Ira Tabas

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. pmc Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis
    Gang Li
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 186:783-92. 2009
  2. pmc Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor
    Tracie DeVries-Seimon
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 171:61-73. 2005
  3. pmc Adaptive suppression of the ATF4-CHOP branch of the unfolded protein response by toll-like receptor signalling
    Connie W Woo
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Nat Cell Biol 11:1473-80. 2009
  4. pmc Toll-like receptor activation suppresses ER stress factor CHOP and translation inhibition through activation of eIF2B
    Connie W Woo
    Department of Medicine, Columbia University, New York 10032, USA
    Nat Cell Biol 14:192-200. 2012
  5. pmc NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis
    Gang Li
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 191:1113-25. 2010
  6. pmc Anti-inflammatory therapy in chronic disease: challenges and opportunities
    Ira Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Science 339:166-72. 2013
  7. pmc Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress
    Ira Tabas
    Department of Medicine, Anatomy and Cell Biology, Columbia University, New York, NY 10032, USA
    Nat Cell Biol 13:184-90. 2011
  8. ncbi request reprint A two-carbon switch to sterol-induced autophagic death
    Ira Tabas
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Autophagy 3:38-41. 2007
  9. ncbi request reprint Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications
    Ira Tabas
    Department of Medicine, Columbia University Medical Center, 630 W 168th St, New York, NY 10032, USA
    Circulation 116:1832-44. 2007
  10. ncbi request reprint Apoptosis and efferocytosis in mouse models of atherosclerosis
    Ira Tabas
    Departments of Medicine, Pathology and Cell Biology, and Physiology and Cellular Biophysics I T, Columbia University, New York, NY 10032, USA
    Curr Drug Targets 8:1288-96. 2007

Collaborators

Detail Information

Publications73

  1. pmc Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis
    Gang Li
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 186:783-92. 2009
    ..Macrophages from insulin-resistant ob/ob mice, another model of ER stress, also have elevated IICR. These data shed new light on how the CHOP pathway of apoptosis triggers calcium-dependent apoptosis through an ERO1-alpha-IP3R pathway...
  2. pmc Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor
    Tracie DeVries-Seimon
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 171:61-73. 2005
    ..These findings have important implications for understanding how the UPR, MAPKs, and the SRA might conspire to cause macrophage death, lesional necrosis, and plaque destabilization in advanced atherosclerotic lesions...
  3. pmc Adaptive suppression of the ATF4-CHOP branch of the unfolded protein response by toll-like receptor signalling
    Connie W Woo
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Nat Cell Biol 11:1473-80. 2009
    ..We speculate that this mechanism evolved to promote survival of TLR-expressing cells that experience prolonged levels of physiological ER stress in the course of the host response to invading pathogens...
  4. pmc Toll-like receptor activation suppresses ER stress factor CHOP and translation inhibition through activation of eIF2B
    Connie W Woo
    Department of Medicine, Columbia University, New York 10032, USA
    Nat Cell Biol 14:192-200. 2012
    ....
  5. pmc NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis
    Gang Li
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Cell Biol 191:1113-25. 2010
    ..These data provide new insight into how ER stress, oxidative stress, and PKR activation can be integrated to induce apoptosis in a pathophysiologically relevant manner...
  6. pmc Anti-inflammatory therapy in chronic disease: challenges and opportunities
    Ira Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Science 339:166-72. 2013
    ..However, new advances in understanding inflammatory signaling and its links to resolution pathways, together with new drug development, offer promise in this area of translational biomedical research...
  7. pmc Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress
    Ira Tabas
    Department of Medicine, Anatomy and Cell Biology, Columbia University, New York, NY 10032, USA
    Nat Cell Biol 13:184-90. 2011
    ..The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress...
  8. ncbi request reprint A two-carbon switch to sterol-induced autophagic death
    Ira Tabas
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Autophagy 3:38-41. 2007
    ....
  9. ncbi request reprint Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications
    Ira Tabas
    Department of Medicine, Columbia University Medical Center, 630 W 168th St, New York, NY 10032, USA
    Circulation 116:1832-44. 2007
    ....
