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. 2000 May 9;97(10):5255–5260. doi: 10.1073/pnas.97.10.5255

Figure 3.

Figure 3

Activation of PAR2 in stably transfected fibroblasts by FVIIa and FXa. KOLFs expressing TF, PAR2, or TF + PAR2 were used. Results shown are representative of several lines tested. Figures show representative experiments (mean ± SD; n = 3). (A) PI hydrolysis induced by FVIIa (Top), FXa (Middle), or a combination of picomolar FVIIa and zymogen FX (Bottom), all relative to saturating PAR2 agonist (SLIGRL, 100 μM). The maximal response to SLIGRL varied with PAR2 expression and the lower maximal response in KOLFPAR2 relative to KOLFTF+PAR2 is likely caused by different PAR2 expression levels in the particular clones shown. (B) Dose responses for FVIIa-induced PI hydrolysis in KOLFTF+PAR2 in the presence or absence of plasma concentrations of FX. (C) Calcium transients induced by FXa (1 unit/ml) or FVIIa (100 pM) + FX (1 unit/ml) in Fura-2 loaded KOLFTF+PAR2 cells. 1 unit/ml FXa or FX = 174 nM. Increases in cytosolic calcium were measured fluorometrically. Agonists were added at time indicated by arrows. (D) Dose-response for FXa- or Gla-domainless FXa-induced PI hydrolysis. (E) Inhibition of FXa-induced PAR2 activation by preincubation of cells with the indicated concentrations of active site-inhibited FXa .