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βA amyloid peptide (25-35) induced APP expression in cultured astrocytes

✍ Scribed by M.T. Moreno-Flores; O. Salinero; F. Wandosell

Publisher
John Wiley and Sons
Year
1998
Tongue
English
Weight
282 KB
Volume
52
Category
Article
ISSN
0360-4012

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✦ Synopsis

Alzheimer's disease is characterized by an accumulation of senile or neuritic plaques surrounded by activated microglia and reactive astrocytes, the cell processes of which are frequently in contact with the amyloid core. The major component of this amyloid deposit is the amyloid peptide (␤A or ␤A4). These reactive glia are characterized by their hypertrophic phenotype and by the overexpression of some molecules such as glial fibrillary acidic protein and the amyloid precursor protein (APP).

The purpose of this work was to analyze whether APP expression was modified in astrocytes by the presence of ␤A peptide. To study this, the effects of ␤-Amyloid (25-35) on cultured astrocytes were analyzed and compared with those of a scrambled peptide. Our data indicated that the addition of previously polymerized ␤A peptide induced a marked morphological change from a flat, polygonal shape to a stellated, process-bearing morphology. This change occurred with an increase in APP immunoreactivity that is dependent of phosphatases PP2A or PP1, since it was inhibited by okadaic acid. Upregulation of APP protein expression appears to be mainly nontranscriptional, because the increase of APP protein precedes the increase of mRNA expression. The analysis of several APP isoforms indicated that this increment is not due to changes of a single isoform.

Our data may correlate with some in vivo reports of astrocytic APP induction after brain insult, suggesting an important role for ␤A peptide in the initial process and/or maintenance of the reactive phenotype in vivo.

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