Inhibition of glucocorticoid-induced cataracts in chick embryos by RU486: A model for studies on the role of glucocorticoids in development

Hideo Nishigori, Hiroshi Kosano, Izumi O. Umeda, Hidekazu Nishigori

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Cataract formation can be induced by glucocorticoid treatment of developing chick embryos. We show here that this response can be blocked very effectively by use of the antiglucocorticoid RU486. When dexamethasone (0.02 μmol/egg) was administered from day 13 to 16 chick embryos, their lenses (over 80%) became cataract (GC-induced cataract; stage IV-V) within 48 hrs. These GC-induced cataract formations were prevented by administration of RU486 (0.2 μmol/egg) on day 9. However, RU486 also inhibited hatching even though the embryos showed normal growth and appearance. In control embryos, more than 90% live chicks (39/42 chicks) were hatched on day 22. Chick embryos treated with RU486 on day 9 appeared to grow normally until 21, but could not hatch. When chick embryos were treated with RU486 (0.2 μmol/egg) on day 15, more than 80% live embryos (34/42 chicks) were hatched on day 23 with normal appearance, which was one day delay comparing to the control. These observations indicate that endogenous glucocorticoids are involved in the ability to hatch and that RU486 is able to block the actions of endogenous glucocorticoids. Thus, RU486 should be a very useful tool for studies on other biochemical and physiological aspects of chick embryo development that are under glucocorticoid control.

Original languageEnglish
Pages (from-to)3027-3033
Number of pages7
JournalLife Sciences
Volume75
Issue number25
DOIs
Publication statusPublished - 2004 Nov 5

Keywords

  • Cataract
  • Delayed hatch
  • Developing chick embryo
  • Dexamethasone
  • Glucocorticoid
  • Mifepristone
  • RU486

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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