Arteriosclerosis, Thrombosis, and Vascular Biology -- Table of Contents (24 [10])

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Volume 24, Issue 10; October 1, 2004

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

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	Editorials
	Estrogen and HDL: All that Glitters Is not Gold David M. Herrington and John S. Parks Arterioscler Thromb Vasc Biol. 2004;24:1741-1742, doi:10.1161/01.ATV.0000142357.90351.92. Full Text \| PDF
	CRP and Risk of Coronary Heart Disease: Can Exercise Training Cool Down the Flames? Jean-Pierre Després Arterioscler Thromb Vasc Biol. 2004;24:1743-1745, doi:10.1161/01.ATV.0000143482.82230.bb. Full Text \| PDF
	Molecular Phenotypes of Atherosclerosis: Fingering the Perpetrators Peter F. Davies Arterioscler Thromb Vasc Biol. 2004;24:1746-1747, doi:10.1161/01.ATV.0000144777.98578.9e. Full Text \| PDF
	Vascular Cross-Talk: A Conversation Margarete Mehrabian and Hooman Allayee Arterioscler Thromb Vasc Biol. 2004;24:1748-1749, doi:10.1161/01.ATV.0000143939.91227.63. Full Text \| PDF
	Brief Reviews
	Hepatic Lipase, Lipoprotein Metabolism, and Atherogenesis Silvia Santamarina-Fojo, Herminia González-Navarro, Lita Freeman, Elke Wagner, and Zengxuan Nong Arterioscler Thromb Vasc Biol. 2004;24:1750-1754; published online before print July 29 2004, doi:10.1161/01.ATV.0000140818.00570.2d. Abstract \| Full Text \| PDF Hepatic lipase is a multifunctional protein that modulates lipoprotein metabolism and atherosclerosis. Hepatic lipase functions as a lipase and as a ligand that facilitates lipoprotein uptake by cell surface receptors and proteoglycans. These multiple functions have a major and complex impact on atherogenesis.
	Regulation of Plasma High-Density Lipoprotein Levels by the ABCA1 Transporter and the Emerging Role of High-Density Lipoprotein in the Treatment of Cardiovascular Disease H. Bryan Brewer, Jr, Alan T. Remaley, Edward B. Neufeld, Federica Basso, and Charles Joyce Arterioscler Thromb Vasc Biol. 2004;24:1755-1760; published online before print August 19 2004, doi:10.1161/01.ATV.0000142804.27420.5b. Abstract \| Full Text \| PDF High-density lipoproteins (HDL) protect against cardiovascular disease. Current approaches to increasing HDL to determine its efficacy in reducing atherosclerosis involve acute HDL therapy with infusions of apoA-I or apoA-I mimetic peptides and chronic long-term therapy with selective agents to increase HDL, including CETP inhibitors.
	Endothelium-Targeted Gene and Cell-Based Therapies for Cardiovascular Disease Luis G. Melo, Massimiliano Gnecchi, Alok S. Pachori, Deling Kong, Kai Wang, Xiaoli Liu, Richard E. Pratt, and Victor J. Dzau Arterioscler Thromb Vasc Biol. 2004;24:1761-1774; published online before print August 12 2004, doi:10.1161/01.ATV.0000142363.15113.88. Abstract \| Full Text \| PDF \| Data Supplement Endothelial dysfunction plays a pivotal role in cardiovascular disease. The recent isolation of endothelial progenitor cells together with the availability of promoter sequences and vectors capable of rendering endothelial-specific transgene expression may offer opportunities for the design of novel therapeutic strategies for improvement of endothelial function in cardiovascular disease.
	Finding Vulnerable Atherosclerotic Plaques: Is It Worth the Effort? Mohammad Madjid, Alireza Zarrabi, Silvio Litovsky, James T. Willerson, and Ward Casscells Arterioscler Thromb Vasc Biol. 2004;24:1775-1782; published online before print August 12 2004, doi:10.1161/01.ATV.0000142373.72662.20. Abstract \| Full Text \| PDF Techniques to identify and treat vulnerable plaques are the focus of enormous research. Here, we discuss the potential benefit of locating individual vulnerable plaques. We review the multifocal nature of the disease in autopsy series and studies using angiography, IVUS, thermography, and angioscopy. The use of new imaging techniques and the development of predictive models may enable physicians to identify plaques that may benefit from local therapies.
	Vascular Biology
