Mechanism underlying the stimulation by IGF-1 of LHCGR expression in porcine granulosa cells.

IGF-1 plays important roles in mammalian fertility by promoting cell growth and increasing steroid hormone secretion. Although IGF-1 significantly upregulated luteinizing hormone/choriogonadotropin receptor (LHCGR) gene expression in granulosa cells in a previous study, the mechanism was unclear. The present experiment was designed to primarily explore the regulation of LHCGR expression by IGF-1. First, based on a porcine LHCGR double-luciferase reporter experiment, c-Fos significantly inhibited the activity of the LHCGR promoter. Second, porcine granulosa cells were cultured in vitro with IGF-1, and we observed that the expression of LHCGR was significantly increased and the expression of c-Fos mRNA significantly reduced. After c-Fos overexpression in granulosa cells, IGF-1 attenuated the inhibitory effect of c-Fos on LHCGR. Furthermore, the level of LHCGR mRNA stimulated by IGF-1 in the presence of SB203580 was markedly lower than that of IGF-1 alone action. In conclusion, IGF-1 enhanced the expression of LHCGR by regulating c-Fos in granulosa cells, which may be mediated by the p38MAPK-signaling pathway. • c-Fos significantly inhibited the activity of the LHCGR promoter. • IGF-1 promoted the expression of LHCGR gene by suppressing c-Fos. • IGF-1 may regulate c-Fos through the p38MAPK-signaling pathway, consequently influencing the expression of LHCGR. [ABSTRACT FROM AUTHOR]