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Disruption of β-arrestins blocks glucocorticoid receptor and severely retards lung and liver development in mice

【摘要】:正In this study,the role of β-arrestin 1 andβ-arrestin 2 in fetal lung and liver development was examined using Arrb1~(-/-) Arrb2~(-/-) mouse embryos.β-arrestin 1/2 dual-null mice died shortly after birth and morphological examination revealed an obvious pulmonary hypoplasia and severe hepatic impairment. Western blot analysis demonstrated that GR protein levels in Arrb1~(-/-)Arrb2~(-/-) lung and liver tissues were significantly decreased compared to wild type embryos.Expression of GR proteins was confirmed in the nuclei of typeⅡpneumocytes of 18.5 day embryos(E18.5) by immunofluorescence.The production of hepatic glucose and mRNA level of gluconeogenic enzymes were dramatically reduced in E18.5 Arrb1~(-/-)Arrb2~(-/-) liver.These results suggest that GR is an important downstream effector of theβ-arrestin signaling pathway involved in regulation of lung and liver development.However,no obvious changes in GR expression were detected following in vitro modulation ofβ-arrestin 1/2,thus indicating the existence of an indirect regulatory relationship between GR and theβ-arrestin signaling pathway.

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