	Leukotriene B₄ Strongly Increases Monocyte Chemoattractant Protein-1 in Human Monocytes Li Huang, Annie Zhao, Frederick Wong, Julia M. Ayala, Mary Struthers, Feroze Ujjainwalla, Samuel D. Wright, Marty S. Springer, Jilly Evans, and Jisong Cui Arterioscler Thromb Vasc Biol. 2004;24:1783-1788; published online before print July 22 2004, doi:10.1161/01.ATV.0000140063.06341.09. Abstract \| Full Text \| PDF Leukotriene B4 (LTB4), a product of the 5-lipoxygenase (5-LO) pathway of arachidonic acid metabolism, has been implicated in atherosclerosis. However, the molecular mechanisms for the atherogenic effect of LTB4 are not well understood. This study shows that the LTB4-induced MCP-1 in human monocytes may play a critical role in the atherogenicity of LTB4.
	Proinflammatory Cytokines Regulate LOX-1 Expression in Vascular Smooth Muscle Cells Oliver Hofnagel, Birgit Luechtenborg, Katrin Stolle, Stefan Lorkowski, Heike Eschert, Gabriele Plenz, and Horst Robenek Arterioscler Thromb Vasc Biol. 2004;24:1789-1795; published online before print July 22 2004, doi:10.1161/01.ATV.0000140061.89096.2b. Abstract \| Full Text \| PDF The proinflammatory cytokines interleukin (IL)-1{alpha}, IL-1ß, and tumor necrosis factor (TNF)-{alpha} promote the expression of LOX-1 in cultured smooth muscle cells (SMC), and LOX-1 expression colocalizes with these cytokines in advanced atherosclerotic lesions. Therefore, LOX-1 expression in SMC may be upregulated locally by these cytokines during atherogenesis.
	PECAM-1 Interacts With Nitric Oxide Synthase in Human Endothelial Cells: Implication for Flow-Induced Nitric Oxide Synthase Activation N. Dusserre, N. L’Heureux, K.S. Bell, H.Y. Stevens, J. Yeh, L.A. Otte, L. Loufrani, and J.A. Frangos Arterioscler Thromb Vasc Biol. 2004;24:1796-1802; published online before print July 29 2004, doi:10.1161/01.ATV.0000141133.32496.41. Abstract \| Full Text \| PDF \| Data Supplement We hypothesized that the particular sublocalization of eNOS at the cell-cell junction would render it responsive to activation by FSS temporal gradients. Our results suggest that eNOS is complexed with PECAM-1 at the cell-cell junction and is likely involved in the modulation of eNOS activity by FSS temporal gradients.
	Expression of Angiopoietin-2 in Endothelial Cells Is Controlled by Positive and Negative Regulatory Promoter Elements Anja Hegen, Stefanie Koidl, Karin Weindel, Dieter Marmé, Hellmut G. Augustin, and Ulrike Fiedler Arterioscler Thromb Vasc Biol. 2004;24:1803-1809; published online before print July 29 2004, doi:10.1161/01.ATV.0000140819.81839.0e. Abstract \| Full Text \| PDF \| Data Supplement This study shows that (1) the Ang-2 promoter becomes specifically activated in endothelial cells, (2) Ang-2 promoter activity is regulated by VEGF and FGF-2, (3) negative regulatory elements control low basal Ang-2 promoter activity, and (4) Ets-1 and Elf-1 act as regulators of endothelial cell specific Ang-2 expression.
	ADP Receptor P2Y₁₂ Is Expressed in Vascular Smooth Muscle Cells and Stimulates Contraction in Human Blood Vessels Anna-Karin Wihlborg, Lingwei Wang, Oscar Östberg Braun, Atli Eyjolfsson, Ronny Gustafsson, Tomas Gudbjartsson, and David Erlinge Arterioscler Thromb Vasc Biol. 2004;24:1810-1815; published online before print August 12 2004, doi:10.1161/01.ATV.0000142376.30582.ed. Abstract \| Full Text \| PDF ADP causes platelet aggregation by P2Y12 receptor activation. We show that P2Y12 is expressed on vascular smooth muscle cells, and also that it has contractile function. These results give rise to new aspects of P2Y12-blocking drugs, such as having double therapeutic benefit in their prevention of thrombosis and vasospasm.
	Endogenous Nitric Oxide Synthesis Inhibitor Asymmetric Dimethyl L-Arginine Accelerates Endothelial Cell Senescence Fortunato Scalera, Jürgen Borlak, Bibiana Beckmann, Jens Martens-Lobenhoffer, Thomas Thum, Michael Täger, and Stefanie M. Bode-Böger Arterioscler Thromb Vasc Biol. 2004;24:1816-1822; published online before print August 12 2004, doi:10.1161/01.ATV.0000141843.77133.fc. Abstract \| Full Text \| PDF We aimed to investigate the role of asymmetrical dimethylarginine (ADMA), a novel cardiovascular risk factor, in endothelial cell senescence. We found that at concentrations corresponding to plasma levels at pathophysiological conditions, ADMA accelerates aging in endothelial cells, probably via increased oxygen radical formation by inhibiting nitric oxide elaboration via decreased dimethylarginine dimethylaminohydrolase activity.
