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Volume 16, Number 19,
Issue of October 1, 1996
pp. 5914-5922
Copyright ©1996 Society for Neuroscience
Cholinergic Stimulation of AP-1 and NF B Transcription Factors
Is Differentially Sensitive to Oxidative Stress in SH-SY5Y
Neuroblastoma: Relationship to Phosphoinositide Hydrolysis
Received April 23, 1996; revised July 1, 1996; accepted July 8, 1996.
Xiaohua Li,
Ling Song, and
Richard S. Jope
Department of Psychiatry and Behavioral Neurobiology, University of
Alabama at Birmingham, Birmingham, Alabama 35294-0017
Oxidative stress appears to contribute to neuronal dysfunction in a
number of neurodegenerative conditions, notably including Alzheimer's
disease, in which cholinergic receptor-linked signal transduction
activity is severely impaired. To test whether oxidative stress could
contribute to deficits in cholinergic signaling, responses to carbachol
were measured in human neuroblastoma SH-SY5Y cells exposed to
H2O2. DNA binding activities of two
transcription factors that are respondent to oxidative conditions, AP-1
and NF B, were measured in nuclear extracts.
H2O2 and carbachol individually induced dose-
and time-dependent increases in AP-1 and NFB. In contrast, when
given together, H2O2 concentration dependently
(30-300 µM) inhibited the increase after carbachol in
AP-1. Carbachol's stimulation of NFB was not inhibited except with
a high concentration (300 µM) of
H2O2, which was associated with impaired
activation of protein kinase C. Lower concentrations of
H2O2 (30-300 µM) inhibited
carbachol-induced [3H]phosphoinositide hydrolysis, and
this inhibition correlated (r = 0.95) with the
inhibition of carbachol-induced AP-1. Activation of
[3H]phosphoinositide hydrolysis by the calcium ionophore
ionomycin was unaffected by H2O2, indicating
that phospholipase C and phosphoinositides were impervious to this
treatment. In contrast, activation with NaF of G-proteins coupled to
phospholipase C was concentration dependently inhibited by
H2O2, indicating impaired G-protein function.
These effects of H2O2 are similar to signaling
impairments reported in Alzheimer's disease brain, which involve
deficits in receptor- and G-protein-stimulated phosphoinositide
hydrolysis, but not phospholipase C activity. Thus, these findings
indicate that oxidative stress may contribute to impaired
phosphoinositide signaling in neurological disorders in which oxidative
stress occurs, and that oxidative stress can differentially influence
transcription factors activated by cholinergic stimulation.
Key words:
oxidative stress;
transcription factors;
AP-1;
NFB;
phosphoinositide;
cholinergic signaling
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