A sustained elevation in retinoic acid receptor-beta 2 mRNA and protein occurs during retinoic acid-induced fetal dysmorphogenesis.
Mech Dev
; 45(3): 243-53, 1994 Mar.
Article
em En
| MEDLINE
| ID: mdl-8011556
ABSTRACT
We have previously shown that oral treatment of pregnant mice with all-trans retinoic acid (RA) at doses which cause 100% fetal dysmorphogenesis results in a rapid elevation in the mRNA of one specific isoform of the RA receptor-beta, RAR-beta 2, in susceptible embryonic regions. To further investigate the involvement of RAR-beta 2 mRNA in teratogenesis, we have examined its expression in mouse embryos exposed to marginal/nonteratogenic and teratogenic dosing regimens of both 13-cis RA and all-trans RA. We have found that the mere elevation in embryonic RAR-beta 2 mRNA levels and free retinoid levels is not sufficient to result in dysmorphogenesis. Rather, retinoid-induced dysmorphogenesis of embryos appears to occur only when RAR-beta 2 mRNA and unbound retinoid levels remain elevated for at least 6-9 h following retinoid treatment resulting in a significant and prolonged elevation in RAR-beta protein levels.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Teratogênicos
/
Tretinoína
/
RNA Mensageiro
/
Receptores do Ácido Retinoico
Limite:
Animals
Idioma:
En
Revista:
Mech Dev
Ano de publicação:
1994
Tipo de documento:
Article