	Oxidized Low-Density Lipoproteins Stimulate Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) Release by Coronary Smooth Muscle Cells Cornelia Haug, Christina Lenz, Fredy Díaz, and Max G. Bachem Arterioscler Thromb Vasc Biol. 2004;24:1823-1829; published online before print August 19 2004, doi:10.1161/01.ATV.0000142806.59283.11. Abstract \| Full Text \| PDF \| Data Supplement This study demonstrates that oxidized low-density lipoproteins stimulate the release of soluble extracellular matrix metalloproteinase inducer (EMMPRIN) by human coronary artery smooth muscle cells, an effect which seems to result from enhanced EMMPRIN shedding. In addition, we have shown that isolated purified EMMPRIN stimulates MMP synthesis in coronary smooth muscle cells.
	REDD2 Gene Is Upregulated by Modified LDL or Hypoxia and Mediates Human Macrophage Cell Death C. Cuaz-Pérolin, C. Furman, G. Larigauderie, L. Legedz, C. Lasselin, C. Copin, M. Jaye, G. Searfoss, K.T. Yu, N. Duverger, A. Nègre-Salvayre, J.-C. Fruchart, and M. Rouis Arterioscler Thromb Vasc Biol. 2004;24:1830-1835; published online before print August 12 2004, doi:10.1161/01.ATV.0000142366.69080.c3. Abstract \| Full Text \| PDF \| Data Supplement The regulated in development and DNA damage response 2 (REDD2) gene is highly expressed in macrophages foam cells and in human atherosclerotic plaques. REDD2 overexpression in U-937 monocytic cells and HMEC endothelial cells increased the sensitivity for oxLDL-induced cytotoxicity. Therefore, REDD2 might play an important role in arterial pathology.
	In Vivo Transcriptional Response of Cardiac Endothelium to Lipopolysaccharide J. Gregory Maresh, Huaxia Xu, Nan Jiang, and Ralph V. Shohet Arterioscler Thromb Vasc Biol. 2004;24:1836-1841; published online before print August 19 2004, doi:10.1161/01.ATV.0000143097.90868.c8. Abstract \| Full Text \| PDF \| Data Supplement Fluorescent cell sorting was used to isolate green fluorescent protein expressing endothelial cells from the hearts of mice exposed to lipopolysaccharide. In vivo transcriptional changes were distinct compared with in vitro experiments and identified novel regulated genes. This method can be generalized to the exploration of in vivo endothelial responses in any organ.
	Inhibition of Rho-Kinase Leads to Rapid Activation of Phosphatidylinositol 3-Kinase/Protein Kinase Akt and Cardiovascular Protection Sebastian Wolfrum, Andreas Dendorfer, Yoshiyuki Rikitake, Timothy J. Stalker, Yulan Gong, Rosario Scalia, Peter Dominiak, and James K. Liao Arterioscler Thromb Vasc Biol. 2004;24:1842-1847; published online before print August 19 2004, doi:10.1161/01.ATV.0000142813.33538.82. Abstract \| Full Text \| PDF Acute inhibition of Rho-kinase in endothelial cells leads to the activation of the PI3-kinase/protein kinase Akt pathway and nitric oxide (NO) production. This correlated with a reduction in the inflammatory response after ischemia/reperfusion in postcapillary venules, as well as in myocardial infarct size. Therefore, inhibition of Rho-kinase may be an important therapeutic target in cardiovascular diseases.
	Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways Hajime Fujimoto, Minoru Ohno, Seiji Ayabe, Hisae Kobayashi, Nobukazu Ishizaka, Hiroko Kimura, Ken-ichi Yoshida, and Ryozo Nagai Arterioscler Thromb Vasc Biol. 2004;24:1848-1853; published online before print August 12 2004, doi:10.1161/01.ATV.0000142364.85911.0e. Abstract \| Full Text \| PDF The role of carbon monoxide (CO) in myocardial ischemia-reperfusion was studied. Pre-inhalation of 1000 ppm CO reduced cardiac ischemia-reperfusion injury in vivo. CO resulted in phosphorylation of p38MAPK, Akt, and eNOS. Inhibition of these pathways attenuated the cytoprotection by CO. Thus, CO protects against ischemia-reperfusion by activating p38MAPK, Akt, and eNOS.
