The relationship of expression of statin, the nuclear protein of nonproliferating cells, to the differentiation and cell cycle of astroglia in cultures and in situ.
Cells in the quiescent, nonproliferative state express a protein, statin, in their nuclei. When the cells reenter the cell cycle, statin disappears and another protein, cyclin, appears. We have examined mouse astroglia at various stages of differentiation in cultures and astroglia in adult mouse brains for the presence of statin. In cultures initiated from the neopallium of newborn mice, the glial fibrillary acidic protein (GFAP)+ stellate astrocytes were statin-negative (statin-) but cyclin-positive (cyclin+). In the same cultures, large flat cells (senescent cells) were statin+ but cyclin-. In frozen sections of the brains of adult mice and in brain smears, GFAP+ astrocytes were statin-. Neither stellate astrocytes grown in cultures for 30 or more days nor astrocytes in adult mouse brain were labeled when pulsed with bromodeoxyuridine (BudR). When astroglia were treated with dibutyrl cyclic adenosine monophosphate (dBcAMP), large stellate cells that closely resemble reactive astrocytes in situ formed. These cells were all statin+ from 11-62 days in vitro; however, reactive astrocytes in mouse neopallium, 4-50 days after a stab wound, were statin-. In colony cultures, senescent cells became statin+, whereas stellate astrocytes and their precursor cells remained statin-. These observations indicate that normal astrocytes both in cultures and in situ retain the potential to divide and probably progress through the cell cycle at a very slow rate.