MicroRNA-150 regulates steroidogenesis of mouse testicular Leydig cells by targeting STAR

Xu-Jing Geng1, Dong-Mei Zhao1, Gen-Hong Mao1

  • 1Reproductive Medical Center, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Reproduction (Cambridge, England)
|June 15, 2017
PubMed

Insights

MicroRNA-150 (miR-150) negatively regulates steroid production in mouse Leydig cells. Inhibiting miR-150 increases steroidogenesis, while its overexpression reduces it, impacting male fertility.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Reproductive Biology

Background:

  • Leydig cells are crucial for male reproductive development and androgen production.
  • MicroRNAs (miRNAs) are implicated in spermatogenesis, but their role in Leydig cell steroidogenesis is unclear.
  • miR-150 is predominantly expressed in mouse Leydig cells.

Purpose of the Study:

  • To investigate the role of miR-150 in regulating steroidogenesis in mouse Leydig cells.
  • To determine if miR-150 directly targets the Steroidogenic Acute Regulatory Protein (STAR).

Main Methods:

  • Leydig cells were treated with miR-150 antagomirs (knockdown) and agomirs (overexpression).
  • Steroid production and STAR expression levels were measured.
  • Luciferase reporter assays were used to validate STAR as a miR-150 target.
  • Intratesticular injections were performed to assess in vivo effects.

Main Results:

  • miR-150 knockdown significantly increased STAR expression and steroid production.
  • miR-150 overexpression significantly reduced STAR expression and steroid production.
  • The Steroidogenic Acute Regulatory Protein (STAR) gene was identified as a direct target of miR-150.
  • miR-150 inhibition or overexpression altered steroidogenesis and spermatogenesis in vivo.

Conclusions:

  • miR-150 acts as a negative regulator of steroidogenesis in mouse Leydig cells.
  • miR-150 controls Leydig cell function by targeting STAR expression.
  • These findings highlight miR-150's importance in male reproductive health.

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