	Cortical Microvascular Remodeling in the Stenotic Kidney: Role of Increased Oxidative Stress Xiang-Yang Zhu, Alejandro R. Chade, Martin Rodriguez-Porcel, Michael D. Bentley, Erik L. Ritman, Amir Lerman, and Lilach O. Lerman Arterioscler Thromb Vasc Biol. 2004;24:1854-1859; published online before print August 12 2004, doi:10.1161/01.ATV.0000142443.52606.81. Abstract \| Full Text \| PDF \| Data Supplement To explore the mechanisms of renal injury distal to renal artery stenosis (RAS), we studied cortical microvascular architecture in stenotic pig kidneys. We observed that antioxidant intervention improved renal growth factor expression and blunted microvascular remodeling. These findings underscore the role of increased oxidative stress in modulating intrarenal microvascular architecture in RAS.
	Exogenous NADPH Increases Cerebral Blood Flow Through NADPH Oxidase–Dependent and –Independent Mechanisms Laibaik Park, Josef Anrather, Ping Zhou, Kelly Frys, Gang Wang, and Costantino Iadecola Arterioscler Thromb Vasc Biol. 2004;24:1860-1865; published online before print August 12 2004, doi:10.1161/01.ATV.0000142446.75898.44. Abstract \| Full Text \| PDF \| Data Supplement We investigated the mechanisms of the increase in cerebral blood flow (CBF) produced by NADPH. We found that the CBF response to NADPH is mediated by NADPH oxidase, but that nitric oxide synthase also plays a role. Therefore, the cerebrovascular effects of NADPH include both NADPH oxidase-dependent and -independent mechanisms.
	Atherosclerosis and Lipoproteins
	Contrasting Effects of Oral Versus Transdermal Estrogen on Serum Amyloid A (SAA) and High-Density Lipoprotein–SAA in Postmenopausal Women Aamer Abbas, Paul J. Fadel, Zhongyun Wang, Debbie Arbique, Ishwarlal Jialal, and Wanpen Vongpatanasin Arterioscler Thromb Vasc Biol. 2004;24:e164-e167; published online before print July 29 2004, doi:10.1161/01.ATV.0000140198.16664.8e. Abstract \| Full Text \| PDF In this study, we determine whether the route of estrogen administration influences serum amyloid A (SAA), another acute-phase protein produced by the liver, and the SAA content of the high-density lipoprotein (HDL-SAA) in postmenopausal women. Oral estrogen increased SAA and altered HDL composition to contain a higher level of SAA by a first-pass hepatic mechanism. Because elevated SAA levels predict adverse prognosis in healthy postmenopausal women, and elevated HDL-SAA levels have been shown to interfere with HDL function, the administration route may be an important consideration in minimizing side effects of estrogen replacement therapy on cardiovascular outcomes.
	C-Reactive Protein-Induced In Vitro Vasorelaxation Is an Artefact Caused by the Presence of Sodium Azide in Commercial Preparations Carmen W. van den Berg, Karolina E. Taylor, and Derek Lang Arterioscler Thromb Vasc Biol. 2004;24:e168-e171; published online before print August 19 2004, doi:10.1161/01.ATV.0000142807.92781.d9. Abstract \| Full Text \| PDF We constructed a congenic mouse strain in which chromosome 15 interval from MRL/MpJ is placed on the genetic background of BALB/c. Analysis of the congenic strain showed that the underlying gene, termed Hyplip2, increases plasma cholesterol and triglyceride levels, accompanied by a dramatic {approx}30-fold increase in atherosclerotic lesions.
	Can Exercise Training With Weight Loss Lower Serum C-Reactive Protein Levels? Koichi Okita, Hirotaka Nishijima, Takeshi Murakami, Tatsuya Nagai, Noriteru Morita, Kazuya Yonezawa, Kenji Iizuka, Hideaki Kawaguchi, and Akira Kitabatake Arterioscler Thromb Vasc Biol. 2004;24:1868-1873; published online before print July 29 2004, doi:10.1161/01.ATV.0000140199.14930.32. Abstract \| Full Text \| PDF C-reactive protein (CRP) is a promising predictor for cardiovascular disease and may be a mediator for atherogenesis. Although it has been reported that diet-induced weight loss lowered CRP levels, the effect of exercise training on CRP is still unclear. We examined effects of exercise training with weight loss on CRP levels, finding that exercise training with weight reduction disproportionately lowered CRP levels. Considering inflammatory status, there might be an optimal pace of exercise with weight loss.
