Table 1

Effect of pertussis toxin and the p38 kinase inhibitor on the proliferative response induced by somatostatin and in combination with bFGF in CHO-K1 cells expressing human recombinant sst2, sst3, or sst4 receptors

BasalSRIFbFGFSRIF+bFGF
CHOsst2 162  ± 6169  ± 13248  ± 31-a 179  ± 111-b
+Pertussis157  ± 6175  ± 10249  ± 4 245  ± 2
+PD 169316148  ± 3157  ± 11234  ± 4 238  ± 3
CHOsst3 154  ± 4152  ± 9239  ± 51-a 249  ± 101-a
+Pertussis160  ± 1155  ± 10237  ± 1244  ± 5
+PD 169316145  ± 2152  ± 8236  ± 4237  ± 6
CHOsst4 152  ± 4238  ± 71-a 236  ± 161-a 158  ± 21-b
+Pertussis157  ± 10 160  ± 4 252  ± 3 234  ± 7
+PD 169316146  ± 5236  ± 5236  ± 6 230  ± 1

Immediately after denudation, cell monolayers were incubated in incomplete media (basal), somatostatin (100 nM; SRIF), bFGF (10 ng/ml), or somatostatin and bFGF (SRIF+bFGF) either in the presence and absence of PD 169316 (10 μM) or after an initial pretreatment of confluent monolayers with pertussis toxin (18 h at 100 ng/ml). Values are expressed as the mean cell number (× 103 ± S.E.M.) harvested from a single coverslip 24 h after partial denudation (n = 3)

    • ↵1-a  Treatment is significantly different (P < 0.01) from basal.

    • ↵1-b  Treatment is significantly different from that in the presence of bFGF alone (P < 0.01).

    • Values highlighted in bold indicate the treatment is significantly different (P < 0.01) from that in the absence of pertussis toxin and PD 169316.