Selective macrophage ascorbate deficiency suppresses early atherosclerosis.

[1]  M. Linton,et al.  Combined Vitamin C and Vitamin E Deficiency Worsens Early Atherosclerosis in Apolipoprotein E–Deficient Mice , 2010, Arteriosclerosis, thrombosis, and vascular biology.

[2]  J. M. May,et al.  Chelation of intracellular iron enhances endothelial barrier function: a role for vitamin C? , 2010, Archives of biochemistry and biophysics.

[3]  F. Liu,et al.  Effect of high mobility group box-1 protein on apoptosis of peritoneal macrophages. , 2009, Archives of biochemistry and biophysics.

[4]  S. Watkins,et al.  Reducing endoplasmic reticulum stress through a macrophage lipid chaperone alleviates atherosclerosis , 2009, Nature Medicine.

[5]  M. Lotze,et al.  The Receptor for Advanced Glycation End-products (RAGE) Sustains Autophagy and Limits Apoptosis, Promoting Pancreatic Tumor Cell Survival , 2009, Cell Death and Differentiation.

[6]  Hong Wang,et al.  Advanced glycation endproducts alter functions and promote apoptosis in endothelial progenitor cells through receptor for advanced glycation endproducts mediate overpression of cell oxidant stress , 2009, Molecular and Cellular Biochemistry.

[7]  J. M. May,et al.  Oxidized lipoprotein induces the macrophage ascorbate transporter (SVCT2): protection by intracellular ascorbate against oxidant stress and apoptosis. , 2009, Archives of biochemistry and biophysics.

[8]  M. Cooper,et al.  RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetes. , 2009, Journal of the American Society of Nephrology : JASN.

[9]  K. Ley,et al.  Immune and inflammatory mechanisms of atherosclerosis (*). , 2009, Annual review of immunology.

[10]  J. Oates,et al.  Macrophage EP4 deficiency increases apoptosis and suppresses early atherosclerosis. , 2008, Cell metabolism.

[11]  S. Ye,et al.  Advanced Glycation End-Product of Low Density Lipoprotein Activates the Toll-Like 4 Receptor Pathway Implications for Diabetic Atherosclerosis , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[12]  K. Hirata,et al.  RAGE mediates oxidized LDL-induced pro-inflammatory effects and atherosclerosis in non-diabetic LDL receptor-deficient mice. , 2008, Cardiovascular research.

[13]  J. Manson,et al.  Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial. , 2008, JAMA.

[14]  D. Schrijvers,et al.  Mertk Receptor Mutation Reduces Efferocytosis Efficiency and Promotes Apoptotic Cell Accumulation and Plaque Necrosis in Atherosclerotic Lesions of Apoe−/− Mice , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[15]  J. Witztum,et al.  Macrophage Apoptosis Exerts Divergent Effects on Atherogenesis as a Function of Lesion Stage , 2008, Circulation.

[16]  T. Miyazaki,et al.  Ascorbate inhibits apoptosis of Kupffer cells during warm ischemia/reperfusion injury. , 2008, Hepato-gastroenterology.

[17]  Tomohiro Miike,et al.  Effects of an anti-oxidative ACAT inhibitor on apoptosis/necrosis and cholesterol accumulation under oxidative stress in THP-1 cell-derived foam cells. , 2008, Life sciences.

[18]  R. Ramasamy,et al.  Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- mice. , 2008, The Journal of clinical investigation.

[19]  C. Fernández-Hernando,et al.  Phospholipase C beta3 deficiency leads to macrophage hypersensitivity to apoptotic induction and reduction of atherosclerosis in mice. , 2008, The Journal of clinical investigation.

[20]  S. Vannucci,et al.  Hypoxia-inducible Factor-1 Mediates Neuronal Expression of the Receptor for Advanced Glycation End Products following Hypoxia/Ischemia* , 2007, Journal of Biological Chemistry.

[21]  Knight Sc,et al.  Advanced Glycation: A Novel Outlook on Atherosclerosis , 2007 .

[22]  J. Manson,et al.  A randomized factorial trial of vitamins C and E and beta carotene in the secondary prevention of cardiovascular events in women: results from the Women's Antioxidant Cardiovascular Study. , 2007, Archives of internal medicine.

[23]  F. Q. Schafer,et al.  A simple and sensitive assay for ascorbate using a plate reader. , 2007, Analytical biochemistry.

[24]  M. Vissers,et al.  Ascorbate deficiency results in impaired neutrophil apoptosis and clearance and is associated with up‐regulation of hypoxia‐inducible factor 1α , 2007, Journal of leukocyte biology.

[25]  M. Currie,et al.  Modulation of hypoxia-inducible factor-1 alpha in cultured primary cells by intracellular ascorbate. , 2007, Free radical biology & medicine.

[26]  H. Asard,et al.  An ascorbate-reducible cytochrome b561 is localized in macrophage lysosomes. , 2006, Biochimica et biophysica acta.

[27]  G. Mann,et al.  Ascorbate does not protect macrophages against apoptosis induced by oxidised low density lipoprotein. , 2006, Archives of biochemistry and biophysics.

[28]  Trevor A. Mori,et al.  Protective effect of vitamin E supplements on experimental atherosclerosis is modest and depends on preexisting vitamin E deficiency. , 2006, Free radical biology & medicine.

[29]  D. Accili,et al.  Macrophage insulin receptor deficiency increases ER stress-induced apoptosis and necrotic core formation in advanced atherosclerotic lesions. , 2006, Cell metabolism.

