Reelin regulates male mouse reproductive capacity via the sertoli cells.

J Cell Biochem

College of Veterinary Medicine, Shaanxi Centre of Stem Cells Engineering & Technology, Northwest A&F University, Yangling, Shaanxi, China.

Published: February 2019

AI Article Synopsis

  • Reelin plays a crucial role in brain development and is linked to reproductive functions in mice, as seen in reeler mutant mice that lack the protein.
  • These mutant mice exhibit irregular development of spermatogenic cells and reduced offspring production due to variations in sex hormone expression.
  • The study suggests potential pathways involving GDNF and ERK that may regulate changes in Sertoli cells and male germ cell niches, shedding light on the relationship between reelin and male reproductive health.

Article Abstract

Reelin plays important roles in brain development. Reeler mutant mice that lack the protein reelin (RELN) suffer from cell type- and region-dependent changes in their neocortical layers, and adult reeler mutant mice have dilated seminiferous tubules. Meanwhile, the mechanism by which Reelin regulates the spermatogenic cell development in mice and their reproductive abilities remains unclear. In the present study, we used reeler mutant mice to investigate the effects of Reelin on reproduction in mice. The results indicated variations in sex hormone expression among the reeler mice, indicating that they produce few offspring and their spermatogenic cells are irregularly developed. Moreover, glial cell line-derived neurotrophic factor (GDNF)/GDNF family receptor alpha 1, Ras/extracellular regulated protein kinases (ERK), and promyelocytic leukemia zinc finger (PLZF)/chemokine (C-X-C motif) receptor 4 (CXCR4) serve as potential regulatory pathways that respond to the changes in sertoli cells and the niche of male germ cells. Our findings provided valuable insights into the role of reeler in the reproductive abilities of male mice and development of their spermatogonia stem cells.

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Source
http://dx.doi.org/10.1002/jcb.26824DOI Listing

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