Dm. Hallam et Le. Maroun, ANTI-GAMMA INTERFERON CAN PREVENT THE PREMATURE DEATH OF TRISOMY-16 MOUSE CORTICAL-NEURONS IN CULTURE, Neuroscience letters, 252(1), 1998, pp. 17-20
Previous reports have indicated that human trisomy 21 and mouse trisom
y 16 neurons exhibit decreased viability in culture when compared to e
uploid control cultures and that trisomic cells are significantly more
sensitive to the anti-cellular effects of the interferons. In the stu
dy reported here, cortical neurons from euploid and trisomy 16 mouse f
etuses were treated with either anti-gamma-interferon or non-specific
IgG and neuron morphology and viability measured photographically. The
addition of anti-gamma-interferon IgG to the culture media had no eff
ect on euploid neurons, but significantly increased trisomy neuron via
bility throughout the 5-day culture period. Assay of both DNA fragment
ation and phosphatidylserine externalization suggested that the trisom
ic neurons were undergoing apoptosis at a significantly higher rate th
an their euploid counterparts and that this increase in apoptosis coul
d be almost completely prevented by addition of either ligand purified
monoclonal or ligand purified polyclonal anti-gamma-interferon IgG. T
aken together, these data suggest that endogenous interferon plays an
important role in the premature death of the trisomy neuron. (C) 1998
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