Extracellular histones are major mediators of death in sepsis
- Jun Xu, Xiaomei Zhang, C. Esmon
- Biology, MedicineNature Network Boston
- 9 October 2009
It is concluded that extracellular histones are potential molecular targets for therapeutics for sepsis and other inflammatory diseases.
The interactions between inflammation and coagulation
- C. Esmon
- Biology, MedicineBritish Journal of Haematology
- 1 November 2005
Downregulation of anticoagulant pathways not only promotes thrombosis but also amplifies the inflammatory process, such as manifested in severe sepsis or inflammatory bowel disease.
Extracellular Histones Are Mediators of Death through TLR2 and TLR4 in Mouse Fatal Liver Injury
- Jun Xu, Xiaomei Zhang, M. Monestier, N. Esmon, C. Esmon
- BiologyJournal of Immunology
- 1 September 2011
The studies imply that histone release contributes to death in inflammatory injury and in chemical-induced cellular injury, both of which are mediated in part through the TLRs.
Future research directions in acute lung injury: summary of a National Heart, Lung, and Blood Institute working group.
- M. Matthay, G. Zimmerman, A. Harabin
- MedicineAmerican Journal of Respiratory and Critical Care…
- 1 April 2003
Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI.
Extracellular histones promote thrombin generation through platelet-dependent mechanisms: involvement of platelet TLR2 and TLR4.
- F. Semeraro, C. T. Ammollo, C. Esmon
- BiologyBlood
- 18 August 2011
Data show that histone-activated platelets possess a procoagulant phenotype that drives plasma thrombin generation and suggest that TLR2 and TLR4 mediate the activation process.
The roles of protein C and thrombomodulin in the regulation of blood coagulation.
- C. Esmon
- Biology, MedicineJournal of Biological Chemistry
- 1 December 1984
The data presented here suggest that deficiencics in protein S, thrombomodulin, or the platelet receptor for activated protein C might also result in a thromBotic tendency.
Identification, cloning, and regulation of a novel endothelial cell protein C/activated protein C receptor.
- K. Fukudome, C. Esmon
- BiologyJournal of Biological Chemistry
- 21 October 1994
The protein C pathway
- C. Esmon
- Biology, MedicineChest
- 1 September 2000
Animal studies and preliminary clinical results suggest that protein C/ activated protein C supplementation may be useful in reversing microvascular dysfunction, probably augmenting inflammatory responses and contributing to endothelial cell dysfunction.
The protein C pathway.
- C. Esmon
- Biology, MedicineCritical Care Medicine
- 1 September 2003
Animal studies and preliminary clinical results suggest that protein C/activated protein C supplementation may be useful in reversing microvascular dysfunction, and the mechanisms by which inflammation impairs the function of this pathway are reviewed.
The endothelial cell protein C receptor augments protein C activation by the thrombin-thrombomodulin complex.
- D. Stearns-Kurosawa, S. Kurosawa, J. Mollica, G. Ferrell, C. Esmon
- BiologyProceedings of the National Academy of Sciences…
- 17 September 1996
It is demonstrated that monoclonal antibodies that block protein C binding to the endothelial cell protein C receptor (EPCR) reduce protein C activation rates by the thrombin-thrombomodulin complex on endothelium, but that antibodies that bind to EPCR without blockingprotein C binding have no effect.
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