Regulation and role of the insulin-like growth factor I system in rat luteal cells

The relationship between insulin-like growth factor I (IGF-I), a hormone wh ich has potent metabolic effects and stimulates protein synthesis, and prol actin and oestradiol was examined to investigate a possible mechanism for t he luteal cell hypertrophy that is responsible for the increase in size of the corpus luteum. A luteal cell line (GG-CL) derived from large luteal cel ls of the pregnant rat corpus luteum was used. IGF-I, IGF-I receptor and oe strogen receptor beta mRNA, contents were determined by semiquantitative RT -PCR. The results revealed that prolactin upregulates the expression of IGF -I mRNA in luteal cells, but not that of its receptor. IGF-I had no effect on the expression of its receptor but caused a dose-related increase in the expression of oestrogen receptor beta. Furthermore, whereas IGF-I upregula ted oestrogen receptor beta expression, oestradiol downregulated expression of mRNA for both IGF-I and its receptor. This effect of oestradiol is not mediated through progesterone which is stimulated by oestradiol in the corp us luteum. The developmental studies indicate that mRNA for IGF-I and its r eceptor are not expressed in tandem throughout pregnancy. Whereas the recep tor mRNA is expressed at higher concentrations in early pregnancy, that of its ligand is highly expressed close to parturition. Collectively, the resu lts indicate that prolactin stimulates luteal IGF-I production, which in tu rn acts on the luteal cell to stimulate expression of oestrogen receptor be ta. Luteal cells with increased oestrogen receptor beta can respond fully t o oestradiol, leading to cell hypertrophy.