Comp Biochem Physiol C Toxicol Pharmacol 2009 Aug 01;1502:314-21. doi: 10.1016/j.cbpc.2009.05.013.

Corticosteroids disrupt amphibian metamorphosis by complex modes of action including increased prolactin expression.

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Although thyroid hormones (TH) are the primary morphogens regulating amphibian metamorphosis, other hormones including corticosteroids are known to participate in this regulation. The present study investigated effects of corticosteroids on larval development of the amphibian Xenopus laevis. Premetamorphic tadpoles (stage 51) were treated with aldosterone (ALDO; 100 nM), corticosterone (B; 10, 100, 500 nM) and dexamethasone (DEX; 10, 100, 500 nM) for 21 days and organismal responses were assessed by gross morphology determining stage development, whole body length (WBL), and hind limb length (HLL). B and DEX reduced WBL and HLL and caused abnormal development including the lack of fore limb emergence while ALDO treatment showed no significant effect. Gene expression analyses using RT-PCR revealed up-regulation of prolactin (PRL) in brain, but down-regulation of type III deiodinase in tail tissue induced by the glucocorticoids B and DEX. Additionally, stromelysin-3 transcript in tail tissue was decreased by B. ALDO at 100 nM had no effect on mRNA expression, neither in brain nor in tail tissue. These findings indicate that corticosteroids modulate TH-dependent metamorphosis by complex mechanisms that even include indirect effects triggered by increased PRL mRNA expression.

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Species referenced: Xenopus laevis
Genes referenced: prl.1 prl.2