Document Detail

Astroglia-derived retinoic acid is a key factor in glia-induced neurogenesis.
MedLine Citation:
PMID:  17438145     Owner:  NLM     Status:  MEDLINE    
Astroglial cells are essential components of the neurogenic niches within the central nervous system. Emerging evidence suggests that they are among the key regulators of postnatal neurogenesis. Although astrocytes have been demonstrated to possess the potential to instruct stem cells to adopt a neuronal fate, little is known about the nature of the glia-derived instructive signals. Here we propose that all-trans retinoic acid, one of the most powerful morphogenic molecules regulating neuronal cell fate commitment, may be one of the glia-derived factors directing astroglia-induced neurogenesis. According to data obtained from several complementary approaches, we show that cultured astrocytes express the key enzyme mRNAs of retinoic acid biosynthesis and actively produce all-trans retinoic acid. We show that blockage of retinoic acid signaling by the pan-RAR antagonist AGN193109 prevents glia-induced neuron formation by noncommitted stem cells. Therefore, we provide strong in vitro evidence for retinoic acid action in astroglia-induced neuronal differentiation.
Z Környei; E Gócza; R Rühl; B Orsolits; E Vörös; B Szabó; B Vágovits; E Madarász
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-04-16
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  21     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-08-01     Completed Date:  2007-11-05     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2496-509     Citation Subset:  IM    
Institute of Experimental Medicine, Hungarian Academy of Sciences, Laboratory of Cellular and Developmental Neurobiology, H-1083 43 Szigony U., Budapest, Hungary.
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MeSH Terms
Animals, Newborn
Astrocytes / physiology*
Brain / growth & development*
Cell Differentiation
Central Nervous System / physiology
Genes, Reporter
Mice, Transgenic
Neuroglia / physiology*
Neurons / cytology,  physiology
Stem Cells / physiology
Tretinoin / physiology*
Tumor Suppressor Protein p53 / deficiency
Reg. No./Substance:
0/Tumor Suppressor Protein p53; 302-79-4/Tretinoin

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

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