  10. ncbi request reprint Apoptosis and efferocytosis in mouse models of atherosclerosis
    Ira Tabas
    Departments of Medicine, Pathology and Cell Biology, and Physiology and Cellular Biophysics I T, Columbia University, New York, NY 10032, USA
    Curr Drug Targets 8:1288-96. 2007
    ..Advances in these areas offer great hope for eventual translation into innovative therapeutic strategies to combat atherothrombotic vascular disease...
  11. pmc Macrophage apoptosis in advanced atherosclerosis
    Ira Tabas
    Department of Medicine, Columbia University Medical Center, New York, New York, USA
    Ann N Y Acad Sci 1173:E40-5. 2009
    ..Further understanding of the mechanisms and consequences of this event may lead to novel therapies directed at preventing the clinical progression of atheromata...
  12. pmc Macrophage apoptosis in atherosclerosis: consequences on plaque progression and the role of endoplasmic reticulum stress
    Ira Tabas
    Department of Medicine, Columbia University, New York, New York 10032, USA
    Antioxid Redox Signal 11:2333-9. 2009
    ....
  13. pmc The role of endoplasmic reticulum stress in the progression of atherosclerosis
    Ira Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Circ Res 107:839-50. 2010
    ....
  14. pmc Macrophage death and defective inflammation resolution in atherosclerosis
    Ira Tabas
    Department of Medicine, Physiology and Cellular Biophysics, Columbia University, New York, New York 10032, USA
    Nat Rev Immunol 10:36-46. 2010
    ..In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis...
  15. pmc The impact of macrophage insulin resistance on advanced atherosclerotic plaque progression
    Ira Tabas
    Department of Medicine, Columbia University, 630 West 168th St, New York, NY 10032, USA
    Circ Res 106:58-67. 2010
    ..These processes may therefore provide an important mechanistic link among insulin resistance, plaque necrosis, and atherothrombotic vascular disease and suggest novel therapeutic approaches to this expanding health problem...
  16. ncbi request reprint Consequences and therapeutic implications of macrophage apoptosis in atherosclerosis: the importance of lesion stage and phagocytic efficiency
    Ira Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Arterioscler Thromb Vasc Biol 25:2255-64. 2005
    ..Further understanding of the mechanisms involved in macrophage apoptosis and phagocytic clearance might lead to novel therapeutic strategies directed against the progression of advanced plaques...
  17. ncbi request reprint Secretory sphingomyelinase
    I Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Chem Phys Lipids 102:123-30. 1999
    ....
  18. ncbi request reprint Nonoxidative modifications of lipoproteins in atherogenesis
    I Tabas
    Department of Medicine and Anatomy, Columbia University, New York, New York 10032, USA
    Annu Rev Nutr 19:123-39. 1999
    ..The focus is on the evidence that these modifications occur in atherosclerotic lesions and on the potential role of these modified lipoproteins in atherogenesis, with an emphasis on macrophage foam cell formation...
  19. pmc Cholesterol in health and disease
    Ira Tabas
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Clin Invest 110:583-90. 2002
  20. ncbi request reprint Cholesterol and phospholipid metabolism in macrophages
    I Tabas
    Department of Medicine and Anatomy, Columbia University, 630 West 168th Street, New York, NY, 10032, USA
    Biochim Biophys Acta 1529:164-74. 2000
    ....
  21. pmc Consequences of cellular cholesterol accumulation: basic concepts and physiological implications
    Ira Tabas
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Clin Invest 110:905-11. 2002
  22. ncbi request reprint Apoptosis and plaque destabilization in atherosclerosis: the role of macrophage apoptosis induced by cholesterol
    I Tabas
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Cell Death Differ 11:S12-6. 2004
  23. ncbi request reprint Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-alpha and interleukin-6: model of NF-kappaB- and map kinase-dependent inflammation in advanced atherosclerosis
    Yankun Li
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    J Biol Chem 280:21763-72. 2005
    ..Moreover, this model may help explain the relationship between FC accumulation and inflammation in vulnerable plaques...
