Expression of Neuronal Antigens by Astrocytes Derived from EGF-Generated Neuroprogenitor Cells

Previous studies have demonstrated that astrocytes reacting to CNS injury can express antigens normally associated with neurons. The origin of the reactive astrocytes, i.e., whether they are newly differentiated glial cells or preexisting astrocytes somehow triggered to express neuronal markers, rem...

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Bibliographic Details
Published inExperimental neurology Vol. 141; no. 1; pp. 67 - 78
Main Authors Schinstine, Malcolm, Iacovitti, Lorraine
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Inc 01.09.1996
Elsevier
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Summary:Previous studies have demonstrated that astrocytes reacting to CNS injury can express antigens normally associated with neurons. The origin of the reactive astrocytes, i.e., whether they are newly differentiated glial cells or preexisting astrocytes somehow triggered to express neuronal markers, remains difficult to determine using anin vivomodel system. Anin vitromodel may prove more manageable. In the present study, primary brain cultures and EGF-generated neuroprogenitor cells were used to study the expression of neuronal antigens by established (primary) and nascent astrocytes, respectively. Astrocytes derived directly from dissociated mouse brains exhibited a flat morphology typical of type 1 astrocytes. These cells were nestin and GFAP positive and, in most cases, the antigens were colocalized. Primary astrocytes did not appear to express the putative neuronal markers GABA,Tau,or MAP2. Nascent astrocytes derived from EGF-generated progenitor cells showed a similar pattern of GFAP and nestin immunoreactivity. Contrary to primary astrocytes, many GFAP-intensive, stellate astrocytes exhibitedTauand MAP2. These cells also exhibited an intense nestin immunoreactivity. These data suggest that the reactive astrocytes expressing neuronal antigens in response to CNS trauma may be derived from neural progenitor cells rather than from previously differentiated astrocytes.
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content type line 23
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.1996.0140