Document Detail


The ameboid phenotype of NG2 (+) cells in the region of apoptotic dentate granule neurons in trimethyltin intoxicated mice shares antigen properties with microglia/macrophages.
MedLine Citation:
PMID:  18023017     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
NG2+, stellate cells present in the adult central nervous system (CNS) have been recently recognized as a distinct glial class, identified as multipotent progenitor cells. Antigenically, they are indistinguishable from oligodendroglia progenitor cells. In response to a variety of CNS insults, these cells become rapidly activated and undergo morphological changes accompanied by increased cellular proliferation. The role they play with respect to injured neurons is not clear. In our studies, we performed immunocytochemical investigations and identified a response of NG2-expressing cells in the model of selective neurodegeneration of murine dentate gyrus granule cells induced by systemic administration of trimethyltin. Dying neurons exhibited features of apoptotic cells. Around the region of neurodegeneration, we observed activation of NG2+ stellate cells and microglia. During the peak of apoptosis, we detected the appearance of NG2+ cells of the ameboid phenotype, intermingled with granule neurons. These cells also expressed markers of microglia/macrophages, OX42- and ED1-recognized antigens, an antigen recognized by O4 antibody-a marker of more differentiated cells of the oligodendroglia lineage and, in some cases, also a protein of mature oligodendroglia adenomatus polyposis coli. They also expressed nestin. Our results suggest that the injury induces a parallel transformation of both the activated glial classes: NG2+ stellate cells and resident microglia, into ameboid cells, sharing properties of both oligodendrocyte and monocyte lineages. These cells may play a role in the phagocytosis. If this assumption is verified by electron microscopy, it would indicate a novel function of NG2 transformed cells under CNS injury conditions.
Authors:
Anna Fiedorowicz; Izabela Figiel; Małgorzata Zaremba; Karolina Dzwonek; Barbara Oderfeld-Nowak
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Glia     Volume:  56     ISSN:  0894-1491     ISO Abbreviation:  Glia     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-06     Completed Date:  2008-03-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8806785     Medline TA:  Glia     Country:  United States    
Other Details:
Languages:  eng     Pagination:  209-22     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2007 Wiley-Liss, Inc.
Affiliation:
Department of Molecular and Cellular Neurobiology, Laboratory of Mechanisms of Neurodegeneration and Neuroprotection, Nencki Institute of Experimental Biology, Polish Academy of Science, Warsaw, Poland.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens / metabolism*
Antigens, CD11b / metabolism
Apoptosis / drug effects*
DNA Fragmentation / drug effects
Dentate Gyrus / cytology*,  drug effects
Ectodysplasins / metabolism
Female
Gene Expression
In Situ Nick-End Labeling / methods
Intermediate Filament Proteins / metabolism
Mice
Mice, Inbred BALB C
Nerve Tissue Proteins / metabolism
Neuroglia / physiology*
Neurons / drug effects*
Neurotoxins / toxicity*
O Antigens / metabolism
Proteoglycans / metabolism*
Time Factors
Trimethyltin Compounds / toxicity*
Grant Support
ID/Acronym/Agency:
3P05AI3422/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Antigens; 0/Antigens, CD11b; 0/Ectodysplasins; 0/Eda protein, mouse; 0/Intermediate Filament Proteins; 0/Nerve Tissue Proteins; 0/Neurotoxins; 0/O Antigens; 0/Proteoglycans; 0/Trimethyltin Compounds; 0/chondroitin sulfate proteoglycan 4; 0/nestin; 1631-73-8/trimethyltin

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


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