  24. pmc ABCA1 and ABCG1 protect against oxidative stress-induced macrophage apoptosis during efferocytosis
    Laurent Yvan-Charvet
    Division of Molecular Medicine, Department of Medicine, 630 W 168th St, Columbia University, New York, NY 10032, USA
    Circ Res 106:1861-9. 2010
    ..The ATP-binding cassette transporters ABCA1 and ABCG1 have a major role in promoting cholesterol efflux from macrophages to apolipoprotein A-1 and HDL and are upregulated during the phagocytosis of apoptotic cells (efferocytosis)...
  25. ncbi request reprint Macrophage insulin receptor deficiency increases ER stress-induced apoptosis and necrotic core formation in advanced atherosclerotic lesions
    Seongah Han
    Department of Medicine, Columbia University, New York, New York 10032, USA
    Cell Metab 3:257-66. 2006
    ..These studies suggest that defective insulin signaling and reduced Akt activity impair the ability of macrophages to deal with ER stress-induced apoptosis within atherosclerotic plaques...
  26. pmc Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress
    Tracie A Seimon
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Cell Metab 12:467-82. 2010
    ..These findings provide insight into how atherogenic lipoproteins trigger macrophage apoptosis in the setting of ER stress and how TLR activation might promote macrophage apoptosis and plaque necrosis in advanced atherosclerosis...
  27. pmc Defective phagocytosis of apoptotic cells by macrophages in atherosclerotic lesions of ob/ob mice and reversal by a fish oil diet
    Suzhao Li
    Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA
    Circ Res 105:1072-82. 2009
    ..Defective clearance of apoptotic cells by macrophages (efferocytosis) is thought to lead to increased necrotic core formation and inflammation in atherosclerotic lesions...
  28. pmc Forkhead transcription factors (FoxOs) promote apoptosis of insulin-resistant macrophages during cholesterol-induced endoplasmic reticulum stress
    Takafumi Senokuchi
    Department of Medicine, Columbia University, New York, New York, USA
    Diabetes 57:2967-76. 2008
    ..However, the molecular mechanisms of increased apoptosis in insulin-resistant macrophages remain unclear...
  29. pmc Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP
    Edward Thorp
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Cell Metab 9:474-81. 2009
    ..These data provide direct evidence for a causal link between the ER stress effector CHOP and plaque necrosis and suggest that interventions weakening this arm of the UPR may lessen plaque progression...
  30. ncbi request reprint Pivotal advance: macrophages become resistant to cholesterol-induced death after phagocytosis of apoptotic cells
    Dongying Cui
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Leukoc Biol 82:1040-50. 2007
    ..These findings have implications for macrophage physiology in both AC clearance and atherosclerotic plaque progression...
  31. pmc Acid sphingomyelinase promotes lipoprotein retention within early atheromata and accelerates lesion progression
    Cecilia M Devlin
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Arterioscler Thromb Vasc Biol 28:1723-30. 2008
    ..We now sought to test a direct causative role for acid SMase in lipoprotein retention and atherogenesis in vivo...
  32. pmc Brief report: increased apoptosis in advanced atherosclerotic lesions of Apoe-/- mice lacking macrophage Bcl-2
    Edward Thorp
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Arterioscler Thromb Vasc Biol 29:169-72. 2009
    ..The goal herein was to determine the effect of macrophage-targeted deletion of Bcl-2 on macrophage apoptosis in atherosclerotic lesions of Apoe(-/-) mice...
  33. pmc Combinatorial pattern recognition receptor signaling alters the balance of life and death in macrophages
    Tracie A Seimon
    Department of Medicine and Anatomy, Columbia University, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 103:19794-9. 2006
    ..PRR-induced macrophage death may play important roles in advanced atherosclerosis and in other innate immunity-related processes in which the balance between macrophage survival and death is critical...
  34. pmc TNFalpha induces ABCA1 through NF-kappaB in macrophages and in phagocytes ingesting apoptotic cells
    Marie Christine Gerbod-Giannone
    Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 103:3112-7. 2006
    ..In atherosclerotic plaques, this process may help phagocytic macrophages to efflux excess lipids derived from the ingestion of cholesterol-rich apoptotic corpses...