	C-Reactive Protein Genotypes Affect Baseline, but not Exercise Training–Induced Changes, in C-Reactive Protein Levels Thomas O. Obisesan, Christiaan Leeuwenburgh, Tracey Phillips, Robert E. Ferrell, Dana A. Phares, Steven J. Prior, and James M. Hagberg Arterioscler Thromb Vasc Biol. 2004;24:1874-1879; published online before print July 22 2004, doi:10.1161/01.ATV.0000140060.13203.22. Abstract \| Full Text \| PDF We determined whether CRP gene variants affect baseline CRP levels and whether these variants interact with exercise training to affect CRP levels. CRP +219G/A and -732A/G genotypes and exercise training appear to modulate CRP levels. However, the training-induced CRP reductions appear to be independent of genotype at these loci.
	Mast Cells in Neovascularized Human Coronary Plaques Store and Secrete Basic Fibroblast Growth Factor, a Potent Angiogenic Mediator Helena Lappalainen, Petri Laine, Markku O. Pentikäinen, Antti Sajantila, and Petri T. Kovanen Arterioscler Thromb Vasc Biol. 2004;24:1880-1885; published online before print July 29 2004, doi:10.1161/01.ATV.0000140820.51174.8d. Abstract \| Full Text \| PDF Basic fibroblast growth factor (bFGF) was found in mast cells (MCs) in human atherosclerotic coronary arteries. MCs contained bFGF and were located near microvessels. With increasing severity of atherosclerosis, proportion of intimal MCs positive for bFGF increased. By releasing bFGF, coronary MCs may participate in the neovascularization of coronary plaques.
	Antimonocyte Chemoattractant Protein-1 Gene Therapy Attenuates Graft Vasculopathy Akio Saiura, Masataka Sata, Ken-ichi Hiasa, Shiro Kitamoto, Miwa Washida, Kensuke Egashira, Ryozo Nagai, and Masatoshi Makuuchi Arterioscler Thromb Vasc Biol. 2004;24:1886-1890; published online before print July 29 2004, doi:10.1161/01.ATV.0000141045.49616.6f. Abstract \| Full Text \| PDF In a murine cardiac allograft model, the gene transfer of the dominant negative form of MCP-1 to the recipients significantly reduced the number of mononuclear cells accumulating in the luminal side of the graft coronary arteries at 1 week and attenuated the development of the lesion at 8 weeks.
	Blockade of Keratinocyte-Derived Chemokine Inhibits Endothelial Recovery and Enhances Plaque Formation After Arterial Injury in ApoE-Deficient Mice Elisa A. Liehn, Andreas Schober, and Christian Weber Arterioscler Thromb Vasc Biol. 2004;24:1891-1896; published online before print August 26 2004, doi:10.1161/01.ATV.0000143135.71440.75. Abstract \| Full Text \| PDF \| Data Supplement Blocking keratinocyte-derived chemokine (KC) enhanced plaque formation after arterial injury in apoE-/[minus] mice and inhibited endothelial recovery, whereas the relative macrophage and smooth muscle cell content in the plaques remained unaltered. Macrophages and endothelial cells covering the plaque expressed KC. The stimulating effect of KC on endothelial chemotaxis and wound repair was confirmed in vitro.
	${alpha}$ (1,3)Fucosyltransferases FucT-IV and FucT-VII Control Susceptibility to Atherosclerosis in Apolipoprotein E–/– Mice Jonathon W. Homeister, Alan Daugherty, and John B. Lowe Arterioscler Thromb Vasc Biol. 2004;24:1897-1903; published online before print August 12 2004, doi:10.1161/01.ATV.0000141844.28073.df. Abstract \| Full Text \| PDF \| Data Supplement Roles for leukocyte selectin ligands in atherogenesis are implied by atheroprotection in selectin-deficient mice. In apoE-/- mice, deficiency of {alpha}(1,3)fucosyltransferase IV or VII leads to subtle or marked atheroprotection, respectively, and corresponding reductions in monocyte P-selectin counter-receptor activity. These observations assign {alpha}(1,3)fucosyltransferases IV and VII to controlling roles in atherogenesis.
	High-Density Lipoproteins Retard the Progression of Atherosclerosis and Favorably Remodel Lesions Without Suppressing Indices of Inflammation or Oxidation Robin P. Choudhury, James X. Rong, Eugene Trogan, Valerie I. Elmalem, Hayes M. Dansky, Jan L. Breslow, Joseph L. Witztum, John T. Fallon, and Edward A. Fisher Arterioscler Thromb Vasc Biol. 2004;24:1904-1909; published online before print August 19 2004, doi:10.1161/01.ATV.0000142808.34602.25. Abstract \| Full Text \| PDF \| Data Supplement We have studied the progression of atherosclerosis in male apoE-/- and hAI/apoE-/- mice fed a Western diet. Elevation of HDL retarded the size progression of atherosclerosis, reduced plaque lipid content, and increased plaque collagen, despite greatly elevated non-HDL cholesterol. These changes occurred without evidence of reduced aortic inflammation or LDL oxidation.
