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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
Summary
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.
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