Fig. 6.
(A) COX-2 Luciferase activity in FPS cells transiently transfected with the full length COX-2 promoter C2.1 or series of 5’deletions (DRA, STY, ALU, RSA, HIN) and HIN with a mutation in the cAMP response element (HINcrem; −59/−53). FPS cells were treated with vehicle, 100 nM PGE2 or 100nM PGF2α for 4 h. CRE Luciferase activity in FPS cells transiently transfected with the cis-acting DNA binding sequence of the cAMP response element (CRE). FPS cells were treated with 100 nM PGE2 (B) or 100 nM PGF2α (C) for 4 h in the presence/absence of the FP receptor antagonist AL8810 (50 μM), EP2 receptor antagonist (AH6809; 10 μM), EP4 receptor antagonist (ONOAE2227; 1 μM) or chemical inhibitors of phospholipase Cβ (U73122, 10 μM), protein kinase A (4C3MQ, 1 μM), protein kinase C (GF109203x, 10 μM), EGFR kinase (AG1478, 200 nM) or ERK1/2 kinase (PD98059, 50 μM). Data are presented as mean ± S.E.M. b is significantly different from a and c is significantly different from a and b; P < 0.05.