	Inhibition of Cholesteryl Ester Transfer Protein Activity by JTT-705 Increases Apolipoprotein E–Containing High-Density Lipoprotein and Favorably Affects the Function and Enzyme Composition of High-Density Lipoprotein in Rabbits Bo Zhang, Ping Fan, Eiso Shimoji, Huali Xu, Kazuma Takeuchi, Cheng Bian, and Keijiro Saku Arterioscler Thromb Vasc Biol. 2004;24:1910-1915; published online before print August 26 2004, doi:10.1161/01.ATV.0000143389.00252.bc. Abstract \| Full Text \| PDF \| Data Supplement The effects of CETP inhibition on the function and composition of HDL particles were examined in rabbits. JTT-705 significantly inhibited CETP activities, decreased FERHDL values, and increased apoE-containing HDL and activities of paraoxonase and HDL-associated PAF-AH. In conclusion, inhibition of CETP activity favorably affected the size distribution of HDL subpopulations and the apolipoprotein and enzyme composition of HDL.
	Hemodynamic Regulation of CD34⁺ Cell Localization and Differentiation in Experimental Aneurysms Eiketsu Sho, Mien Sho, Hiroshi Nanjo, Koichi Kawamura, Hirotake Masuda, and Ronald L. Dalman Arterioscler Thromb Vasc Biol. 2004;24:1916-1921; published online before print August 19 2004, doi:10.1161/01.ATV.0000142805.20398.74. Abstract \| Full Text \| PDF \| Data Supplement Vascular progenitor cells (CD34+ cells) localize within murine AAA, contributing to aneurysmal formation and progression. Luminal flow conditions regulate CD34+ cell differentiation and localization.
	Gene Expression Phenotypes of Atherosclerosis David Seo, Tao Wang, Holly Dressman, Edward E. Herderick, Edwin S. Iversen, Chunming Dong, Korkut Vata, Carmelo A. Milano, Fabio Rigat, Jennifer Pittman, Joseph R. Nevins, Mike West, and Pascal J. Goldschmidt-Clermont Arterioscler Thromb Vasc Biol. 2004;24:1922-1927; published online before print August 5 2004, doi:10.1161/01.ATV.0000141358.65242.1f. Abstract \| Full Text \| PDF \| Data Supplement To improve our understanding of the genetic factors that influence atherosclerosis, we performed a genomic analysis of fresh human aorta. We have identified unique gene expression phenotypes that define disease state and, potentially, disease susceptibility, and we have generated a novel list of candidate genes for further study.
	Hyplip2, a New Gene for Combined Hyperlipidemia and Increased Atherosclerosis Xuping Wang, Peter Gargalovic, Jack Wong, Jennifer L. Gu, Xiaohui Wu, Hongxiu Qi, Pingzi Wen, Li Xi, Bing Tan, Rocky Gogliotti, Lawrence W. Castellani, Aurobindo Chatterjee, and Aldons J. Lusis Arterioscler Thromb Vasc Biol. 2004;24:1928-1934; published online before print August 26 2004, doi:10.1161/01.ATV.0000143385.30354.bb. Abstract \| Full Text \| PDF \| Data Supplement We have investigated the vasorelaxant properties of CRP using commercial preparations of CRP, CRP purified from ascites, and our in-house recombinant CRP. We conclude that CRP has no vasorelaxant properties, and previous studies reporting such responses are artifacts caused by sodium azide present in commercial preparations of CRP.
	Quantitative Trait Loci for Apolipoprotein B, Cholesterol, and Triglycerides in Familial Combined Hyperlipidemia Pedigrees Rita M. Cantor, Tjerk de Bruin, Naoko Kono, Susan Napier, Atila van Nas, Hooman Allayee, and Aldons J. Lusis Arterioscler Thromb Vasc Biol. 2004;24:1935-1941; published online before print August 12 2004, doi:10.1161/01.ATV.0000142358.46276.a7. Abstract \| Full Text \| PDF FCHL QTL were identified at 1p21-31 and 17p11-q21 for apolipoprotein B, 12p13 for total serum cholesterol, and 4p15-16 for serum triglycerides by nonparametric linkage analyses of a full genome scan of 150 sibpairs in 22 familial combined hyperlipidemia sibships. Multiple QTL were observed at 4q34-35, 16p12-13, and 17p11-q21.