  35. ncbi request reprint Interleukin-3/granulocyte macrophage colony-stimulating factor receptor promotes stem cell expansion, monocytosis, and atheroma macrophage burden in mice with hematopoietic ApoE deficiency
    Mi Wang
    From the Division of Molecular Medicine, Department of Medicine M Wang, M S, S A, A J M, C W, I T, M Westerterp, A R T and Department of Pharmacology M Wang, Columbia University, New York, NY Department of Medicine, University of California San Diego, La Jolla A G, J W and Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands M Westerterp
    Arterioscler Thromb Vasc Biol 34:976-84. 2014
    ..We investigated the role of the CBS in cholesterol-driven HSPC expansion, monocytosis, and atherosclerosis...
  36. pmc Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways
    Jenelle M Timmins
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    J Clin Invest 119:2925-41. 2009
    ..These findings raise the possibility that CaMKII inhibitors could be useful in preventing apoptosis in pathological settings involving ER stress-induced apoptosis...
  37. pmc Calcium signaling through CaMKII regulates hepatic glucose production in fasting and obesity
    Lale Ozcan
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Cell Metab 15:739-51. 2012
    ..This same pathway is also involved in excessive HGP in the setting of obesity. These results reveal a calcium-mediated signaling pathway involved in FoxO1 nuclear localization and hepatic glucose homeostasis...
  38. ncbi request reprint Sitosterol-containing lipoproteins trigger free sterol-induced caspase-independent death in ACAT-competent macrophages
    Liping Bao
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Biol Chem 281:33635-49. 2006
    ..Pending future in vivo studies, this concept may provide at least one mechanism for accelerated plaque necrosis and atherothrombotic disease in patients with sitosterolemia...
  39. ncbi request reprint Suppression of macrophage eicosanoid synthesis by atherogenic lipoproteins is profoundly affected by cholesterol-fatty acyl esterification and the Niemann-Pick C pathway of lipid trafficking
    Andrew R Leventhal
    Department of Medicine and Anatomy and Cell Biology, Columbia University, New York, New York 10032, USA
    J Biol Chem 279:8084-92. 2004
    ....
  40. pmc Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism
    Yankun Li
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Biol Chem 283:34833-43. 2008
    ..These data suggest a novel action and mechanism of eNampt that could affect the balance of macrophage survival and death in the setting of obesity, which in turn could play important roles in obesity-associated diseases...
  41. pmc Niemann-Pick C heterozygosity confers resistance to lesional necrosis and macrophage apoptosis in murine atherosclerosis
    Bo Feng
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 100:10423-8. 2003
    ..Moreover, by showing that lesional necrosis can be diminished by a subtle defect in intracellular trafficking, these findings suggest therapeutic strategies to stabilize atherosclerotic plaques...
  42. pmc Mertk receptor mutation reduces efferocytosis efficiency and promotes apoptotic cell accumulation and plaque necrosis in atherosclerotic lesions of apoe-/- mice
    Edward Thorp
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Arterioscler Thromb Vasc Biol 28:1421-8. 2008
    ..Herein we test the hypothesis that the Mertk(KD) mutation would result in increased accumulation of apoptotic cells and promote necrotic core expansion in a mouse model of advanced atherosclerosis...
  43. ncbi request reprint The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages
    Bo Feng
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Nat Cell Biol 5:781-92. 2003
    ..We propose that cholesterol trafficking to endoplasmic reticulum membranes, resulting in activation of the CHOP arm of the UPR, is the key signalling step in cholesterol-induced apoptosis in macrophages...
  44. ncbi request reprint Cholesterol-induced apoptotic macrophages elicit an inflammatory response in phagocytes, which is partially attenuated by the Mer receptor
    Yankun Li
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Biol Chem 281:6707-17. 2006
    ..Thus, the proinflammatory milieu of advanced atherosclerotic lesions may be promoted, or at least not dampened, by contact between FC-induced apoptotic macrophages and neighboring phagocytes prior to apoptotic cell ingestion...