[30]  S. Ram,et al.  Comparative cytoprotective activity of vitamin C, E and beta-carotene against chromium induced oxidative stress in murine macrophages. , 2006, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[31]  I. Tabas.  Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis: The Importance of Lesion Stage and Phagocytic Efficiency , 2005, Arteriosclerosis, thrombosis, and vascular biology.

[32]  Liying Li,et al.  Ascorbate uptake and antioxidant function in peritoneal macrophages. , 2005, Archives of biochemistry and biophysics.

[33]  A. Bookout,et al.  A role for the apoptosis inhibitory factor AIM/Spalpha/Api6 in atherosclerosis development. , 2005, Cell metabolism.

[34]  K. Salnikow,et al.  Ascorbate Depletion: A Critical Step in Nickel Carcinogenesis? , 2005, Environmental health perspectives.

[35]  C. Print,et al.  Hypoxia-induced neutrophil survival is mediated by HIF-1α–dependent NF-κB activity , 2005, The Journal of experimental medicine.

[36]  M. Linton,et al.  Reduced Macrophage Apoptosis Is Associated With Accelerated Atherosclerosis in Low-Density Lipoprotein Receptor–Null Mice , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[37]  M. Linton,et al.  Macrophages, inflammation, and atherosclerosis , 2003, International Journal of Obesity.

[38]  K. Kivirikko,et al.  Characterization of the Human Prolyl 4-Hydroxylases That Modify the Hypoxia-inducible Factor* , 2003, Journal of Biological Chemistry.

[39]  R. Jaenisch,et al.  HIF-1α Is Essential for Myeloid Cell-Mediated Inflammation , 2003, Cell.

[40]  R. Collins,et al.  MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20536 high-risk individuals: a randomised placebo-controlled trial , 2002 .

[41]  R. Nussbaum,et al.  Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival , 2002, Nature Medicine.

[42]  N. Maeda,et al.  Vulnerable Atherosclerotic Plaque Morphology in Apolipoprotein E-Deficient Mice Unable to Make Ascorbic Acid , 2002, Circulation.

[43]  P. Libby,et al.  Inflammation and Atherosclerosis , 2002, Circulation.

[44]  O. Arrigoni,et al.  Ascorbic acid: much more than just an antioxidant. , 2002, Biochimica et biophysica acta.

[45]  J. Tamaoki,et al.  Acute cigarette smoke exposure induces apoptosis of alveolar macrophages. , 2001, American journal of physiology. Lung cellular and molecular physiology.

[46]  G. Semenza,et al.  HIF-1, O2, and the 3 PHDs How Animal Cells Signal Hypoxia to the Nucleus , 2001, Cell.

[47]  A. Schmidt,et al.  The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. , 2001, The Journal of clinical investigation.

[48]  Robert V Farese,et al.  Increased atherosclerosis in hyperlipidemic mice deficient in alpha -tocopherol transfer protein and vitamin E. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[49]  H. Perlman,et al.  Macrophages Require Constitutive NF-κB Activation To Maintain A1 Expression and Mitochondrial Homeostasis , 2000, Molecular and Cellular Biology.

[50]  Mayur B. Patel,et al.  Macrophage Lipoprotein Lipase Promotes Foam Cell Formation and Atherosclerosis in Low Density Lipoprotein Receptor-deficient Mice* , 2000, The Journal of Biological Chemistry.

[51]  N. Maeda,et al.  Aortic wall damage in mice unable to synthesize ascorbic acid. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[52]  K. Williams,et al.  Atherosclerosis--an inflammatory disease. , 1999, The New England journal of medicine.

[53]  M. Linton,et al.  Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in vivo. , 1999, The Journal of clinical investigation.

[54]  Taro Tokui,et al.  A family of mammalian Na+-dependent L-ascorbic acid transporters , 1999, Nature.

[55]  R. Asmis,et al.  Dehydroascorbic acid prevents apoptosis induced by oxidized low-density lipoprotein in human monocyte-derived macrophages. , 1998, European journal of biochemistry.

[56]  M. Linton,et al.  Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[57]  Y. Zou,et al.  Enhanced cellular oxidant stress by the interaction of advanced glycation end products with their receptors/binding proteins. , 1994, The Journal of biological chemistry.

[58]  C. Rebouche.  Ascorbic acid and carnitine biosynthesis. , 1991, The American journal of clinical nutrition.

[59]  P. Bergsten,et al.  Millimolar concentrations of ascorbic acid in purified human mononuclear leukocytes. Depletion and reaccumulation. , 1990, The Journal of biological chemistry.

[60]  R. Williams,et al.  Quantitative assessment of atherosclerotic lesions in mice. , 1987, Atherosclerosis.

[61]  I. Chatterjee,et al.  SYNTHESIS AND SOME MAJOR FUNCTIONS OF VITAMIN C IN ANIMALS * , 1975, Annals of the New York Academy of Sciences.

[62]  Willis Gc.  The reversibility of atherosclerosis. , 1957, Canadian Medical Association journal.

[63]  Willis Gc.  An experimental study of intimal ground substance in atherosclerosis. , 1953 .

[64]  S. Knight,et al.  Advanced glycation: a novel outlook on atherosclerosis. , 2007, Current pharmaceutical design.

[65]  A. Coats.  MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20 536 high-risk individuals: a randomised placebo-controlled trial , 2002 .

[66]  M. Hampton,et al.  Regulation of Apoptosis by Vitamin C SPECIFIC PROTECTION OF THE APOPTOTIC MACHINERY AGAINST EXPOSURE TO CHLORINATED OXIDANTS* , 2001 .

[67]  D. Harrison,et al.  Reversibility of atherosclerosis. , 1990, Cardiovascular clinics.

[68]  G. C. Willis.  An experimental study of intimal ground substance in atherosclerosis. , 1953, Canadian Medical Association journal.