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MicroRNA-130a inhibits spermatogenesis by directly targeting androgen receptor in mouse Sertoli cells

Cailing Li1, Bo Yang1, Peng Pan2

  • 1Guangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Institute of Urology, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, China.

Molecular Reproduction and Development
|September 8, 2018
PubMed

Insights

MicroRNAs (miRNAs) regulate male fertility. This study identifies miR-130a as a key factor that inhibits androgen receptor (AR) signaling, leading to impaired spermatogenesis and increased germ cell death.

Area of Science:

  • Reproductive Biology
  • Molecular Endocrinology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are crucial for spermatogenesis.
  • The role of miRNAs in androgen/androgen receptor (AR) signaling during spermatogenesis is not fully understood.

Purpose of the Study:

  • To investigate the function of miR-130a in regulating androgen receptor (AR) signaling and spermatogenesis.
  • To determine the impact of miR-130a on male fertility.

Main Methods:

  • Bioinformatic analysis to identify potential miRNA targets.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) for miRNA expression analysis.
  • In vitro and in vivo experiments to assess the effect of miR-130a on AR expression and spermatogenesis.

Main Results:

  • miR-130a directly targets the 3' untranslated region of AR.
  • miR-130a expression is high in testes and decreases with age.
  • Overexpression of miR-130a inhibits AR expression and causes defects in spermatogenesis, including increased germ cell apoptosis.

Conclusions:

  • miR-130a acts as a negative regulator of AR expression in mouse Sertoli cells.
  • Dysregulation of miR-130a can lead to impaired spermatogenesis and male infertility.
Keywords:
Sertoli cellandrogen receptor (AR)miR-130aspermatogenesis

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