Regulation of Sertoli cell activin A and inhibin B by tumour necrosis factor α and interleukin 1α: interaction with follicle-stimulating hormone/adenosine 3',5'-cyclic phosphate signalling

Mol Cell Endocrinol. 2011 Mar 30;335(2):195-203. doi: 10.1016/j.mce.2011.01.014. Epub 2011 Jan 20.

Abstract

Regulation of crucial events during spermatogenesis involves dynamic changes in cytokine production and interactions across the cycle of the seminiferous epithelium. Regulation of activin A and inhibin B production by the inflammatory cytokines, tumour necrosis factor α (TNFα) and interleukin 1α (IL1α), alone and in conjunction with FSH or a cAMP analogue (dibutyryl cAMP), was examined in cultures of Sertoli cells from 20-day old rats. Both TNFα and IL1α stimulated activin A secretion and expression of its subunit (β(A)) mRNA, and suppressed inhibin B secretion and expression of its subunit (α and β(B)) mRNAs. The actions of TNFα and IL1α were opposed by FSH and dibutyryl cAMP. Both cytokines inhibited FSH/dibutyryl cAMP-stimulated inhibin B secretion and mRNA expression as well as stem cell factor mRNA expression. Both cytokines also inhibited FSH-induced cAMP production, and reduced baseline FSH receptor mRNA expression. These data highlight the reciprocal relationship that exists between FSH/cAMP signalling and inflammatory cytokine signalling pathways in the control of Sertoli cell function, and production of activin A/inhibin B in particular. It is anticipated that these interactions play important roles in the fine control of events during the cycle of the seminiferous epithelium and in the inhibition of spermatogenesis during inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bucladesine / pharmacology
  • Cells, Cultured
  • Cyclic AMP / antagonists & inhibitors
  • Cyclic AMP / metabolism*
  • Down-Regulation
  • Follicle Stimulating Hormone / pharmacology*
  • Follicle Stimulating Hormone / physiology
  • Inhibin-beta Subunits / genetics
  • Inhibin-beta Subunits / metabolism*
  • Inhibins / genetics
  • Inhibins / metabolism*
  • Interleukin-1alpha / pharmacology*
  • Interleukin-1alpha / physiology
  • Male
  • Phosphodiesterase Inhibitors / pharmacology
  • Protein Subunits / genetics
  • Protein Subunits / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, FSH / genetics
  • Recombinant Proteins / pharmacology
  • Sertoli Cells
  • Signal Transduction
  • Sphingosine / analogs & derivatives
  • Sphingosine / pharmacology
  • Stem Cell Factor / genetics
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Tumor Necrosis Factor-alpha / physiology
  • Up-Regulation

Substances

  • Interleukin-1alpha
  • N-acetylsphingosine
  • Phosphodiesterase Inhibitors
  • Protein Subunits
  • Receptors, FSH
  • Recombinant Proteins
  • Stem Cell Factor
  • Tumor Necrosis Factor-alpha
  • inhibin B
  • inhibin beta A subunit
  • Inhibins
  • Bucladesine
  • Follicle Stimulating Hormone
  • Inhibin-beta Subunits
  • Cyclic AMP
  • Sphingosine