| First Author | Zhang M | Year | 2011 |
| Journal | Mech Dev | Volume | 128 |
| Issue | 7-10 | Pages | 368-75 |
| PubMed ID | 21824517 | Mgi Jnum | J:178360 |
| Mgi Id | MGI:5298183 | Doi | 10.1016/j.mod.2011.07.003 |
| Citation | Zhang M, et al. (2011) Disruption of beta-arrestins blocks glucocorticoid receptor and severely retards lung and liver development in mice. Mech Dev 128(7-10):368-75 |
| abstractText | In this study, the role of beta-arrestin 1 and beta-arrestin 2 in fetal lung and liver development was examined using Arrb1(-/-)Arrb2(-/-) mouse embryos. beta-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 type II pneumocytes of 18.5day 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 the beta-arrestin signaling pathway involved in regulation of lung and liver development. However, no obvious changes in GR expression following in vitro modulation of beta-arrestin 1/2 indicated the existence of an indirect regulatory relationship between GR and the beta-arrestin signaling pathway. |
