Fig. 1.

For paracrine-mediated effects of gastrin, 93 bp of the plasminogen activator inhibitor-2 (PAI-2) promoter is sufficient. A: in cells expressing the CCK-2 receptor and transfected with PAI-2-luc vectors, there was a reduction in luciferase activity in response to G17 (1 nM, 8 h) of the 93-bp PAI-2 luciferase construct compared with the 196-bp construct, *P < 0.05, t-test, n = 3. B: in contrast, when the 93-bp construct was transfected into cells not expressing CCK-2 receptors, but cocultured with cells expressing this receptor, the response to G17 (attributable to the action of paracrine mediators) was similar for both constructs and was comparable to the response to the 93-bp construct according to the protocol illustrated in A. Schematic cartoons underneath A and B illustrate the experimental design in each case (see Fig. 7 for a summary of the relevant signaling pathways). Note that in A, AGS cells not expressing the CCK-2 receptor and not transfected with PAI-2-luc vectors are included to ensure that total cell numbers were the same in the 2 conditions; in these circumstances PAI-2-luc responses are expected to reflect either direct effects of gastrin or effects consequent on activation of autocrine signaling pathways.