	Low-Density Lipoprotein Particle Size Loci in Familial Combined Hyperlipidemia: Evidence for Multiple Loci From a Genome Scan Michael D. Badzioch, Robert P. Igo, Jr, France Gagnon, John D. Brunzell, Ronald M. Krauss, Arno G. Motulsky, Ellen M. Wijsman, and Gail P. Jarvik Arterioscler Thromb Vasc Biol. 2004;24:1942-1950; published online before print August 26 2004, doi:10.1161/01.ATV.0000143499.09575.93. Abstract \| Full Text \| PDF \| Data Supplement We used lod score and Markov chain Monte Carlo linkage analysis to perform a genome scan of adjusted LDL size in 4 large families with familial combined hyperlipidemia. We identified significant evidence of linkage to chromosomes 9p, 16q23, and 11q22 and confirmatory evidence for 14q24-31. LDL size is influenced by multiple loci.
	Segment-Specific Effects of Cardiovascular Risk Factors on Carotid Artery Intima-Medial Thickness in Women at Midlife Laura L. Schott, Rachel P. Wildman, Sarah Brockwell, Laurey R. Simkin-Silverman, Lewis H. Kuller, and Kim Sutton-Tyrrell Arterioscler Thromb Vasc Biol. 2004;24:1951-1956; published online before print August 5 2004, doi:10.1161/01.ATV.0000141119.02205.6b. Abstract \| Full Text \| PDF Associations between segment-specific intima-medial thickness and cardiovascular risk factors in middle-aged women were examined through ultrasound in the common, bifurcation, and internal carotid arteries. Segment-specific effects, indicating cardiovascular risk factors may differentially affect intima-medial thickness and were evident in regression models and a repeated measures model with all 3 locations.
	Thrombosis
	C-Reactive Protein, Fibrin D-Dimer, and Risk of Ischemic Heart Disease: The Caerphilly and Speedwell Studies G.D.O. Lowe, P.M. Sweetnam, J.W.G. Yarnell, A. Rumley, C. Rumley, D. Bainton, and Y. Ben-Shlomo Arterioscler Thromb Vasc Biol. 2004;24:1957-1962; published online before print August 12 2004, doi:10.1161/01.ATV.0000141842.27810.a9. Abstract \| Full Text \| PDF \| Data Supplement We assessed the associations of C-reactive protein and fibrin D-dimer in the prediction of ischemic heart disease in the Caerphilly and Speedwell cohorts of 3213 men aged 49 to 66 years. Both C-reactive protein and D-dimer were significantly associated with risk, indicating that inflammatory and thrombogenic markers are potentially additive predictors.
	PI3K-Akt Pathway Suppresses Coagulation and Inflammation in Endotoxemic Mice Gernot Schabbauer, Michael Tencati, Brian Pedersen, Rafal Pawlinski, and Nigel Mackman Arterioscler Thromb Vasc Biol. 2004;24:1963-1969; published online before print August 19 2004, doi:10.1161/01.ATV.0000143096.15099.ce. Abstract \| Full Text \| PDF \| Data Supplement In this study, we analyzed the role of the phosphoinositide 3-kinase (PI3K)-Akt pathway in a mouse model of endotoxemia. Inhibition of PI3K strongly enhanced LPS-induced coagulation and inflammation, which resulted in reduced survival of endotoxemic mice.
	Serum Lipid Levels and the Risk of Venous Thrombosis Carine J.M. Doggen, Nicholas L. Smith, Rozenn N. Lemaitre, Susan R. Heckbert, Frits R. Rosendaal, and Bruce M. Psaty Arterioscler Thromb Vasc Biol. 2004;24:1970-1975; published online before print August 26 2004, doi:10.1161/01.ATV.0000143134.87051.46. Abstract \| Full Text \| PDF In a population-based case-control study including 477 postmenopausal women with a first venous thrombosis and 1986 control subjects, elevated triglyceride levels were associated with a 2-fold increased risk of venous thrombosis, whereas high HDL cholesterol was associated with a decreased risk. Total cholesterol levels were not associated with venous thrombosis.
	Letters to the Editor
	Clinical Significance of Coronary Calcification Raimund Erbel, Axel Schmermund, Moeen Abedin, Yin Tintut, and Linda L. Demer Arterioscler Thromb Vasc Biol. 2004;24:e172, doi:10.1161/01.ATV.0000142384.70383.ea. Full Text \| PDF
	Aortic Stiffness Does Not Mediate the Relation Between Pulse Pressure and CRP Jacques Amar, Jean Bernard Ruidavets, Jean Ferrieres, John R. Cockcroft, Yasmin, Carmel M. McEniery, and Ian B. Wilkinson Arterioscler Thromb Vasc Biol. 2004;24:e173, doi:10.1161/01.ATV.0000142444.02057.e7. Full Text \| PDF
	Corrections
	Correction Arterioscler Thromb Vasc Biol. 2004;24:1976. Full Text \| PDF

