Factor VIIa induces anti-inflammatory signaling via EPCR and PAR1
Copyright policy )Factor VIIa induces anti-inflammatory signaling via EPCR and PAR1
Key Points The coagulation protease FVIIa attenuates TNF-α- and LPS-induced inflammation both in vitro and in vivo via an EPCR-dependent mechanism. FVIIa-EPCR-PAR1-mediated anti-inflammatory signaling transmits through the β-arrestin-1-dependent pathway.
- Oklahoma Medical Research Foundation United States
- The University of Texas Health Science Center at Tyler United States
- The University of Texas System United States
Inflammation, Lipopolysaccharides, Tumor Necrosis Factor-alpha, Endothelial Protein C Receptor, Factor VIIa, Mice, Gene Expression Regulation, Human Umbilical Vein Endothelial Cells, Animals, Humans, Receptor, PAR-1, Inflammation Mediators, Biomarkers, beta-Arrestins, Signal Transduction
Inflammation, Lipopolysaccharides, Tumor Necrosis Factor-alpha, Endothelial Protein C Receptor, Factor VIIa, Mice, Gene Expression Regulation, Human Umbilical Vein Endothelial Cells, Animals, Humans, Receptor, PAR-1, Inflammation Mediators, Biomarkers, beta-Arrestins, Signal Transduction
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