miR-317 regulates the proliferation and apoptosis of duck follicle granulosa cells by targeting VIPR1

  • 0Institute of Animal Husbandry and Veterinary Medicine, Fujian Academy of Agricultural Sciences, Fujian Key Laboratory of Animal Genetics and Breeding, Fuzhou, Fujian 350013, PR China.

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Summary

This summary is machine-generated.

MicroRNA-317 (miR-317) influences duck follicle granulosa cell proliferation and apoptosis. miR-317 overexpression promotes proliferation, while its inhibition increases apoptosis and negatively regulates VIPR1 expression, offering insights into follicular atresia.

Area Of Science

  • Reproductive Biology
  • Molecular Endocrinology
  • Avian Physiology

Background

  • Vasoactive intestinal peptide receptor 1 (VIPR1) binds VIP, a prolactin (PRL) release factor, influencing PRL secretion and bird nesting behavior.
  • Understanding the role of microRNAs in regulating avian reproductive processes, such as follicular atresia, is crucial for agricultural applications.

Purpose Of The Study

  • To investigate the regulatory effects of miR-317 on VIPR1 gene and protein expression in duck follicle granulosa cells.
  • To elucidate the impact of miR-317 modulation on cell proliferation and apoptosis in duck follicular cells.

Main Methods

  • Histological analysis (HE staining) of Muscovy duck ovaries during nesting and laying periods.
  • Isolation and identification (immunofluorescence for FSHR and LHR) of primary follicle granulosa cells.
  • Transfection with miR-317 mimics or inhibitors, followed by EdU staining (proliferation), Annexin-V/TUNEL assays (apoptosis), qRT-PCR, and Western blotting (VIPR1 expression).

Main Results

  • miR-317 overexpression significantly increased granulosa cell proliferation and decreased VIPR1 expression at both gene and protein levels.
  • miR-317 inhibition significantly promoted granulosa cell apoptosis and increased VIPR1 expression.
  • Histological analysis showed distinct nuclear characteristics in granulosa cells during brooding versus laying periods.

Conclusions

  • miR-317 plays a dual role: promoting proliferation and inhibiting VIPR1 expression when overexpressed, while promoting apoptosis and upregulating VIPR1 when inhibited in duck follicle granulosa cells.
  • These findings reveal a molecular mechanism underlying follicular atresia in ducks and provide a potential target for managing broodiness in Muscovy ducks.