The Mechanism of Melatonin and Its Receptor MT2 Involved in the Development of Bovine Granulosa Cells

Ovarian granulosa cells (GCs) are a critical approach to investigate the mechanism of gene regulation during folliculogenesis. The objective of this study was to investigate the role of in bovine GCs, and assess whether silencing affected GCs response to melatonin. We found that silencing significan...

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Published inInternational journal of molecular sciences Vol. 19; no. 7; p. 2028
Main Authors Wang, Shujuan, Liu, Wenju, Pang, Xunsheng, Dai, Sifa, Liu, Guodong
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 12.07.2018
MDPI
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Summary:Ovarian granulosa cells (GCs) are a critical approach to investigate the mechanism of gene regulation during folliculogenesis. The objective of this study was to investigate the role of in bovine GCs, and assess whether silencing affected GCs response to melatonin. We found that silencing significantly decreased the secretion of progesterone and estradiol, and increased the concentration of inhibin B and activin B. To further reveal the regulatory mechanism of silencing on steroids synthesis, it was found that the expression of and enzymes (steroid hormone synthesis) were down-regulated, while genes related to hormonal synthesis ( , , and ) were up-regulated without affecting the expression of , suggesting that silencing may regulate hormone abundance. Furthermore, silencing significantly increased the expression of and , and decreased the expression of and without significant difference in the expression of and . In addition, silencing didn't affect the effect of melatonin on increasing the expression of , , and , and progesterone level, or decreasing , and expression, and production of inhibin B. Moreover, silencing could disrupt the role of melatonin in decreasing the , and expression, and activin B secretion. In conclusion, these results reveal that melatonin and MT2 are essential regulator of bovine GCs function by modulating reproduction-related genes expression, hormones secretion and other regulators of folliculogenesis.
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These authors contributed equally to this work.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms19072028