Spotlight

TOC Spotlight File

Volume 24, Issue 10; October 1, 2004

Editorials

Estrogen and HDL: All that Glitters Is not Gold

CRP and Risk of Coronary Heart Disease: Can Exercise Training Cool Down the Flames?

Molecular Phenotypes of Atherosclerosis: Fingering the Perpetrators

Vascular Cross-Talk: A Conversation

Brief Reviews

Hepatic Lipase, Lipoprotein Metabolism, and Atherogenesis

Regulation of Plasma High-Density Lipoprotein Levels by the ABCA1 Transporter and the Emerging Role of High-Density Lipoprotein in the Treatment of Cardiovascular Disease

Endothelium-Targeted Gene and Cell-Based Therapies for Cardiovascular Disease

Finding Vulnerable Atherosclerotic Plaques: Is It Worth the Effort?

Vascular Biology

Leukotriene B4 Strongly Increases Monocyte Chemoattractant Protein-1 in Human Monocytes

Proinflammatory Cytokines Regulate LOX-1 Expression in Vascular Smooth Muscle Cells

PECAM-1 Interacts With Nitric Oxide Synthase in Human Endothelial Cells: Implication for Flow-Induced Nitric Oxide Synthase Activation

Expression of Angiopoietin-2 in Endothelial Cells Is Controlled by Positive and Negative Regulatory Promoter Elements

ADP Receptor P2Y12 Is Expressed in Vascular Smooth Muscle Cells and Stimulates Contraction in Human Blood Vessels

Endogenous Nitric Oxide Synthesis Inhibitor Asymmetric Dimethyl L-Arginine Accelerates Endothelial Cell Senescence

Oxidized Low-Density Lipoproteins Stimulate Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) Release by Coronary Smooth Muscle Cells

REDD2 Gene Is Upregulated by Modified LDL or Hypoxia and Mediates Human Macrophage Cell Death

In Vivo Transcriptional Response of Cardiac Endothelium to Lipopolysaccharide

Inhibition of Rho-Kinase Leads to Rapid Activation of Phosphatidylinositol 3-Kinase/Protein Kinase Akt and Cardiovascular Protection

Carbon Monoxide Protects Against Cardiac Ischemia—Reperfusion Injury In Vivo via MAPK and Akt—eNOS Pathways

Cortical Microvascular Remodeling in the Stenotic Kidney: Role of Increased Oxidative Stress

Exogenous NADPH Increases Cerebral Blood Flow Through NADPH Oxidase–Dependent and –Independent Mechanisms

Atherosclerosis and Lipoproteins

Contrasting Effects of Oral Versus Transdermal Estrogen on Serum Amyloid A (SAA) and High-Density Lipoprotein–SAA in Postmenopausal Women

C-Reactive Protein-Induced In Vitro Vasorelaxation Is an Artefact Caused by the Presence of Sodium Azide in Commercial Preparations

Can Exercise Training With Weight Loss Lower Serum C-Reactive Protein Levels?

C-Reactive Protein Genotypes Affect Baseline, but not Exercise Training–Induced Changes, in C-Reactive Protein Levels

Mast Cells in Neovascularized Human Coronary Plaques Store and Secrete Basic Fibroblast Growth Factor, a Potent Angiogenic Mediator

Antimonocyte Chemoattractant Protein-1 Gene Therapy Attenuates Graft Vasculopathy

Blockade of Keratinocyte-Derived Chemokine Inhibits Endothelial Recovery and Enhances Plaque Formation After Arterial Injury in ApoE-Deficient Mice

(1,3)Fucosyltransferases FucT-IV and FucT-VII Control Susceptibility to Atherosclerosis in Apolipoprotein E–/– Mice

High-Density Lipoproteins Retard the Progression of Atherosclerosis and Favorably Remodel Lesions Without Suppressing Indices of Inflammation or Oxidation

Inhibition of Cholesteryl Ester Transfer Protein Activity by JTT-705 Increases Apolipoprotein E–Containing High-Density Lipoprotein and Favorably Affects the Function and Enzyme Composition of High-Density Lipoprotein in Rabbits

Hemodynamic Regulation of CD34+ Cell Localization and Differentiation in Experimental Aneurysms

Gene Expression Phenotypes of Atherosclerosis

Hyplip2, a New Gene for Combined Hyperlipidemia and Increased Atherosclerosis

Quantitative Trait Loci for Apolipoprotein B, Cholesterol, and Triglycerides in Familial Combined Hyperlipidemia Pedigrees

Low-Density Lipoprotein Particle Size Loci in Familial Combined Hyperlipidemia: Evidence for Multiple Loci From a Genome Scan

Segment-Specific Effects of Cardiovascular Risk Factors on Carotid Artery Intima-Medial Thickness in Women at Midlife

Thrombosis

C-Reactive Protein, Fibrin D-Dimer, and Risk of Ischemic Heart Disease: The Caerphilly and Speedwell Studies

PI3K-Akt Pathway Suppresses Coagulation and Inflammation in Endotoxemic Mice

Serum Lipid Levels and the Risk of Venous Thrombosis

Letters to the Editor

Clinical Significance of Coronary Calcification

Aortic Stiffness Does Not Mediate the Relation Between Pulse Pressure and CRP

Corrections

Correction

Spotlight

Leukotriene B₄ Strongly Increases Monocyte Chemoattractant Protein-1 in Human Monocytes

ADP Receptor P2Y₁₂ Is Expressed in Vascular Smooth Muscle Cells and Stimulates Contraction in Human Blood Vessels

${alpha}$ (1,3)Fucosyltransferases FucT-IV and FucT-VII Control Susceptibility to Atherosclerosis in Apolipoprotein E–/– Mice

Hemodynamic Regulation of CD34⁺ Cell Localization and Differentiation in Experimental Aneurysms