Astroglial cells play an important role in orchestrating the migration and positioning of neurons during central nervous system development. Primary astroglia, as well as astrocytoma cells will extend long stable processes when co-cultured with granule neurons. In order to determine the function of the glial fibrillary acidic protein (GFAP), the major intermediate filament protein in astroglia and astrocytoma cells, we suppressed the expression of GFAP by stable transfection of an anti-sense GFAP construct in human astrocytoma U251MG cells. The resulting AS2-U251 cells can no longer extend stable processes in the presence of granule neurons. To show that this effect is due specifically to the absence of GFAP, we reintroduced a fully encoding rat brain GFAP cDNA into these AS2-U251 cells. The resulting rat GFAP appeared as a filamentous network and the reexpression of GFAP rescued the ability of these astrocytoma cells to form stable processes when co-cultured with neurons. From these results, it is clear that the glial specific intermediate filament protein, GFAP, is required for process extension of these astrocytoma cells in response to granule neurons.
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1 November 1994
Article|
November 01 1994
Reexpression of glial fibrillary acidic protein rescues the ability of astrocytoma cells to form processes in response to neurons.
W J Chen,
W J Chen
Department of Pathology, Columbia University College of Physicians and Surgeons, New York 10032.
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R K Liem
R K Liem
Department of Pathology, Columbia University College of Physicians and Surgeons, New York 10032.
Search for other works by this author on:
W J Chen
Department of Pathology, Columbia University College of Physicians and Surgeons, New York 10032.
R K Liem
Department of Pathology, Columbia University College of Physicians and Surgeons, New York 10032.
Online ISSN: 1540-8140
Print ISSN: 0021-9525
J Cell Biol (1994) 127 (3): 813–823.
Citation
W J Chen, R K Liem; Reexpression of glial fibrillary acidic protein rescues the ability of astrocytoma cells to form processes in response to neurons.. J Cell Biol 1 November 1994; 127 (3): 813–823. doi: https://doi.org/10.1083/jcb.127.3.813
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