Journal
MOLECULAR ENDOCRINOLOGY
Volume 25, Issue 8, Pages 1280-1288Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2009-0380
Keywords
-
Categories
Funding
- Deutsche Forschungsgemeinschaft [SFB 488, SFB 636]
- European Union [LSHM-CT-2005-018652 (CRESCENDO)]
- Bundesministerium fur Bildung und Forschung (BMBF) [FZK 01GS08153, 01GS08142]
- Hepato-Sys project [0313074C]
- Helmholtz Gemeinschaft Deutscher Forschungszentren through Initiative CoReNe (Network III) [E2]
- Alliance HelMA [HA-215]
- Deutsche Krebshilfe [108567]
Ask authors/readers for more resources
Corticosteroid treatment is an established therapy for preterm infants, and germline inactivation of the glucocorticoid receptor (GR) gene in the mouse leads to respiratory failure and postnatal lethality. Although glucocorticoids have been thought to critically act in epithelial cells inducing the functional maturation of the lung, inactivation of the GR gene exclusively in the epithelium of the developing murine lung did not impair survival. In contrast, mice lacking GR specifically in mesenchyme-derived cells displayed a phenotype strongly reminiscent of GR knockout animals and died immediately after birth. Detailed analysis of gene expression allows the conclusion that GR acts in cells of the fibroblast lineage controlling their proliferation rate and the composition of the extracellular matrix. (Molecular Endocrinology 25: 1280-1288, 2011)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available