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Animals 2019, 9(2), 54; https://doi.org/10.3390/ani9020054

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

Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, National Engineering Research Centre for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong 510642, China
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Received: 24 November 2018 / Revised: 25 January 2019 / Accepted: 1 February 2019 / Published: 12 February 2019
(This article belongs to the Section Animal Reproduction)
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Simple Summary

In 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.

Abstract

Previous studies have strongly recommended that KISS-1 metastasis suppressor (KISS1) plays an essential gatekeeper of the initiation of reproductive maturation in mammals. However, KISS1 has been recently reported to highly express in ovarian granulosa cells (GCs). But the biological functionalities of KISS1 on cell apoptosis, cell cycle, and synthesis of estradiol-17β (E2) have not been explored in GCs. In this study, using porcine GCs as a cellular model, the overexpression plasmid of KISS1 was built to explore the biological effects of KISS1 on the PI3K signaling pathway, estrogen signaling pathway, cell apoptosis, cell cycle, and E2 secretion. We found that mRNA of KISS1 highly expressed in the ovary and significantly increased from immature to mature follicles in gilts. Overexpression of KISS1 could significantly increase the mRNA expression of PIK3CG, PIK3C1, and PDK1, and significantly decreased the mRNA levels of FOXO3, TSC2, and BAD of PI3K signaling pathway. Furthermore, results of the flow cytometry showed that overexpression of KISS1 significantly inhibited the apoptosis of GCs and decreased the percentage of GCs at G0/G1 phase of the cell cycle. Additionally, overexpression of KISS1 could increase the mRNA levels of Star, CYP17, 3B-HSD, 17B-HSD of estrogen synthesis signaling pathway, significantly increase the concentration of E2 in the supernatant of the cultured GCs, and up-regulate the mRNA expression levels of ESR1 and ESR2. These results suggested that KISS1 might suppress cell apoptosis through activating the PI3K signaling pathway and stimulate synthesis of E2 via boosting the estrogen synthesis signaling pathway. This study would be of great interests for exploring the biological functionalities of KISS1 in the folliculogenesis and sex steroid production of the ovaries in mammals. View Full-Text
Keywords: KISS1; Granulosa cells; Cell apoptosis; Cell cycle; Synthesis of E2 KISS1; Granulosa cells; Cell apoptosis; Cell cycle; Synthesis of E2
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Xin, X.; Li, Z.; Zhong, Y.; Li, Q.; Wang, J.; Zhang, H.; Yuan, X.; Li, J.; Zhang, Z. KISS1 Suppresses Apoptosis and Stimulates the Synthesis of E2 in Porcine Ovarian Granulosa Cells. Animals 2019, 9, 54.

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