C Esmon

Summary

Affiliation: University of Oklahoma Health Sciences Center
Country: USA

Publications

  1. pmc Valves of the deep venous system: an overlooked risk factor
    Erin G Brooks
    Department of Pathology, University of Vermont, Burlington, VT 05482, USA
    Blood 114:1276-9. 2009
  2. ncbi request reprint Regulation of blood coagulation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Biochim Biophys Acta 1477:349-60. 2000
  3. ncbi request reprint The interactions between inflammation and coagulation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Br J Haematol 131:417-30. 2005
  4. ncbi request reprint Protein C pathway in sepsis
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA
    Ann Med 34:598-605. 2002
  5. ncbi request reprint Is APC activation of endothelial cell PAR1 important in severe sepsis?: No
    C T Esmon
    OK Med Res Fndn and Howard Hughes Med Inst, Cardiovascular Biology, Oklahoma City, OK 73104, USA
    J Thromb Haemost 3:1910-1. 2005
  6. ncbi request reprint Coagulation inhibitors in inflammation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Howard Hughes Medical Institute, Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
    Biochem Soc Trans 33:401-5. 2005
  7. ncbi request reprint Coagulation and inflammation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA
    J Endotoxin Res 9:192-8. 2003
  8. ncbi request reprint Inflammation and thrombosis
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    J Thromb Haemost 1:1343-8. 2003
  9. ncbi request reprint The impact of the inflammatory response on coagulation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, OK, USA
    Thromb Res 114:321-7. 2004
  10. ncbi request reprint The discovery of thrombomodulin
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    J Thromb Haemost 2:209-13. 2004

Collaborators

Detail Information

Publications53

  1. pmc Valves of the deep venous system: an overlooked risk factor
    Erin G Brooks
    Department of Pathology, University of Vermont, Burlington, VT 05482, USA
    Blood 114:1276-9. 2009
    ..001; for VWF, P = .01). These data support our hypothesis and suggest that variation in valvular sinus thromboresistance may be an important factor in venous thrombogenesis...
  2. ncbi request reprint Regulation of blood coagulation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Biochim Biophys Acta 1477:349-60. 2000
    ..Initial clinical studies suggest that supplementation with protein C may be useful in the treatment of acute inflammatory diseases such as sepsis...
  3. ncbi request reprint The interactions between inflammation and coagulation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Br J Haematol 131:417-30. 2005
    ..When the inflammation-coagulation interactions overwhelm the natural defence systems, catastrophic events occur, such as manifested in severe sepsis or inflammatory bowel disease...
  4. ncbi request reprint Protein C pathway in sepsis
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA
    Ann Med 34:598-605. 2002
    ..This reduction may be due to both the anticoagulant effects as demonstrated by a reduction in D-dimer and inflammatory effects as demonstrated by a reduction in interleukin 6...
  5. ncbi request reprint Is APC activation of endothelial cell PAR1 important in severe sepsis?: No
    C T Esmon
    OK Med Res Fndn and Howard Hughes Med Inst, Cardiovascular Biology, Oklahoma City, OK 73104, USA
    J Thromb Haemost 3:1910-1. 2005
  6. ncbi request reprint Coagulation inhibitors in inflammation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Howard Hughes Medical Institute, Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
    Biochem Soc Trans 33:401-5. 2005
    ..This review examines the ways in which these pathways are down-regulated by inflammation, thus limiting clot formation and decreasing the natural anti-inflammatory mechanisms that these pathways possess...
  7. ncbi request reprint Coagulation and inflammation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA
    J Endotoxin Res 9:192-8. 2003
    ....
  8. ncbi request reprint Inflammation and thrombosis
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    J Thromb Haemost 1:1343-8. 2003
    ..This review will summarize the interactions between inflammation and coagulation...
  9. ncbi request reprint The impact of the inflammatory response on coagulation
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, OK, USA
    Thromb Res 114:321-7. 2004
    ..Inflammatory mediators like interleukin 6 can increase both platelet count and their responsiveness to agonists like thrombin. All of these events tend to shift the hemostatic balance in favor of clot formation...
