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

Mol Reprod Dev. 2018 Oct;85(10):768-777. doi: 10.1002/mrd.23058. Epub 2018 Oct 7.

Abstract

MicroRNAs (miRNAs) have been shown to play a key role in spermatogenesis. However, whether the miRNAs influence androgen/androgen receptor (AR) signaling during spermatogenesis remains unclear. Using a bioinformatic approach, a potential miRNA, miR-130a, which could bind to Ar-3'untranslated region directly was identified. The expression pattern of miR-130a was further characterized by quantitative real-time polymerase chain reaction. It was found that miR-130a was abundant in testis and its expression level was negatively correlated with age. Overexpression of miR-130a could inhibit AR expression both in vitro and in vivo. Moreover, the mice with an intratesticular injection of miR-130a showed defects in spermatogenesis and increased germ cell apoptosis. Taken together, these results suggest that miR-130a could negatively regulate AR expression in mouse Sertoli cell, which further cause defects in spermatogenesis.

Keywords: Sertoli cell; androgen receptor (AR); miR-130a; spermatogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Line
  • Gene Expression Regulation*
  • Male
  • Mice
  • MicroRNAs / biosynthesis*
  • MicroRNAs / genetics
  • Receptors, Androgen / biosynthesis*
  • Receptors, Androgen / genetics
  • Sertoli Cells / cytology
  • Sertoli Cells / metabolism*
  • Spermatogenesis*

Substances

  • MIRN130 microRNA, mouse
  • MicroRNAs
  • Receptors, Androgen