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Extracellular Histones Trigger Disseminated Intravascular Coagulation by Lytic Cell Death.

Yan Zhang1,2,3, Congqing Wu2,4, Lan Li5

  • 1Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.

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|June 24, 2022
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Summary
This summary is machine-generated.

Extracellular histones cause blood clotting (coagulation) by inducing cell death, independent of inflammasome or TLR pathways. This discovery reveals a new mechanism for histone-induced thrombosis.

Keywords:
DICcell deathcoagulationhistonesplateletthrombocytopeniatissue factor

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Area of Science:

  • Biochemistry
  • Immunology
  • Hematology

Background:

  • Extracellular histones are linked to sepsis-induced mortality via unknown mechanisms.
  • Previous research implicated inflammasome activation and pyroptosis in triggering coagulation via tissue factor (TF).

Purpose of the Study:

  • To elucidate the molecular mechanisms by which extracellular histones induce coagulation.
  • To investigate the roles of inflammasome pathways, TLRs, and cell death in histone-induced coagulopathy.

Main Methods:

  • Utilized various gene-deficient mouse models to study histone-induced coagulation in vivo.
  • Incubated histones with macrophages to assess cell death and phosphatidylserine (PS) exposure.
  • Assessed coagulation parameters, fibrin deposition, and the effect of TF neutralization.

Main Results:

  • Histones induced coagulation activation and fibrin deposition in vivo.
  • Histone-induced coagulopathy was independent of caspase 1/11, gasdermin D (GSDMD), TLR2, and TLR4.
  • Histones induced lytic cell death and phosphatidylserine (PS) exposure in macrophages, which is crucial for TF activity.
  • Neutralization of TF significantly reduced histone-induced coagulation.

Conclusions:

  • Lytic cell death is a novel mechanism driving histone-induced coagulation activation.
  • Extracellular histones promote thrombosis through a pathway involving cell lysis and TF exposure, distinct from inflammasome or TLR signaling.