  45. pmc Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo
    Wah Seng Lim
    Department of Medicine, Columbia University, 630 W 168th St, New York, NY 10032, USA
    Circulation 117:940-51. 2008
    ....
  46. pmc Improvement in lipid and protein trafficking in Niemann-Pick C1 cells by correction of a secondary enzyme defect
    Cecilia Devlin
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Traffic 11:601-15. 2010
    ..These data show that correcting one aspect of a complex lysosomal lipid storage disease can reduce the cellular consequences even if the primary genetic defect is not corrected...
  47. pmc Increased CD36 protein as a response to defective insulin signaling in macrophages
    Chien Ping Liang
    Department of Medicine, Division of Molecular Medicine, Columbia University, New York, New York 10032, USA
    J Clin Invest 113:764-73. 2004
    ..The results suggest that defective macrophage insulin signaling predisposes to foam cell formation and atherosclerosis in insulin-resistant states and that this is reversed in vivo by treatment with PPAR-gamma activators...
  48. pmc The impact of insulin resistance on macrophage death pathways in advanced atherosclerosis
    Ira Tabas
    Department of Medicine, 630 West 168th Street, Columbia University, New York, NY 10032, USA
    Novartis Found Symp 286:99-109; discussion 109-12, 162-3, 196-203. 2007
    ....
  49. ncbi request reprint Pioglitazone increases macrophage apoptosis and plaque necrosis in advanced atherosclerotic lesions of nondiabetic low-density lipoprotein receptor-null mice
    Edward Thorp
    Department of Medicine, Columbia University, 630 W 168th St, New York, NY 10032, USA
    Circulation 116:2182-90. 2007
    ..However, the effects of TZDs on advanced lesion progression are unknown...
  50. pmc Macrophage autophagy plays a protective role in advanced atherosclerosis
    Xianghai Liao
    Department of Medicine, Columbia University, New York, NY 10032, USA
    Cell Metab 15:545-53. 2012
    ..These findings reveal a protective process in oxidatively stressed macrophages relevant to plaque necrosis, suggesting a mechanism-based strategy to therapeutically suppress atherosclerosis progression and its clinical sequelae...
  51. pmc FoxOs integrate pleiotropic actions of insulin in vascular endothelium to protect mice from atherosclerosis
    Kyoichiro Tsuchiya
    Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
    Cell Metab 15:372-81. 2012
    ..The data demonstrate that FoxO inhibition in endothelial cells has the potential to mediate wide-ranging therapeutic benefits for diabetes-associated cardiovascular disease...
  52. pmc Homozygosity for an allele encoding deacetylated FoxO1 protects macrophages from cholesterol-induced inflammation without increasing apoptosis
    Kyoichiro Tsuchiya
    Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, NY, USA
    Arterioscler Thromb Vasc Biol 31:2920-8. 2011
    ..We sought to identify the mechanism whereby FoxO1 dampens inflammation without promoting apoptosis. We hypothesized that nutrient-dependent FoxO1 acetylation plays a role in this process...
  53. ncbi request reprint The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis
    Yankun Li
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Leukoc Biol 81:483-91. 2007
    ..Moreover, possible perturbation of stimulated pinocytosis during the progression of advanced atherosclerosis may contribute to the heightened inflammatory state of these lesions...
  54. ncbi request reprint Direct observation of rapid internalization and intracellular transport of sterol by macrophage foam cells
    Daniel Wüstner
    Department of Biochemistry, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA
    Traffic 6:396-412. 2005
    ..Our results indicate that elevation of sterol levels in Mphis enhances transport of sterol from the plasma membrane by a non-vesicular pathway...
  55. ncbi request reprint Enrichment of endoplasmic reticulum with cholesterol inhibits sarcoplasmic-endoplasmic reticulum calcium ATPase-2b activity in parallel with increased order of membrane lipids: implications for depletion of endoplasmic reticulum calcium stores and apoptos
    Yankun Li
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    J Biol Chem 279:37030-9. 2004
    ..This biophysical model may underlie the critical connection between excess cholesterol, unfolded protein response induction, macrophage death, and plaque destabilization in advanced atherosclerosis...
