Han Ying, Chen Yanhong, Yang Feng, Sun Xiaomei, Zeng Shenming
National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics, Breeding, and Reproduction of the Ministry of Agriculture and Rural Affairs, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China; College of Agronomy, Liaocheng University, Liaocheng, 252000, Shandong, China.
National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics, Breeding, and Reproduction of the Ministry of Agriculture and Rural Affairs, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China.
Theriogenology. 2021 Jul 15;169:56-64. doi: 10.1016/j.theriogenology.2021.04.011. Epub 2021 Apr 22.
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.
胰岛素样生长因子-1（IGF-1）通过促进细胞生长和增加甾体激素分泌，在哺乳动物生育中发挥重要作用。尽管在先前的一项研究中IGF-1显著上调了颗粒细胞中促黄体生成素/绒毛膜促性腺激素受体（LHCGR）基因的表达，但其机制尚不清楚。本实验旨在初步探究IGF-1对LHCGR表达的调控作用。首先，基于猪LHCGR双荧光素酶报告实验，c-Fos显著抑制LHCGR启动子的活性。其次，用IGF-1体外培养猪颗粒细胞，我们观察到LHCGR的表达显著增加，而c-Fos mRNA的表达显著降低。在颗粒细胞中过表达c-Fos后，IGF-1减弱了c-Fos对LHCGR的抑制作用。此外，在存在SB203580的情况下，IGF-1刺激的LHCGR mRNA水平明显低于IGF-1单独作用时。总之，IGF-1通过调节颗粒细胞中的c-Fos增强LHCGR的表达，这可能是由p38丝裂原活化蛋白激酶信号通路介导的。
