BMP15 regulates AMH expression via the p38 MAPK pathway in granulosa cells from goat
Anti-Mullerian hormone (AMH), a member of the TGF-β superfamily, is produced by granulosa cells (GCs) of preantral and small antral follicles and plays a role in regulating the recruitment of primordial follicles and the FSH-dependent development of follicles. However, the regulation of AMH expressi...
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Veröffentlicht in: | Theriogenology 2018-09, Vol.118, p.72-79 |
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Zusammenfassung: | Anti-Mullerian hormone (AMH), a member of the TGF-β superfamily, is produced by granulosa cells (GCs) of preantral and small antral follicles and plays a role in regulating the recruitment of primordial follicles and the FSH-dependent development of follicles. However, the regulation of AMH expression in follicles remains poorly understood. The objectives of this study were to determine the following: 1. the association between bone morphogenetic protein 15 (BMP15) and AMH; 2. whether BMP15 can regulate the expression of AMH by inhibiting the p38 MAPK pathway; and 3. whether SRY-related HMG box 9 (SOX9), a transcription factor for AMH, is involved in the regulation of AMH expression by BMP15. In this study, an inhibitor of p38 MAPK and an siRNA specific for p38 MAPK were used to prevent the function of the p38 MAPK signaling pathway. Then, AMH mRNA expression and AMH secretion were detected in goat GCs using an RT-PCR assay and ELISA, respectively, after treatment with BMP15. The results indicated that BMP15 up-regulates the transcription of AMH and that the inhibition of p38 MAPK decreases the BMP15-induced expression of AMH and SOX9, suggesting that BMP15 up-regulates the expression of AMH via the p38 MAPK signaling pathway, and this process involves the SOX9 transcription factor.
•Transitional idea is that BMPs can regulate AMH expression via SMAD signaling pathway.•BMP15 up-regulates the expression of AMH through p38 MAPK signaling pathway.•The inhibitor of p38 MAPK and siRNA specific for p38 MAPK can reduce the BMP15-induced AMH and SOX9 expression. |
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ISSN: | 0093-691X 1879-3231 |
DOI: | 10.1016/j.theriogenology.2018.05.032 |