  56. pmc Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs
    Manikandan Subramanian
    Columbia University, Department of Medicine, New York, New York 10032, USA
    J Clin Invest 123:179-88. 2013
    ..In the absence of MYD88 signaling in CD11c+ DCs, the loss of this protective Treg response trumps the loss of proatherogenic T effector cell activation...
  57. pmc Impaired MEK signaling and SERCA expression promote ER stress and apoptosis in insulin-resistant macrophages and are reversed by exenatide treatment
    Chien Ping Liang
    Department of Medicine, Columbia University, New York, New York, USA
    Diabetes 61:2609-20. 2012
    ..Increased signaling via GLP-1 receptor or the CREBP activator protein kinase A thus offers a way to rescue insulin-resistant macrophages from excessive ER stress responses and apoptosis in insulin resistance and type 2 diabetes...
  58. pmc Activation of ER stress and mTORC1 suppresses hepatic sortilin-1 levels in obese mice
    Ding Ai
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Clin Invest 122:1677-87. 2012
    ..Thus, in mouse models of obesity, induction of mTORC1 and ER stress led to repression of hepatic Sort1 and increased VLDL secretion via Atf3. This pathway may contribute to dyslipidemia in metabolic disease...
  59. pmc CD11c(+) dendritic cells maintain antigen processing, presentation capabilities, and CD4(+) T-cell priming efficacy under hypercholesterolemic conditions associated with atherosclerosis
    René R S Packard
    Leducq Center for Cardiovascular Research and Donald W Reynolds Cardiovascular Clinical Research Center, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circ Res 103:965-73. 2008
    ..In particular, DCs remain functional antigen-presenting cells and maintain their ability to prime CD4(+) T cells even when cholesterol-loaded...
  60. ncbi request reprint Minimally oxidized LDL offsets the apoptotic effects of extensively oxidized LDL and free cholesterol in macrophages
    Agnes Boullier
    Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093 0682, USA
    Arterioscler Thromb Vasc Biol 26:1169-76. 2006
    ..Indeed, there is evidence of macrophage death in lesions, but how the surviving macrophages avoid death induced by OxLDL, FC, and other factors is not known...
  61. pmc The role of macrophages and dendritic cells in the clearance of apoptotic cells in advanced atherosclerosis
    Edward Thorp
    Department of Medicine, Division of Molecular Medicine, Columbia University, New York, NY 10032, USA
    Eur J Immunol 41:2515-8. 2011
    ..In this Viewpoint, we discuss how reduced efferocytosis by macrophages and CD11c(HI) DC-like cells may combine to reduce overall plaque stability and therefore promote susceptibility to acute atherothrombosis...
  62. pmc ACAT inhibition reduces the progression of preexisting, advanced atherosclerotic mouse lesions without plaque or systemic toxicity
    James X Rong
    Marc and Ruti Bell Vascular Biology and Disease Research Program of the Leon H Charney Division of Cardiology and the Department of Medicine Cardiology, New York University School of Medicine, Smilow 7, 522 First Ave, New York, NY 10029, USA
    Arterioscler Thromb Vasc Biol 33:4-12. 2013
    ..In this report, we tested F1394 effects on preestablished, advanced lesions of apolipoprotein-E-deficient mice...
  63. pmc Shedding of the Mer tyrosine kinase receptor is mediated by ADAM17 protein through a pathway involving reactive oxygen species, protein kinase Cδ, and p38 mitogen-activated protein kinase (MAPK)
    Edward Thorp
    Departments of Medicine, Pathology and Cell Biology, and Physiology, and Cellular Biophysics, Columbia University, New York, New York 10032, USA
    J Biol Chem 286:33335-44. 2011
    ....
  64. pmc Loss of subcellular lipid transport due to ARV1 deficiency disrupts organelle homeostasis and activates the unfolded protein response
    Caryn F Shechtman
    Institute of Human Nutrition, Department of Pediatrics, Columbia University Medical Center, New York, NY 10032, USA
    J Biol Chem 286:11951-9. 2011
    ..Thus, loss or down-regulation of ARV1 disturbs membrane and lipid homeostasis, resulting in a disruption of ER integrity, one consequence of which is induction of the UPR...
