Editor

Vitamin E Is Not Deficient in Human Atherosclerotic Plaques

Supplemented -Tocopherol Apparently Does Not Enter the Plaque Compartment

Corrections

Correction

Spotlight

Angiotensin II Stimulates the Release of Interleukin-6 and Interleukin-8 From Cultured Human Adipocytes by Activation of NF- ${kappa}$ B

Basic Fibroblast Growth Factor–Induced Endothelial Proliferation and NO Synthesis Involves Inward Rectifier K⁺ Current

Enhanced P2X₇ Activity in Human Fibroblasts From Diabetic Patients: A Possible Pathogenetic Mechanism for Vascular Damage in Diabetes

Muscarinic (M) Receptors in Coronary Circulation: Gene-Targeted Mice Define the Role of M₂ and M₃ Receptors in Response to Acetylcholine

Supplemented ${alpha}$ -Tocopherol Apparently Does Not Enter the Plaque Compartment