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Related Experiment Videos

Development of anorectal malformations using etretinate

Y Kubota1, T Shimotake, J Yanagihara

  • 1Division of Surgery, Children's Research Hospital, Kyoto Prefectural University of Medicine, Japan.

Journal of Pediatric Surgery
|February 24, 1998
PubMed
Summary

Retinoid exposure in mice caused anorectal malformations (ARM) by disrupting cell proliferation and apoptosis in the cloacal membrane and dorsocaudal region during embryonic development.

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Area of Science:

  • Developmental biology
  • Teratology
  • Embryology

Background:

  • Anorectal malformations (ARM) are congenital defects with complex etiologies.
  • Retinoids, vitamin A analogues, are known teratogens that can cause developmental abnormalities.

Purpose of the Study:

  • To investigate the role of cell proliferation and programmed cell death (apoptosis) in the pathogenesis of etretinate-induced anorectal malformations in murine embryos.

Main Methods:

  • Pregnant mice were administered etretinate, a retinoid, on day 9 of gestation.
  • Embryos were collected and analyzed for cell proliferation (PCNA) and apoptosis (TUNEL) at various developmental stages.

Main Results:

  • Over 95% of etretinate-exposed embryos exhibited ARM, including rectoprostatic urethral or rectocloacal fistulas.

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  • Defective cell proliferation in the cloacal membrane and excessive apoptosis in the dorsocaudal region were observed in ARM embryos.
  • Normal cell proliferation and apoptosis patterns were noted in the urorectal septum.

    • Conclusions:

    • Impaired cellular dynamics, specifically altered cell proliferation and apoptosis in the cloacal membrane and dorsocaudal region, are implicated in the pathogenesis of certain anorectal malformations.
    • Etretinate-induced disruption of these cellular processes provides a model for studying ARM development.