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Related Experiment Video

Updated: Aug 20, 2025

A Novel Stretching Platform for Applications in Cell and Tissue Mechanobiology
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FSAP Protects against Histone-Mediated Increase in Endothelial Permeability In Vitro.

Xue Yan Cui1,2,3,4, Benedicte Stavik1,2, Bernd Thiede5

  • 1Department of Haematology, Oslo University Hospital, 0424 Oslo, Norway.

International Journal of Molecular Sciences
|November 26, 2022
PubMed
Summary

Factor-VII-activating protease (FSAP) inhibits histone-induced increases in endothelial permeability by preventing junction protein rearrangement and TLR-2 upregulation. This suggests FSAP plays a protective role in inflammatory conditions.

Keywords:
FSAPTLRendotheliumhistonepermeability

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Immunology

Background:

  • Factor-VII-activating protease (FSAP) regulates hemostasis and inflammation.
  • Extracellular histones contribute to inflammation and activate FSAP.
  • FSAP's role in endothelial permeability regulation requires mechanistic clarification.

Purpose of the Study:

  • To investigate the in vitro effects of FSAP on histone-induced endothelial permeability.
  • To elucidate the mechanisms by which FSAP modulates endothelial barrier function.

Main Methods:

  • In vitro assessment of endothelial permeability using HUVEC cells.
  • Analysis of junction protein localization (VE-cadherin, ZO-1).
  • Evaluation of Toll-like receptor (TLR) involvement using blocking antibodies and gene expression analysis.

Main Results:

  • Histones increased endothelial permeability and disrupted junctional proteins.
  • Wild-type FSAP serine protease domain (WT-SPD-FSAP) blocked histone-induced permeability and protein rearrangement.
  • FSAP inhibited histone-mediated TLR-2 upregulation, while an inactive variant showed no effect.

Conclusions:

  • FSAP actively inhibits histone-induced endothelial hyperpermeability.
  • FSAP's mechanism involves preventing junctional protein disruption and TLR-2 pathway activation.
  • FSAP's inhibitory function on histone effects may be therapeutically relevant for sepsis, trauma, and stroke.