miR-24-3p inhibits lipid synthesis and progesterone secretion in chicken granulosa cells via ERK1/2 signaling pathway.

Normal follicular development is the basis for ovulation in poultry. Our previous sequencing analysis revealed a high expression of miR-24-3p in chicken follicles from degenerated ovaries, suggesting that miR-24-3p may modulate follicular development. Hence, this study investigated the specific mechanisms of miR-24-3p in regulating chicken follicular development. The results revealed that the proliferation, lipid synthesis, and progesterone secretion were significantly inhibited after miR-24-3p overexpression in chicken granulosa cells, vice versa by miR-24-3p knockdown. Dual-specificity phosphatase 16 ( DUSP16 ) and thousand and one amino acid kinase 1 ( TAOK1 ) were identified as potential target genes of miR-24-3p. Further validation revealed that knockdown of DUSP16 and TAOK1 suppressed proliferation, lipid synthesis, and progesterone secretion in chicken granulosa cells. Moreover, we observed that miR-24-3p, along with knockdown of DUSP16 and TAOK1 , increased the phosphorylation levels of extracellular signal-regulated kinases 1 and 2 (ERK1/2). Our previous study proved that activation of ERK1/2 inhibited lipid synthesis and progesterone secretion of chicken granulosa cells. In summary, we demonstrated that miR-24-3p targeting DUSP16 and TAOK1 disrupts lipid synthesis and progesterone secretion via ERK1/2 signaling pathway in chicken granulosa cells in vitro. These results may provide a new theoretical basis for resolving miRNAs regulation on reproductive performance of chickens. • miR-24-3p disrupts proliferation, lipid synthesis, and progesterone secretion in chicken granulosa cells. • DUSP16 and TAOK1 promote proliferation, lipid synthesis, and progesterone secretion in chicken granulosa cells. • miR-24-3p mediates chicken granulosa cell functions via ERK1/2 signaling. [ABSTRACT FROM AUTHOR]