Direct eNOS activation provides atheroprotection in diabetes-accelerated atherosclerosis

1 Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia. 2 Centre for Heart Lung Innovation, St. Paul’s Hospital, University of British Columbia. 3 Baker IDI Heart and Diabetes Institute, Diabetic Complications Division, Melbourne, Victoria, Australia. 4 Department of Pathology and Laboratory Medicine, University of British Columbia. 5 Department of Immunology, Monash University, Melbourne, Victoria, Australia.

[1]  N. Tzemos,et al.  Is reversal of endothelial dysfunction still an attractive target in modern cardiology? , 2014, World journal of cardiology.

[2]  Amanda J. Moffitt,et al.  The effects of tetrahydrobiopterin (BH4) treatment on brain function in individuals with phenylketonuria☆ , 2013, NeuroImage: Clinical.

[3]  P. Pozzilli,et al.  Is Glucose Control Important for Prevention of Cardiovascular Disease in Diabetes? , 2013, Diabetes Care.

[4]  R. Bergman,et al.  The endothelium in diabetes: Its role in insulin access and diabetic complications , 2013, Reviews in Endocrine and Metabolic Disorders.

[5]  Merlin C. Thomas,et al.  Activation of the Renin-Angiotensin System Mediates the Effects of Dietary Salt Intake on Atherogenesis in the Apolipoprotein E Knockout Mouse , 2012, Hypertension.

[6]  S. Funk,et al.  Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes , 2012, International journal of vascular medicine.

[7]  J. D. de Haan,et al.  Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes , 2011, International journal of vascular medicine.

[8]  L. Beckers,et al.  Caveolin‐1 deficiency decreases atherosclerosis by hampering leukocyte influx into the arterial wall and generating a regulatory T‐cell response , 2011, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[9]  W. Sessa,et al.  A noninhibitory mutant of the caveolin-1 scaffolding domain enhances eNOS-derived NO synthesis and vasodilation in mice. , 2011, The Journal of clinical investigation.

[10]  U. Förstermann,et al.  Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling , 2011, British journal of pharmacology.

[11]  P. Bernatchez,et al.  Amlodipine increases endothelial nitric oxide release by modulating binding of native eNOS protein complex to caveolin-1. , 2011, European journal of pharmacology.

[12]  A. Chigaev,et al.  Nitric oxide/cGMP pathway signaling actively down-regulates α4β1-integrin affinity: an unexpected mechanism for inducing cell de-adhesion , 2011, BMC Immunology.

[13]  Merlin C. Thomas,et al.  Antiatherosclerotic and Renoprotective Effects of Ebselen in the Diabetic Apolipoprotein E/GPx1-Double Knockout Mouse , 2010, Diabetes.

[14]  A. Dávalos,et al.  Endothelial-specific overexpression of caveolin-1 accelerates atherosclerosis in apolipoprotein E-deficient mice. , 2010, The American journal of pathology.

[15]  J. Liao,et al.  Pleiotropic effects of statins. - Basic research and clinical perspectives -. , 2010, Circulation journal : official journal of the Japanese Circulation Society.

[16]  M. A. Lasunción,et al.  Genetic evidence supporting a critical role of endothelial caveolin-1 during the progression of atherosclerosis. , 2009, Cell metabolism.

[17]  I. Kola,et al.  Site-Specific Antiatherogenic Effect of the Antioxidant Ebselen in the Diabetic Apolipoprotein E–Deficient Mouse , 2009, Arteriosclerosis, thrombosis, and vascular biology.

[18]  S. Homer-Vanniasinkam,et al.  Nitric oxide specifically inhibits integrin‐mediated platelet adhesion and spreading on collagen , 2008, Journal of thrombosis and haemostasis : JTH.

[19]  Hong Wang,et al.  [Atherosclerosis and oxidative stress]. , 2008, Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics.

[20]  M. Aviram,et al.  Characterization of oxidative stress in blood from diabetic vs. hypercholesterolaemic patients, using a novel synthesized marker , 2008, Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals.

[21]  I. Kola,et al.  Lack of the Antioxidant Enzyme Glutathione Peroxidase-1 Accelerates Atherosclerosis in Diabetic Apolipoprotein E–Deficient Mice , 2007, Circulation.

[22]  Kenneth K. Wu,et al.  Diabetic atherosclerosis mouse models. , 2007, Atherosclerosis.

