Fig. 3

DGK inhibitor-induced COXII production and PKA activation is mediated via PKC-ERK1/2 signaling. Human ASM cells were pretreated with vehicle, Bis I (10 µM), U0126 (1 µM), or Vx11e (1 µM) for 10 min followed by stimulation with vehicle or DGK I (20 µM) for 24 h. Cells were lysed and immunoblotted for COXII, p-CREB, VASP, and β-actin (A). Graphical representation of mean ± SEM (n = 3–5 distinct donors) for COXII (B), p-CREB (C) and VASP (D). The densitometry data for COXII and p-CREB are normalized to basal conditions. Densitometry data for VASP phosphorylation are presented as percent (%) VASP shift (p-VASP/total VASP). *p < 0.05 (compared to vehicle basal) and ^#p < 0.05 (compared to DGK I basal) using one-way-ANOVA with Bonferroni post-hoc analysis. Please note that the gel images shown are cropped from the full length images