  10. ncbi request reprint The discovery of thrombomodulin
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    J Thromb Haemost 2:209-13. 2004
  11. ncbi request reprint Crosstalk between inflammation and thrombosis
    Charles T Esmon
    Department of Pathology, University of Oklahoma Health Sciences Center, Howard Hughes Medical Institute, 825 NE 13th Street, Oklahoma City, OK 73104, USA
    Maturitas 47:305-14. 2004
    ....
  12. ncbi request reprint Interactions between the innate immune and blood coagulation systems
    Charles T Esmon
    Oklahoma Medical Research Foundation, Dept of Pathology, University of Oklahoma Health Sciences Center, and Howard Hughes Medical Institute, Oklahoma City 73104, USA
    Trends Immunol 25:536-42. 2004
    ..This Review will summarize our current understanding of the mechanisms involved in the crosstalk between these two important systems...
  13. ncbi request reprint Inflammation and the activated protein C anticoagulant pathway
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA
    Semin Thromb Hemost 32:49-60. 2006
    ..Overall this pathway is critical to both regulation of the blood coagulation process, and control of the innate inflammatory response and some of its associated downstream pathologies...
  14. pmc New mechanisms for vascular control of inflammation mediated by natural anticoagulant proteins
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Department of Pathology, University of Oklahoma Health Sciences Center, and Howard Hughes Medical Institute, Oklahoma City, OK 73104, USA
    J Exp Med 196:561-4. 2002
  15. ncbi request reprint The endothelial protein C receptor
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma, USA
    Curr Opin Hematol 13:382-5. 2006
    ..This review covers the most recent evidence that relatively common genetic and acquired abnormalities of endothelial cell protein C receptor do contribute to pathophysiological disease processes...
  16. ncbi request reprint The anticoagulant and anti-inflammatory roles of the protein C anticoagulant pathway
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Department of Pathology, University of Oklahoma Health Sciences Center and Howard Hughes Medical Institute, Oklahoma City, OK 73104, USA
    J Autoimmun 15:113-6. 2000
    ..The ability of the protein C system to modulate both inflammation and coagulation may explain i part why specific defects in the pathway appear to be associated with both arterial and venus thrombosis...
  17. ncbi request reprint The protein C pathway
    C Esmon
    Oklahoma Medical Research Foundation, Oklahoma City 73104, USA
    Crit Care Med 28:S44-8. 2000
    ....
  18. ncbi request reprint Does inflammation contribute to thrombotic events?
    C T Esmon
    Oklahoma Medical Research Foundation, Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Okla, USA
    Haemostasis 30:34-40. 2000
    ..The requirement for multiple simultaneous injurious events probably explains why inflammation alone is not observed as a major cause of thrombosis...
  19. pmc The normal role of Activated Protein C in maintaining homeostasis and its relevance to critical illness
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Howard Hughes Medical Institute, Oklahoma City 73104, USA
    Crit Care 5:S7-12. 2001
    ..In vitro studies and animal models have shown that Activated Protein C blunts the inflammatory and coagulant response to sepsis through a variety of mechanisms...
  20. ncbi request reprint Protein C anticoagulant pathway and its role in controlling microvascular thrombosis and inflammation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA
    Crit Care Med 29:S48-51; discussion 51-2. 2001
    ....
  21. ncbi request reprint Role of coagulation inhibitors in inflammation
    C T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA
    Thromb Haemost 86:51-6. 2001
    ..A phase III trial with tissue factor pathway inhibitor is in progress. In this review, the mechanisms by which the different natural anticoagulants are thought to function will be reviewed...
  22. ncbi request reprint Crosstalk between inflammation and thrombosis
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Department of Pathology, University of Oklahoma Health Sciences Center, Howard Hughes Medical Institute, Oklahoma City, OK 73104, USA
    Maturitas 61:122-31. 2008
    ....
