The main conclusion from these experiments is that endogenous IGF-I is required for activin-dependent stimulation of Inh-a expression in rat GC. The primary experimental evidence to support this conclusion is as follows. flovent inhaler
First, activin treatment leads to a marked increase in the expression of Inh-a mRNA and protein in the GC, and the stimulatory effect is completely blocked by IGFBP-4, IGFBP-5, and anti-IGF-I antibody. These observations support the idea that IGF-I produced by the GC is required for activin to stimulate Inh-a expression. Second, the stimulation of Inh-a mRNA and protein production by activin is totally abolished by the tyrosine kinase inhibitor A23. Taken together, these results are consistent with the interpretation that an IGF-I-dependent tyrosine phosphorylation is obligatory for activin-dependent Inh-a gene expression in rat GC. The functional significance of this autocrine/ paracrine control process is unknown; however, it could have physiological relevance because Inh-a gene expression is important for fertility and tumor suppression in the ovary.