KISS1 Suppresses Apoptosis and Stimulates the Synthesis of E2 in Porcine Ovarian Granulosa Cells

摘要

Simple SummaryIn mammals, KISS-1 metastasis suppressor (KISS1) has emerged to stimulate the secretion of gonadotropin-releasing hormone (GnRH) to initiate the first estrus in the hypothalamus. However, KISS1 was recently demonstrated to be widely expressed in various ovarian compartments, including oocytes, granulosa cells (GCs) and theca cells. But the biological functionalities of KISS1 have not been explored in GCs. In this study, the overexpression plasmid of pcDNA3.1-KISS1 was built to explore the biological effects of KISS1 on the phosphoinositide 3-kinases (PI3K) signaling pathway, estrogen signaling pathway, cell apoptosis, cell cycle, and estradiol-17β (E2) secretion in porcine GCs. We found that overexpression of KISS1 could affect the PI3K signaling pathway, significantly decrease the apoptosis of GCs, and suppress GCs at G0/G1 phase of the cell cycle. Furthermore, overexpression of KISS1 could activate the estrogen synthesis signaling pathway and significantly increase the concentration of E2 in the supernatant and the mRNA expression levels of ESR1 and ESR2. These findings were highly accorded with the supposed role of KISS1 to promote the follicular development. This study would be of great interest for exploring the biological functionalities of KISS1 in regulating the maturation of follicles in mammals.