@entity53 induces vasoactive intestinal peptide and XXXX gene expression in the @entity35 anterior pituitary independently of plasma @entity3695 levels.

@entity172 @entity4089 @entity5 @entity53 @entity62673 @entity3695 @entity35 @entity12180
It is well established that @entity172 are potent stimulators of @entity3695 (PRL) secretion. It has also been demonstrated that @entity53 (E2) can increase the expression and the anterior pituitary levels of the vasoactive intestinal peptide ( @entity12180 ), a peptide which also acts as a potent PRL-releasing factor. It thus remained unknown whether the effects on pituitary @entity12180 were due to E2 itself or to E2-induced @entity4089 ( @entity4089 ). In order to test this hypothesis, various plasma PRL levels were induced in @entity35 either with ectopic pituitary grafts, PRL secreting @entity5 or E2 implants, and @entity12180 mRNA expression in the anterior pituitary was measured by in situ hybridization and Northern blot analyses. Whereas decreases in @entity12180 mRNA can be observed in pituitaries of @entity35 with pure @entity4089 , a 6-fold increase in @entity12180 mRNA can be seen in E2-treated @entity35 . E2 increased both 1.0 and 1.7 Kb @entity12180 mRNA species. The presence of the graft in E2-treated @entity35 significantly reduced the increase in VIPmRNA observed following E2. The direct stimulation by E2 of @entity12180 mRNA expression was further demonstrated by the fact that statistical analysis of the data indicated that both E2 and graft were acting independently of each other, and that a new selective antiestrogen, @entity62673 , almost totally blocked the effect of E2. Moreover, under similar experimental conditions, pituitary PRL mRNA levels were reduced in the graft group and a marked up-regulation was observed similarly in both E2 and in E2 @entity35 bearing ectopic grafts.(ABSTRACT TRUNCATED AT 250 WORDS)