  65. ncbi request reprint An apolipoprotein(a) peptide delays chylomicron remnant clearance and increases plasma remnant lipoproteins and atherosclerosis in vivo
    Cecilia M Devlin
    Department of Medicine, Columbia University, 630 W 168th St, New York, NY 10032, USA
    Arterioscler Thromb Vasc Biol 25:1704-10. 2005
    ..To investigate the effect of KIV(5-8) on lipoprotein metabolism and atherosclerosis in vivo, we created several independent lines of liver-targeted KIV(5-8) transgenic mice...
  66. pmc Mechanisms and consequences of efferocytosis in advanced atherosclerosis
    Edward Thorp
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Leukoc Biol 86:1089-95. 2009
    ....
  67. ncbi request reprint The cytoplasmic domain of the low density lipoprotein (LDL) receptor-related protein, but not that of the LDL receptor, triggers phagocytosis
    Mintoo Patel
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Biol Chem 278:44799-807. 2003
    ..These findings have important implications for atherogenesis and apoptotic cell clearance and for a fundamental cell biological understanding of how the LDL receptor and LRP function in internalization processes...
  68. pmc A reporter for tracking the UPR in vivo reveals patterns of temporal and cellular stress during atherosclerotic progression
    Edward Thorp
    Department of Medicine and Anatomy, Columbia University, New York, NY 10032, USA
    J Lipid Res 52:1033-8. 2011
    ..These mice provide a valuable tool to monitor activation of the UPR in atherosclerosis and will be useful for future studies investigating relationships between pharmacologic and genetic modulators of UPR and atherosclerosis...
  69. pmc Induction of ER stress in macrophages of tuberculosis granulomas
    Tracie A Seimon
    Division of Molecular Medicine, Department of Medicine, Columbia University, New York, New York, United States of America
    PLoS ONE 5:e12772. 2010
    ..Because atherosclerosis shares certain features with tuberculosis (TB) with regard to lesional macrophage accumulation, foam cell formation, and apoptosis, we investigated if the ER stress pathway is activated during TB infection...
  70. ncbi request reprint ABCA1-mediated cholesterol efflux is defective in free cholesterol-loaded macrophages. Mechanism involves enhanced ABCA1 degradation in a process requiring full NPC1 activity
    Bo Feng
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Biol Chem 277:43271-80. 2002
    ..These findings provide new insight into the post-translational regulation of ABCA1 and the pathobiology of the FC-loaded macrophage...
  71. pmc Mechanisms and consequences of macrophage apoptosis in atherosclerosis
    Tracie Seimon
    Department of Medicine, Columbia University, New York, NY 10032, USA
    J Lipid Res 50:S382-7. 2009
    ..Of particular interest is the complex and coordinated role that the endoplasmic reticulum (ER) stress pathway and pattern recognition receptors (PRRs) may play in triggering macrophage apoptosis...
  72. pmc Genetic alterations of IL-1 receptor antagonist in mice affect plasma cholesterol level and foam cell lesion size
    Cecilia M Devlin
    Department of Medicine, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Proc Natl Acad Sci U S A 99:6280-5. 2002
    ..These data demonstrate that in selected models of murine atherosclerosis, chronic IL-1ra depletion or overexpression has potentially important effects on lipoprotein metabolism and foam-cell lesion development...
  73. ncbi request reprint Role of cholesterol and lipid organization in disease
    Frederick R Maxfield
    Department of Biochemistry, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA
    Nature 438:612-21. 2005
    ..These insights have also led to improved understanding of normal physiology...

Research Grants27

  1. Conference on Cellular Biology of Atherosclerosis
    Ira Tabas; Fiscal Year: 2005
    ....
  2. The Unfolded Protein Response in Sterol Cytoxicity
    Ira Tabas; Fiscal Year: 2006
    ..abstract_text> ..
  3. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2006
    ..After achieving these goals, we hope to have a much deeper understanding of the molecular mechanisms of LP-Chol trafficking, particularly in the context of atherosclerotic lesional macrophages that internalize atherogenic lipoproteins. ..
