Table 1.

Cyclooxygenase products either had no effect or slightly stimulated PAI-1-luc expression in MKN45 and AGS-G_R cells

	MKN45 Cells	AGS-GR Cells
Control	1.0 ± 0.13	1.0 ± 0.17
G-17 (10 nM)		3.01 ± 0.12*
PMA (100 ng/ml)	4.14 ± 0.39*
PGE2 (10 μM)	1.82 ± 0.26*	1.73 ± 0.37
PGI2 (10 μM)	1.84 ± 0.45*	1.60 ± 0.37
U-46619 (10 μM)	1.42 ± 0.09	1.10 ± 0.31
PGE2 + G-17		1.94 ± 0.55*
PGE2 + PMA	4.75 ± 0.64*
PGI2 + G-17		2.40 ± 0.56*
PGI2 + PMA	3.37 ± 0.28*
U-46619 + G-17		1.69 ± 0.14a
U-46619 + PMA	3.39 ± 0.91*

Values are means ± SE; n = 5 experiments, ANOVA. Stimulation (6 h) of plasminogen activator inhibitor-1 promoter coupled to luciferase (PAI-1-luc)-transfected MKN45 or AGS-G_R cells with phorbol 12-myristate, 13-acetate (PMA) or gastrin-17 (G-17), respectively, increased PAI-1-luc expression 3- to 4-fold. PGE₂, PGI₂, or a stable ligand of the thromboxane A₂ receptor U-46619 had either no or a small stimulatory effect on PAI-1-luc expression; in combination with PMA or G-17, as appropriate, PGE₂, PGI₂, and U-46619 had no effect or slightly inhibited the response to PMA/G-17.

^*P < 0.05, statistically significant from control.

^aStatistically significant from G-17.