[23]  I. Kola,et al.  Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet Published, JLR Papers in Press, February 28, 2006. , 2006, Journal of Lipid Research.

[24]  C. Triggle,et al.  Endothelial Cell Dysfunction and the Vascular Complications Associated with Type 2 Diabetes: Assessing the Health of the Endothelium , 2005, Vascular health and risk management.

[25]  W. Sessa,et al.  Dissecting the molecular control of endothelial NO synthase by caveolin-1 using cell-permeable peptides. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[26]  B. Ahrén,et al.  The high-fat diet-fed mouse: a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes. , 2004, Diabetes.

[27]  C. Hedrick,et al.  Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells , 2004, Diabetologia.

[28]  G. D. Johnston,et al.  Impaired endothelium-dependent and independent vasodilation in patients with Type 2 (non-insulin-dependent) diabetes mellitus , 1992, Diabetologia.

[29]  J. Phillips,et al.  Rosiglitazone Reduces the Accelerated Neointima Formation After Arterial Injury in a Mouse Injury Model of Type 2 Diabetes , 2003, Circulation.

[30]  R. Groszmann,et al.  Selective inhibition of tumor microvascular permeability by cavtratin blocks tumor progression in mice. , 2003, Cancer cell.

[31]  J. Connell,et al.  High Glucose Inhibits Insulin-stimulated Nitric Oxide Production without Reducing Endothelial Nitric-oxide Synthase Ser1177 Phosphorylation in Human Aortic Endothelial Cells* , 2003, Journal of Biological Chemistry.

[32]  Tomoya Yamashita,et al.  Overexpression of endothelial nitric oxide synthase accelerates atherosclerotic lesion formation in apoE-deficient mice. , 2002, The Journal of clinical investigation.

[33]  Paul L Huang,et al.  Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice , 2001, Circulation.

[34]  C. Dessy,et al.  Hydroxy-Methylglutaryl–Coenzyme A Reductase Inhibition Promotes Endothelial Nitric Oxide Synthase Activation Through a Decrease in Caveolin Abundance , 2001, Circulation.

[35]  R. D. Rudic,et al.  In vivo delivery of the caveolin-1 scaffolding domain inhibits nitric oxide synthesis and reduces inflammation , 2000, Nature Medicine.

[36]  J. Farmer.  Pleiotropic effects of statins , 2000, Current atherosclerosis reports.

[37]  G. Remuzzi,et al.  Leukocyte-endothelial interaction is augmented by high glucose concentrations and hyperglycemia in a NF-kB-dependent fashion. , 1998, The Journal of clinical investigation.

[38]  R. Ross,et al.  Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[39]  D. Harrison,et al.  Expression of multiple isoforms of nitric oxide synthase in normal and atherosclerotic vessels. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[40]  G. Garcı́a-Cardeña,et al.  Dissecting the Interaction between Nitric Oxide Synthase (NOS) and Caveolin , 1997, The Journal of Biological Chemistry.

[41]  P. Tsao,et al.  Adherence of Mononuclear Cells to Endothelium In Vitro Is Increased in Patients With NIDDM , 1997, Diabetes Care.

[42]  G. Garcı́a-Cardeña,et al.  Palmitoylation of endothelial nitric oxide synthase is necessary for optimal stimulated release of nitric oxide: implications for caveolae localization. , 1996, Biochemistry.

[43]  M. Sampson,et al.  Impaired vascular reactivity in insulin-dependent diabetes mellitus is related to disease duration and low density lipoprotein cholesterol levels. , 1996, Journal of the American College of Cardiology.

[44]  P. Libby,et al.  Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. , 1995, The Journal of clinical investigation.

[45]  R. Natarajan,et al.  Evidence That Glucose Increases Monocyte Binding to Human Aortic Endothelial Cells , 1994, Diabetes.

[46]  R. Cohen,et al.  Chronic inhibition of nitric oxide production accelerates neointima formation and impairs endothelial function in hypercholesterolemic rabbits. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[47]  R. Alexander,et al.  Vascular cell adhesion molecule-1 (VCAM-1) gene transcription and expression are regulated through an antioxidant-sensitive mechanism in human vascular endothelial cells. , 1993, The Journal of clinical investigation.

[48]  M. Laakso,et al.  Diabetes and atherosclerosis: an epidemiologic view. , 1987, Diabetes/metabolism reviews.