  23. ncbi request reprint The protein C pathway
    Charles T Esmon
    Howard Hughes Medical Institute, Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Chest 124:26S-32S. 2003
    ..APC has been shown clinically to protect patients with severe sepsis. Protein C and thrombomodulin are in early stage clinical trials for this disease, and each has distinct potential advantages and disadvantages relative to APC...
  24. ncbi request reprint The crystal structure of the endothelial protein C receptor and a bound phospholipid
    Vaheh Oganesyan
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA
    J Biol Chem 277:24851-4. 2002
    ..The EPCR structure is a model for how CD1d binds lipids and further suggests additional potential functions for EPCR in immune regulation, possibly including the anti-phospholipid syndrome...
  25. pmc Effects of membrane and soluble EPCR on the hemostatic balance and endotoxemia in mice
    Xunzhen Zheng
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, The Howard Hughes Medical Institute, Oklahoma City 73104, USA
    Blood 109:1003-9. 2007
    ..In conclusion, mEPCR, but not physiologically elevated sEPCR, regulated protein C activation. Procr heterozygosity results in a mild increase of thrombosis tendency and little influence on the response to endotoxin...
  26. pmc Inhibition of APC anticoagulant activity on oxidized phospholipid by anti-{beta}2-glycoprotein I monoclonal antibodies
    Omid Safa
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK 73104, USA
    Blood 106:1629-35. 2005
    ..We conclude that antibodies to beta(2)-GPI inhibit APC function specifically and contribute to a hypercoaguable state by disrupting specific protein-protein interactions induced by oxidation of PE-containing membranes...
  27. ncbi request reprint Structure and functions of the endothelial cell protein C receptor
    Charles T Esmon
    Department of Pathology, University of Oklahoma Health Sciences Center, Howard Hughes Medical Institute, Oklahoma City, OK, USA
    Crit Care Med 32:S298-301. 2004
    ..Thus, available data suggest a potential role of EPCR in hematopoiesis, autoimmunity, and the control of both the coagulation and inflammation responses to infection and trauma...
  28. pmc The APCs of neuroprotection
    Charles T Esmon
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, and Howard Hughes Medical Institute, Oklahoma City, Oklahoma 73104, USA
    J Clin Invest 119:3205-7. 2009
    ..Here we discuss the potential importance of these data and possible relevance to human neurodegenerative diseases...
  29. ncbi request reprint Disruption of the endothelial cell protein C receptor gene in mice causes placental thrombosis and early embryonic lethality
    Jian Ming Gu
    Cardiovascular Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA
    J Biol Chem 277:43335-43. 2002
    ..We conclude that EPCR is essential for normal embryonic development. Moreover, EPCR plays a key role in preventing thrombosis at the maternal-embryonic interface...
  30. ncbi request reprint Why do animal models (sometimes) fail to mimic human sepsis?
    Charles T Esmon
    Departments of Pathology and Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
    Crit Care Med 32:S219-22. 2004
    ..To describe potential mechanisms that may account for the observation that drugs that work in treating sepsis in animal models often fail in sepsis trials in patients...
  31. pmc Basic mechanisms and pathogenesis of venous thrombosis
    Charles T Esmon
    Oklahoma Medical Research Foundation, Howard Hughes Medical Institute, and Departments of Pathology and Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States
    Blood Rev 23:225-9. 2009
    ....
  32. pmc Extracellular histones are major mediators of death in sepsis
    Jun Xu
    Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
    Nat Med 15:1318-21. 2009
    ..We conclude that extracellular histones are potential molecular targets for therapeutics for sepsis and other inflammatory diseases...
  33. pmc Extraembryonic expression of EPCR is essential for embryonic viability
    Weihong Li
    Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
    Blood 106:2716-22. 2005
    ..Spontaneous thrombin formation in the deficient animals increases with age. These findings show that extraembryonic EPCR expression is critical for embryo development...
