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Cellular effects of factor VII activating protease (FSAP).

Authors
  • Byskov, Kristina1
  • Etscheid, Michael2
  • Kanse, Sandip M3
  • 1 Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. , (Norway)
  • 2 Paul Ehrlich Institute, Langen, Germany. , (Germany)
  • 3 Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. Electronic address: [email protected] , (Norway)
Type
Published Article
Journal
Thrombosis research
Publication Date
Feb 13, 2020
Volume
188
Pages
74–78
Identifiers
DOI: 10.1016/j.thromres.2020.02.010
PMID: 32087413
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Factor VII activating protease (FSAP) is a circulating serine protease of broad specificity that is likely to be involved in many pathophysiological processes. The activation of the circulating zymogen form of FSAP by histones, released from damaged cells, underlines its roles in regulating host responses to tissue damage and inflammation. Some of the direct cellular effects of FSAP are mediated through protease-activated receptors (PARs). Knock-down of each one of the four PARs in endothelial cells indicated that PAR-1 and -3 are involved in regulating endothelial permeability in response to FSAP. Overexpression of PARs in cell lines led to the conclusion that PAR-2 and -1 were the main receptors for FSAP. Studies with synthetic peptides and receptor mutants demonstrate that FSAP cleaves PAR-1 and -2 at their canonical cleavage site. However, PAR-1 is not activated by FSAP in all cells, which may be related to other, as yet, undefined factors. Inhibition of apoptosis by FSAP is mediated through PAR-1 and was observed in neurons, astrocytes and A549 cells. FSAP also mediates cellular effects by modulating the activity of growth factors, generation of bradykinin, C5a and C3a generation or histone inactivation. These cellular effects need to be further investigated at the in vivo level. Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.

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