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of VIIa/TF in TF-overexpressing VIC were assessed by westernblotting (incubation with FVIIa at 50 ng/mL for 30 min) in presence or absence of anti-TF antibody. Results are expressed as median (interquartile range). Results: VIC were defined as CD31(-) and CD68(-). TF and PAR-2 relative mRNA expressions were significantly higher in fibrocalcific vs normal valves (3.2 (1.5-.8) vs 0.18 (0.02-0.29), p<0.05; 1.15 (0.48-1.62) vs 0.16 (0.02-0.22), p<0.05; respectively). Normal VIC constitutively expressed TF (relative mRNA 4.1 (2.1-21.2); activity 36.2 (13.2-101.3) pg/mL) as well as PAR-2 (mRNA and protein by flow cytometry). TF expression was significantly increased in fibrocalcific VIC (relative mRNA 22.8 (9.8-33.8), p=0.05; activity 153 (71.5-247.0) pg/mL, p<0.05) when compared to normal VIC. Following IL-1beta stimulation of VIC, TF expression was significantly upregulated compared to unstimulated cells (relative mRNA 15.4 (12.9-28.2) fold increase, p<0.05; activity 2.7 (2.2-5.5) fold increase, p<0.05). ERK and Smad2 signalling pathways were upregulated in VIIa stimulated TF-overexpressing VIC (pERK/ERK 3.5 (2.9-4.8) fold increase; pSmad2/Smad2/3 1.8 (1.2-1.8) fold increase), an upregulation blunted by VIC preincubation with an anti-TF antibody. Conclusions: Our results demonstrate the implication of TF/VIIa/PAR-2 axis in VIC commitment to fibrocalcific aortic valve disease. Modulation of this pathway may represent a new therapeutic target for early medical treatment of AVS.

Simulating early calcific aortic valve disease within novel in vitro 3D tissue platform