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Slit/Robo signaling regulates Leydig cell steroidogenesis

Emmanuelle Martinot1, Derek Boerboom2

  • 1Département de Biomédecine Vétérinaire, Centre de Recherche en Reproduction Et Fertilité, Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, QC, Canada.

Cell Communication and Signaling : CCS
|January 22, 2021
PubMed
Abstract

Insights

Slit/Robo signaling regulates Leydig cell steroidogenesis, potentially mediating testosterone

Area of Science:

  • Reproductive Biology
  • Endocrinology
  • Cell Signaling

Background:

  • Slit/Robo signaling is known for axon guidance, angiogenesis, and cancer.
  • Its role in testis function and steroidogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the role and mechanism of Slit/Robo signaling in regulating Leydig cell steroidogenesis.
  • To determine if Slit/Robo signaling is involved in testosterone feedback regulation.

Main Methods:

  • Detected Slit/Robo expression in adult mouse testes using immunohistochemistry and RT-qPCR.
  • Investigated steroidogenesis in Leydig cells (in vitro and in vivo) using gene expression, protein analysis, and hormone measurements.
  • Utilized Robo1-null mice and Leydig cell cultures treated with SLIT ligands.

Main Results:

  • Slit1, -2, -3, Robo1, and -2 are expressed in mouse testes, particularly Leydig cells.
  • Exogenous SLIT ligands decreased steroidogenic gene expression (Star, Cyp11a1, Cyp17a1) and CREB phosphorylation in Leydig cells.
  • SLIT2 treatment reduced luteinizing hormone receptor (Lhcgr) expression in MA10 Leydig cells.
  • Robo1-null mice showed increased testicular Star mRNA and testosterone levels.
  • Testosterone treatment enhanced Slit/Robo gene expression in Leydig cells via an AR-independent pathway.

Conclusions:

  • Slit/Robo signaling is a novel regulator of Leydig cell steroidogenesis.
  • This signaling pathway may mediate autocrine/paracrine negative feedback of testosterone on its own synthesis.
Keywords:
AKTCREBLH responsivenessLeydig cellRoboSlitSteroidogenesis

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