  34. ncbi request reprint Distribution of endothelial cell protein C/activated protein C receptor (EPCR) during mouse embryo development
    James T B Crawley
    Oklahoma Medical Research Foundation, Howard Hughes Medical Institute, OK, USA
    Thromb Haemost 88:259-66. 2002
    ..However, not until postnatal day 7 did the intensity and distribution of EPCR staining mimic that observed in adult mice...
  35. ncbi request reprint Inhibition of a thrombin anion-binding exosite-2 mutant by the glycosaminoglycan-dependent serpins protein C inhibitor and heparin cofactor II
    Scott T Cooper
    Department of Pathology, The University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, NC 27599, USA
    Thromb Res 107:67-73. 2002
    ..In contrast, HCII does not require Arg(93), Arg(97) and Arg(101) of thrombin exosite-2 and further supports the hypothesis that HCII uses an allosteric process following glycosaminoglycan binding to inhibit thrombin...
  36. pmc Bench-to-bedside review: functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis
    Steven M Opal
    Infectious Disease Division, Brown University School of Medicine, Providence, Rhode Island, USA
    Crit Care 7:23-38. 2003
    ..The mechanisms by which these highly complex and coregulated defense strategies are linked together are the focus of the present review...
  37. ncbi request reprint Thrombomodulin mutant mice with a strongly reduced capacity to generate activated protein C have an unaltered pulmonary immune response to respiratory pathogens and lipopolysaccharide
    Anita W Rijneveld
    Academic Medical Center, University of Amsterdam, The Netherlands
    Blood 103:1702-9. 2004
    ..These data suggest that the capacity of TM to generate APC does not play a role of importance in the pulmonary response to respiratory pathogens or LPS...
  38. ncbi request reprint Early loss of thrombomodulin expression impairs vein graft thromboresistance: implications for vein graft failure
    Antony Y Kim
    Divisions of Cardiology, The Johns Hopkins School of Medicine, Baltimore, MD 21287, USA
    Circ Res 90:205-12. 2002
    ..Although enhanced local thrombin generation may predispose to early vein graft failure due to thrombosis, it does not seem to contribute significantly to late vein graft failure due to neointimal hyperplasia...
  39. pmc Role of the protein C pathway in the extraintestinal thrombosis associated with murine colitis
    Hideo Yoshida
    Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130 33932, USA
    Gastroenterology 135:882-8. 2008
    ..The objective of this study was to determine whether the protein C pathway contributes to the enhanced extraintestinal thrombosis that is associated with dextran sodium sulfate (DSS)-induced colitis in mice...
  40. ncbi request reprint PAR1 cleavage and signaling in response to activated protein C and thrombin
    Matthew J Ludeman
    Cardiovascular Research Institute, University of California, San Francisco, California 94143 0130, USA
    J Biol Chem 280:13122-8. 2005
    ..Although consistent with reports that sufficiently high concentrations of APC can cleave and activate PAR1 in culture, our data suggest that a significant physiological role for PAR1 activation by APC is unlikely...
  41. pmc Alternative mRNA is favored by the A3 haplotype of the EPCR gene PROCR and generates a novel soluble form of EPCR in plasma
    Beatrice Saposnik
    INSERM U765, Paris, France
    Blood 111:3442-51. 2008
    ..Trace amounts of the EPCR isoform were found in the plasma of A3 subjects. These results suggest that the sEPCRisoform could contribute to the regulatory effect of sEPCR in plasma...
  42. ncbi request reprint Activated protein C protects against diabetic nephropathy by inhibiting endothelial and podocyte apoptosis
    Berend Isermann
    Department of Medicine I and Clinical Chemistry, University of Heidelberg, INF 410, 69120 Heidelberg, Germany
    Nat Med 13:1349-58. 2007
    ..Conversely, maintaining high APC levels during long-term diabetes protects against diabetic nephropathy...
  43. ncbi request reprint A comparative study of the protein C pathway in septic and nonseptic patients with organ failure
    Delphine Borgel
    INSERM Unité 765, Paris, France
    Am J Respir Crit Care Med 176:878-85. 2007
    ..Severe sepsis is associated with an exacerbated procoagulant state with protein C (PC) system impairment. In contrast, the inflammatory and coagulation status of nonseptic patients with organ failure (OF) is less documented...
