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    
Abstract/OtherAbstract:
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.
Authors:
Rosanna Parlato; Christiane Otto; Jan Tuckermann; Stefanie Stotz; Sylvia Kaden; Hermann-Josef Gröne; Klaus Unsicker; Günther Schütz
Related Documents :
7364659 - The presence of erythroid cells in the thymus gland of man.
11443739 - Initiation of cell locomotility is a morphogenetic checkpoint in thyroid epithelial cel...
60869 - Calcitonin cells and unusual follicles of the thyroid of the indian grey mongoose, herp...
15648739 - Transplantation of cultured salivary gland cells into an atrophic salivary gland.
17535349 - Interaction between chromaffin and sustentacular cells in adrenal medulla of viscacha (...
2773669 - Developing rat cerebellum--iii. effects of abnormal thyroid states and undernutrition o...
22171079 - Isometric size-scaling of metabolic rate and the size abundance distribution of phytopl...
18492269 - Straw blood cell count, growth, inhibition and comparison to apoptotic bodies.
810469 - Gentamicin accumulation by sensitive strains of escherichia coli and pseudomonas aerugi...
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    
Affiliation:
Department of Molecular Biology of the Cell I, German Cancer Research Center, Heidelberg, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adrenal Glands / cytology,  metabolism
Adrenal Medulla / metabolism,  pathology
Animals
Cell Survival / genetics*
Cells, Cultured
Chromaffin Cells / cytology*,  metabolism*
Dopamine beta-Hydroxylase / metabolism*
Immunohistochemistry
In Situ Nick-End Labeling
Mice
Phenylethanolamine N-Methyltransferase / metabolism
Receptors, Glucocorticoid / genetics*,  physiology*
Chemical
Reg. No./Substance:
0/Receptors, Glucocorticoid; EC 1.14.17.1/Dopamine beta-Hydroxylase; EC 2.1.1.28/Phenylethanolamine N-Methyltransferase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Impaired bacterial clearance in type 3 deiodinase-deficient mice infected with Streptococcus pneumon...
Next Document:  Hexosamine biosynthesis pathway flux contributes to insulin resistance via altering membrane phospha...