Document Detail

Conditional inactivation of glucocorticoid receptor gene in dopamine-beta-hydroxylase cells impairs chromaffin cell survival.
MedLine Citation:
PMID:  19036879     Owner:  NLM     Status:  MEDLINE    
Glucocorticoid hormones (GCs) have been thought to determine the fate of chromaffin cells from sympathoadrenal progenitor cells. The analysis of mice carrying a germ line deletion of the glucocorticoid receptor (GR) gene has challenged these previous results because the embryonic development of adrenal chromaffin cells is largely unaltered. In the present study, we have analyzed the role of GC-dependent signaling in the postnatal development of adrenal chromaffin cells by conditional inactivation of the GR gene in cells expressing dopamine-beta-hydroxylase, an enzyme required for the synthesis of noradrenaline and adrenaline. These mutant mice are viable, allowing to study whether in the absence of GC signaling further development of the adrenal medulla is affected. Our analysis shows that the loss of GR leads not only to the loss of phenylethanolamine-N-methyl-transferase expression and, therefore, to inhibition of adrenaline synthesis, but also to a dramatic reduction in the number of adrenal chromaffin cells. We provide evidence that increased apoptotic cell death is the main consequence of GR loss. These findings define the essential role of GCs for survival of chromaffin cells and underscore the specific requirement of GCs for adrenergic chromaffin cell differentiation and maintenance.
Rosanna Parlato; Christiane Otto; Jan Tuckermann; Stefanie Stotz; Sylvia Kaden; Hermann-Josef Gröne; Klaus Unsicker; Günther Schütz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-11-26
Journal Detail:
Title:  Endocrinology     Volume:  150     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-24     Completed Date:  2009-04-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1775-81     Citation Subset:  AIM; IM    
Department of Molecular Biology of the Cell I, German Cancer Research Center, Heidelberg, Germany.
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MeSH Terms
Adrenal Glands / cytology,  metabolism
Adrenal Medulla / metabolism,  pathology
Cell Survival / genetics*
Cells, Cultured
Chromaffin Cells / cytology*,  metabolism*
Dopamine beta-Hydroxylase / metabolism*
In Situ Nick-End Labeling
Phenylethanolamine N-Methyltransferase / metabolism
Receptors, Glucocorticoid / genetics*,  physiology*
Reg. No./Substance:
0/Receptors, Glucocorticoid; EC beta-Hydroxylase; EC N-Methyltransferase

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