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Related Experiment Video

Updated: May 19, 2026

Using Ex Vivo Upright Droplet Cultures of Whole Fetal Organs to Study Developmental Processes during Mouse Organogenesis
09:47

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Published on: October 21, 2015

[Diethylstilbestrol affects LGR8 expression in mouse gubernaculum testis].

Xin-Bin Yang1, Xue-Wu Jiang, Shou-Xing Duan

  • 1Department of Pediatric Surgery, The Second Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China. yang-xinbin@163.com

Zhonghua Nan Ke Xue = National Journal of Andrology
|September 1, 2012
PubMed
Summary

Prenatal exposure to diethylstilbestrol (DES) impaired mouse gubernaculum testis development and affected LGR8 receptor expression. This suggests DES may cause cryptorchidism by disrupting the INSL3-LGR8 signaling pathway.

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Published on: August 19, 2011

Area of Science:

  • Reproductive biology
  • Developmental toxicology
  • Endocrinology

Context:

  • Prenatal exposure to endocrine-disrupting chemicals (EDCs) can impact reproductive development.
  • Diethylstilbestrol (DES) is a known EDC with documented effects on the reproductive system.
  • The insulin-like factor 3 (INSL3) and its receptor LGR8 play crucial roles in testicular descent.

Purpose:

  • To investigate the effects of prenatal DES exposure on LGR8 expression in the mouse gubernaculum testis.
  • To examine the impact of exoestrogens on testicular descent in mice.

Summary:

  • Prenatal exposure to DES in mice led to poorly developed gubernacula testes with abnormal morphology.
  • DES exposure altered LGR8 protein and mRNA expression in the gubernaculum testis, with decreased protein and increased mRNA at higher doses.
  • These findings suggest DES interferes with the INSL3-LGR8 signaling pathway, potentially causing cryptorchidism.

Impact:

  • Provides evidence for the mechanism by which DES may induce cryptorchidism.
  • Highlights the sensitivity of the INSL3-LGR8 signaling system to environmental endocrine disruptors.
  • Informs understanding of EDC-induced reproductive abnormalities and their developmental origins.