  44. pmc Endothelial cell protein C receptor acts as a cellular receptor for factor VIIa on endothelium
    Samit Ghosh
    Biomedical Research Division, The University of Texas Health Center at Tyler, Tyler, Texas 75708, USA
    J Biol Chem 282:11849-57. 2007
    ..Overall, the present data provide convincing evidence that EPCR serves as a cellular binding site for FVII/FVIIa. Further studies are needed to evaluate the pathophysiological consequences and relevance of FVIIa binding to EPCR...
  45. pmc Crystal structures of native and thrombin-complexed heparin cofactor II reveal a multistep allosteric mechanism
    Trevor P Baglin
    Department of Haematology, Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, United Kingdom
    Proc Natl Acad Sci U S A 99:11079-84. 2002
    ..Together, these structures reveal a multistep allosteric mechanism that relies on sequential contraction and expansion of the central beta-sheet of HCII...
  46. ncbi request reprint Structure of the antithrombin-thrombin-heparin ternary complex reveals the antithrombotic mechanism of heparin
    Wei Li
    University of Cambridge, Department of Haematology, Division of Structural Medicine, Thrombosis Research Unit, Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, UK
    Nat Struct Mol Biol 11:857-62. 2004
    ..A notably close contact interface, comprised of extensive active site and exosite interactions, explains, in molecular detail, the basis of the antithrombotic properties of therapeutic heparin...
  47. ncbi request reprint Shedding of endothelial protein C receptor contributes to vasculopathy and renal injury in lupus: in vivo and in vitro evidence
    Carlos A Sesin
    Department of Rheumatology, Hospital for Joint Diseases, New York University School of Medicine, New York, New York 10003, USA
    Kidney Int 68:110-20. 2005
    ..This study sought correlation between plasma levels of soluble EPCR and disease manifestation/severity, with a focus on lupus nephritis...
  48. ncbi request reprint Venous thrombosis in the elderly: more questions than answers
    Roy L Silverstein
    Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Blood 110:3097-101. 2007
  49. ncbi request reprint Patients with severe sepsis vary markedly in their ability to generate activated protein C
    Patricia C Y Liaw
    Department of Medicine, McMaster University, Hamilton, Ontario, Canada
    Blood 104:3958-64. 2004
    ..Baseline APC levels were higher in survivors (P = .024), and baseline F1 + 2/APC ratios were lower in survivors (P = .047). Larger studies are warranted to establish whether APC generation profiles aid in managing sepsis...
  50. ncbi request reprint Localization of phosphatidylserine binding sites to structural domains of factor Xa
    Arvind Srivastava
    Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599 7260, USA
    J Biol Chem 277:1855-63. 2002
    ....
  51. pmc Endothelial protein C receptor (CD201) explicitly identifies hematopoietic stem cells in murine bone marrow
    Alejandro B Balazs
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Blood 107:2317-21. 2006
    ..Based on our findings, we believe EPCR represents the first known marker that 'explicitly' identifies hematopoietic stem cells within murine bone marrow...
  52. ncbi request reprint The molecular basis of thrombin allostery revealed by a 1.8 A structure of the "slow" form
    James A Huntington
    Department of Haematology, University of Cambridge, Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Hills Road, CB2 2XY, Cambridge, United Kingdom
    Structure 11:469-79. 2003
    ..These residues constitute an allosteric switch, which is flipped directly through sodium binding, resulting in the fast form with an open active site...
  53. pmc Molecular basis of thrombin recognition by protein C inhibitor revealed by the 1.6-A structure of the heparin-bridged complex
    Wei Li
    Department of Haematology, Division of Structural Medicine, Thrombosis Research Unit, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 0XY, United Kingdom
    Proc Natl Acad Sci U S A 105:4661-6. 2008
    ..These data significantly improve our understanding of the cofactor-dependent roles of PCI in hemostasis...