Edward Thorp

Summary

Affiliation: Northwestern University
Country: USA

Publications

  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Detail Information

Publications13

  1. 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...
  2. 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
    ....
  3. 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)...
  4. 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...
  5. 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...
  6. 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...
  7. 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...
  8. 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...
  9. 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
    ....
  10. 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...
  11. 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...
  12. pmc Regulation of hepatic LDL receptors by mTORC1 and PCSK9 in mice
    Ding Ai
    Department of Medicine, Columbia University, New York, New York 10032, USA
    J Clin Invest 122:1262-70. 2012
    ..We therefore suggest that PCSK9 inhibition could be an effective way to reduce the adverse side effect of increased LDL levels that is observed in transplant patients taking rapamycin as immunosuppressive therapy...
  13. 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...