FSH acts on the proliferation of type A spermatogonia via Nur77 that increases GDNF expression in the Sertoli cells

FEBS Lett. 2011 Aug 4;585(15):2437-44. doi: 10.1016/j.febslet.2011.06.013. Epub 2011 Jun 30.

Abstract

The molecular mechanism responsible for the regulation of GDNF in Sertoli cells remains largely unknown. In the present study, FSH induced the expression of Nur77 and GDNF in mouse testis tissue and human fetal Sertoli cells. Moreover, FSH increased the number of A spermatogonia co-cultured with Sertoli cells. In the additional assays, Nur77 was observed to directly regulate GDNF transcription. Furthermore, overexpression of Nur77 and siRNA-mediated knockdown of Nur77 affected levels of GDNF mRNA and protein in primary human fetal Sertoli cells. These results indicate that FSH-induced Nur77 regulates the expression of GDNF in Sertoli cells to stimulate the proliferation of A spermatogonia in vitro.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Proliferation*
  • Cells, Cultured
  • Follicle Stimulating Hormone / physiology*
  • Glial Cell Line-Derived Neurotrophic Factor / biosynthesis*
  • Glial Cell Line-Derived Neurotrophic Factor / genetics
  • Humans
  • Male
  • Mice
  • Nuclear Receptor Subfamily 4, Group A, Member 1 / biosynthesis*
  • Nuclear Receptor Subfamily 4, Group A, Member 1 / genetics
  • Sertoli Cells / metabolism*
  • Spermatogonia / cytology*
  • Spermatogonia / metabolism
  • Transcription, Genetic
  • Transcriptional Activation

Substances

  • Glial Cell Line-Derived Neurotrophic Factor
  • NR4A1 protein, human
  • Nr4a1 protein, mouse
  • Nuclear Receptor Subfamily 4, Group A, Member 1
  • Follicle Stimulating Hormone