Figure 1.
Figure 1. S1P synergistically potentiates thrombin-induced TF activity expression. (A) Confluent EC monolayers were treated with S1P and LPA in the presence (▪) and absence (□) of 2.4 nM thrombin. (B) The monolayers were treated with varying concentrations of thrombin in the presence (•) and absence (○) of 1 μM S1P. (C) In the presence of 2.4 nM thrombin, ECs were treated with varying concentrations of S1P (•), C2-ceramide (○), sphingosine (▴), PAF (▵), and LPC (▪). TF activity on the EC surface was determined after 5 hours of stimulation as factor Xa generation induced by TF–factor VIIa complex using purified factors VIIa and X as described in “Materials and methods.” These data represent the means ± SDs of 4 points per condition. Similar results were observed in 2 independent experiments using ECs of different lots.

S1P synergistically potentiates thrombin-induced TF activity expression. (A) Confluent EC monolayers were treated with S1P and LPA in the presence (▪) and absence (□) of 2.4 nM thrombin. (B) The monolayers were treated with varying concentrations of thrombin in the presence (•) and absence (○) of 1 μM S1P. (C) In the presence of 2.4 nM thrombin, ECs were treated with varying concentrations of S1P (•), C2-ceramide (○), sphingosine (▴), PAF (▵), and LPC (▪). TF activity on the EC surface was determined after 5 hours of stimulation as factor Xa generation induced by TF–factor VIIa complex using purified factors VIIa and X as described in “Materials and methods.” These data represent the means ± SDs of 4 points per condition. Similar results were observed in 2 independent experiments using ECs of different lots.

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