  4. The Unfolded Protein Response in Sterol Cytotoxicity
    Ira Tabas; Fiscal Year: 2007
    ..abstract_text> ..
  5. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2007
    ..After achieving these goals, we hope to have a much deeper understanding of the molecular mechanisms of LP-Chol trafficking, particularly in the context of atherosclerotic lesional macrophages that internalize atherogenic lipoproteins. ..
  6. Mechanisms of Atherogenesis in Insulin Resistance
    Ira Tabas; Fiscal Year: 2007
    ..abstract_text> ..
  7. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2009
    ..abstract_text> ..
  8. The Unfolded Protein Response in Sterol Cytoxicity
    Ira Tabas; Fiscal Year: 2009
    ....
  9. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    IRA A TABAS; Fiscal Year: 2010
    ..abstract_text> ..
  10. Macrophage Death in Plaque Vulnerability
    Ira Tabas; Fiscal Year: 2005
    ..New insights in this area may suggest new therapeutic strategies to combat cardiovascular disease. ..
  11. The Unfolded Protein Response in Sterol Cytoxicity
    Ira Tabas; Fiscal Year: 2005
    ..abstract_text> ..
  12. FOAM CELL APO (A)/LP(A) RECEPTOR--CLONING AND FUNCTION
    Ira Tabas; Fiscal Year: 1999
    ..The studies in this proposal will lead to the molecular identification of a novel cholesterol-induced receptor on foam cells and should provide important insight into the role of foam cell-apo(a)/Lp(a) interactions in atherogenesis. ..
  13. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 1999
    ..The information gained from these studies may suggest new therapeutic strategies, directed at the level of the lesion foam cell, for further lowering the risk of atherosclerotic heart disease. ..
  14. FORM CELL APO (A)/LP(A) RECEPTOR--CLONING AND FUNCTION
    Ira Tabas; Fiscal Year: 2000
    ..The studies in this proposal will lead to the molecular identification of a novel cholesterol-induced receptor on foam cells and should provide important insight into the role of foam cell-apo(a)/Lp(a) interactions in atherogenesis. ..
  15. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2000
    ..The information gained from these studies may suggest new therapeutic strategies, directed at the level of the lesion foam cell, for further lowering the risk of atherosclerotic heart disease. ..
  16. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2001
    ..In summary, these studies should elucidate novel molecular and cellular mechanisms involved in MO foam cell formation and thus provide new insights into this critical cellular event of atherogenesis. ..
  17. FORM CELL APO (A)/LP(A) RECEPTOR--CLONING AND FUNCTION
    Ira Tabas; Fiscal Year: 2001
    ..The studies in this proposal will lead to the molecular identification of a novel cholesterol-induced receptor on foam cells and should provide important insight into the role of foam cell-apo(a)/Lp(a) interactions in atherogenesis. ..
  18. FORM CELL APO (A)/LP(A) RECEPTOR--CLONING AND FUNCTION
    Ira Tabas; Fiscal Year: 2002
    ..The studies in this proposal will lead to the molecular identification of a novel cholesterol-induced receptor on foam cells and should provide important insight into the role of foam cell-apo(a)/Lp(a) interactions in atherogenesis. ..
  19. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2002
    ..In summary, these studies should elucidate novel molecular and cellular mechanisms involved in MO foam cell formation and thus provide new insights into this critical cellular event of atherogenesis. ..
  20. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2003
    ..In summary, these studies should elucidate novel molecular and cellular mechanisms involved in MO foam cell formation and thus provide new insights into this critical cellular event of atherogenesis. ..
  21. INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGES
    Ira Tabas; Fiscal Year: 2004
    ..In summary, these studies should elucidate novel molecular and cellular mechanisms involved in MO foam cell formation and thus provide new insights into this critical cellular event of atherogenesis. ..
  22. The Unfolded Protein Response in Sterol Cytotoxicity
    Ira Tabas; Fiscal Year: 2004
    ..abstract_text> ..
  23. The Unfolded Protein Response in Sterol Cytoxicity
    IRA A TABAS; Fiscal Year: 2010
    ....