Experiments with immature estrogen-primed rats have provided compelling evidence for the involvement of activin receptor signaling in GC differentiation. These GC express type II activin receptor mRNA and possess ~4000 specific activin receptors on the cell surface. Two activin А-dependent functions have been identified in cultured GC: the expression of inhibin-a subunit (Inh-a) and of FSH receptor. The connection of activin to Inh-a gene expression is of interest because Inh-a null female mice are infertile and their ovaries develop tumors. Since Inh-a plays an important role in fertility and the prevention of ovary tumors, understanding the mechanisms of the regulation of Inh-a expression is important. ventolin inhalers
The accumulated data from rat GC experiments indicate that activin, FSH (reviewed in ), and insulinlike growth factor-I (IGF-I) each can act alone to stimulate Inh-a expression. IGF-I is a 70-amino acid singlechain peptide that can have multiple positive effects on growth and cytodifferentiation in target cells in different body tissues, including the ovaries. There is evidence that endogenous IGF-I is obligatory for FSH-depen-dent steroidogenesis and preovulatory follicle development, and that the IGF-I mechanism requires receptor protein tyrosine kinase (PTK) activity in the GC. Because activin can mimic the stimulatory effects of FSH on Inh-a production, we hypothesized that IGF-I may also act as an autocrine/paracrine regulator for activin-stimulated Inh-a expression. The purpose of this research was to test this hypothesis.