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GnRH regulates gonadotrope cells through GnRH receptor activation of the PKC-, MAPK-, and calcium-activated signaling cascades. Due to the paucity of homologous model systems expressing FSHβ, little is known about the specific mechanisms involved in transcriptional regulation of this gene by GnRH. Previous studies from our laboratory demonstrated that the gonadotrope-derived LβT2 cell line expresses FSHβ mRNA. In the present study we characterized the mechanisms involved in GnRH regulation of the FSHβ promoter using this cell model. Using transfection assays, we show that GnRH regulation of the ovine FSHβ promoter involves at least two elements, present between −4152/−2878 and −2550/−1089 bp, in association with one or several elements within the proximal region of the promoter. Surprisingly, the two activating protein-1 sites previously shown to be involved in the FSHβ response to GnRH in heterologous cells do not play a role in GnRH responsiveness in the gonadotrope cell model. Here we demonstrate that calcium influx itself is not sufficient to confer the response, but it is necessary for both 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and GnRH induction of the FSHβ gene. Moreover, we show that GnRH regulation of FSHβ gene expression is mediated by PKC and establish the presence of multiple PKC isozymes in LβT2 cells. Interestingly, GnRH and TPA induce activity of the FSHβ promoter through different, although possibly overlapping, pools of PKC isoforms. This is further supported by the use of a MAPK inhibitor, which abolishes the induction of FSHβ by GnRH, but not by TPA. In conclusion, we have demonstrated that calcium, PKC, and MAPK signaling systems are all involved in the induction of FSHβ gene expression by GnRH in the LβT2 mouse gonadotrope cell model.

endocrinology

Transcriptional Activation of the Ovine Follicle-Stimulating Hormone-β Gene by Gonadotropin- Releasing Hormone Involves Multiple Signal Transduction Pathways