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In Human Fetal Astrocytes Exposure to Interleukin‐1β Stimulates Acquisition of the GD3 + Phenotype and Inhibits Cell Division
Author(s) -
Lee Sunhee C.,
Liu Wei,
Dickson Dennis W.,
Brosnan Celia F.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64041800.x
Subject(s) - astrocyte , bromodeoxyuridine , population , cell sorting , biology , neuroglia , glial fibrillary acidic protein , flow cytometry , immunocytochemistry , microbiology and biotechnology , cell culture , stimulation , cell division , cell growth , microglia , cell , endocrinology , immunology , medicine , central nervous system , biochemistry , immunohistochemistry , genetics , inflammation , environmental health
In human astrocyte cultures established from second‐trimester fetal brain tissue, ∼5–10% of total astrocyte population in unstimulated cultures were GD3 + /glial fibrillary acidic protein (GFAP) + . The GD3 + cells were always GFAP + and grew as flat, highly spread cells but changed to process‐bearing cells after interleukin‐1β (IL‐1β) stimulation. It is interesting that IL‐1β, a known mitogen for rat astrocytes, suppressed human fetal astrocyte proliferation as determined by [ 3 H]thymidine incorporation, bromodeoxyuridine (BrdU) labeling, and cell counting. The GD3 + population, however, consistently increased in absolute number after IL‐1β stimulation, in a dose‐ and time‐dependent manner. The IL‐1β‐mediated increase in number of GD3 + astrocytes was independent of initial cell density or serum concentration. By flow cytometry, IL‐1β enhanced both the mean fluorescence intensity and the percentage of GD3 + cells. To investigate whether the increase in GD3 + astrocyte cell number was due to proliferation of preexisting GD3 + astrocytes or due to conversion of GD3 − to GD3 + cells, we performed BrdU/GD3 double immunocytochemistry. BrdU/GD3 double‐positive cells were extremely rare in both control and IL‐1β‐stimulated cultures. Moreover, an increase in number of GD3 + astrocytes was still observed in control and IL‐1β‐stimulated cultures where GD3 + cells had been initially eliminated by cell sorting. These results indicate that GD3 + astrocytes in human fetal culture may represent a postmitotic, differentiated, distinct phenotype.