Modulation of prolactin-stimulated @entity42990 XXXX cell mitogenesis by cholera toxin and pertussis toxin.

@entity268 @entity42990 @entity706 @entity4515 @entity5987 @entity21788 @entity35 @entity4514
We have investigated whether cholera toxin (CT)- or pertussis toxin (IAP)-sensitive G proteins are involved in ovine (o) PRL-stimulated mitogenesis in the lactogen-dependent @entity35 @entity42990 @entity706 cell line. Addition of IAP to medium caused a biphasic effect on @entity21788 -stimulated cell number. Low doses (10(-3) ng/ml) enhanced (mean +/- SEM, 15 +/- 3%) whereas higher doses (greater than or equal to 10 ng/ml) inhibited (24 +/- 3%) mitogenesis stimulated by a submaximal dose of @entity21788 (0.1 ng/ml) compared to control values. The @entity268 analog @entity5987 also had a biphasic effect on cell division stimulated by submaximal doses of PRL. Low doses (10(-5) M) enhanced whereas higher doses (10(-3) M) inhibited @entity42990 cell growth in response to PRL. Incubation with CT only inhibited @entity21788 -stimulated mitogenesis in a dose-dependent manner. Maximal inhibition (63 +/- 7%) occurred at a concentration of 10 ng/ml or more. @entity4514 ( @entity4515 ) enhanced mitogenesis stimulated by PRL alone and in the presence of either stimulatory or inhibitory doses of IAP, but @entity4515 did not block IAP inhibition. In contrast, @entity4515 had no effect on cells incubated with CT; the inhibition of PRL-stimulated cell division by CT remained unchanged. Lactogenic receptor-binding sites per cell and affinity were not significantly affected by @entity4515 , IAP, or CT, suggesting a postreceptor mechanism of action. In summary, these data demonstrate that @entity268 modifies PRL-stimulated @entity42990 cell mitogenesis. The differences between IAP and CT (i.e. biphasic effect, degree of inhibition, and differential effect of @entity4515 ) suggest that these agents could also modulate PRL actions in the @entity42990 cell through different mechanisms, including a @entity268 -independent pathway.
