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Related Experiment Video

Updated: Dec 29, 2025

Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
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Citrullinated histone 3 causes endothelial barrier dysfunction.

Jamie E Meegan1, Xiaoyuan Yang1, Richard S Beard1

  • 1Department of Molecular Pharmacology & Physiology, University of South Florida Morsani College of Medicine, Tampa, FL, USA.

Biochemical and Biophysical Research Communications
|July 22, 2018
PubMed
Summary
This summary is machine-generated.

Circulating citrullinated histone 3 (H3Cit) from neutrophil extracellular traps (NETs) directly damages the microvascular endothelial barrier. This damage involves junction opening and cytoskeleton changes, suggesting H3Cit as a therapeutic target for inflammatory injury.

Keywords:
Adherens junctionCytoskeletonH3CitMicrocirculationPermeability

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Area of Science:

  • Immunology
  • Vascular Biology
  • Cellular Biology

Background:

  • Circulating neutrophil extracellular traps (NETs) and their components, particularly histones, are implicated in tissue damage during inflammatory diseases like sepsis.
  • Citrullinated histone 3 (H3Cit), a biomarker for NETs, may actively contribute to the inflammatory response and associated pathologies.

Purpose of the Study:

  • To investigate the direct role of citrullinated histone 3 (H3Cit) in mediating microvascular endothelial barrier dysfunction.
  • To elucidate the cellular mechanisms by which H3Cit impacts endothelial cells.

Main Methods:

  • Exposure of endothelial cells to purified H3Cit.
  • Assessment of endothelial barrier integrity via cell-cell adherens junction status and F-actin cytoskeleton organization.
  • Investigation of key signaling pathways (Rho, MLCK) and the effect of adenylyl cyclase activation (forskolin).

Main Results:

  • H3Cit directly disrupts the microvascular endothelial barrier.
  • Endothelial cell responses include opening of cell-cell adherens junctions and reorganization of the cytoskeleton with increased F-actin stress fibers.
  • Canonical hyperpermeability pathways (Rho, MLCK) were not major mediators; however, forskolin treatment mitigated H3Cit's barrier-disrupting effects.

Conclusions:

  • Citrullinated histone 3 (H3Cit) directly contributes to inflammatory injury by compromising the endothelial barrier.
  • The findings suggest H3Cit-induced endothelial barrier dysfunction as a potential therapeutic target for inflammatory conditions.
  • Modulation of adenylyl cyclase signaling may offer a strategy to counteract H3Cit's detrimental effects.