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Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory

C Mauduit1, F Gasnier, C Rey

  • 1INSERM U407, Centre Hospitalier Lyon-Sud, Pierre Bénite, France. mauduit@lsgrisn1.univ-lyon1.fr

Endocrinology
|June 2, 1998
PubMed
Summary
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Tumor necrosis factor alpha (TNFalpha) inhibits testosterone production by affecting steroidogenic acute regulatory protein (StAR) levels in testicular cells. This suggests TNFalpha directly impacts Leydig cells, influencing cholesterol transport for steroidogenesis.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Testosterone production is regulated by luteinizing hormone (LH) and human chorionic gonadotropin (hCG).
  • Tumor necrosis factor alpha (TNFalpha) is a cytokine implicated in inflammatory processes and cellular regulation.

Purpose of the Study:

  • To pinpoint the inhibitory mechanism of TNFalpha on LH/hCG-stimulated testosterone formation.
  • To investigate TNFalpha's effect on cholesterol metabolism and steroidogenic acute regulatory protein (StAR) in Leydig cells.

Main Methods:

  • Cultured porcine Leydig cells were used as an in vitro model.
  • Cells were stimulated with hCG or 22R-hydroxycholesterol in the presence of varying TNFalpha concentrations.
  • StAR mRNA and protein levels were quantified using RT-PCR and cross-linking experiments.

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Main Results:

  • TNFalpha inhibited hCG-stimulated testosterone secretion but not that induced by 22R-hydroxycholesterol.
  • TNFalpha dose-dependently reduced hCG-induced StAR levels, with maximal inhibition at 20 ng/ml.
  • Maximal inhibition of StAR mRNA and protein by TNFalpha occurred after 48 hours.
  • TNFalpha receptors (P55) were detected on Leydig cells, indicating direct action.

Conclusions:

  • TNFalpha's inhibitory effect on testosterone production likely involves the disruption of cholesterol transport to mitochondria.
  • TNFalpha directly acts on testicular Leydig cells by downregulating StAR expression.
  • This study elucidates a novel mechanism by which TNFalpha modulates steroidogenesis.