Cytokine‐induced expression of type II nitric oxide synthase in astrocytes is downregulated by ATP and glutamate

Cytokine‐induced expression of type II nitric oxide synthase in astrocytes is downregulated by... Combinations of cytokines and/or phorbol ester induce expression of Type II nitric oxide synthase (NOS) mRNA in astrocyte cultures via protein kinase mediated pathways (Simmons and Murphy: GLIA 11:227, 1994; Feinstein et al.: J Neurochem 62:811,1994). Agonists that activate receptors linked to protein kinases did not reproduce this effect of cytokines in astrocytes. On the contrary, ATP and glutamate treatment of astrocytes prior to a combination of interleukin‐1ß and interferon‐γ markedly reduced (30–50%) subsequent NOS mRNA expression. The effect was not seen if treatment coincided with or followed cytokine activation, suggesting that ATP and glutamate were not destabilizing NOS mRNA. The effects of ATP and glutamate were additive and could be mimicked by selective receptor agonists, but were insensitive to a specific inhibitor of protein kinase C. The inhibition of cytokine‐induced NOS mRNA expression caused by these agents was not the result of interference with the activation/translocation of nuclear factor‐ϰB by interleukin‐1ß. These results suggest that exposure of astrocytes to ATP and glutamate, both of which increase markedly in a variety of neuropathologies, could modulate the subsequent responsiveness of these cells to NOS‐inducing stimuli. As such, this may be an important regulatory mechanism in the expression of Type II NOS in vivo. © 1995 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Cytokine‐induced expression of type II nitric oxide synthase in astrocytes is downregulated by ATP and glutamate

Glia, Volume 15 (1) – Sep 1, 1995

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Publisher
Wiley
Copyright
Copyright © 1995 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
DOI
10.1002/glia.440150109
pmid
8847103
Publisher site
See Article on Publisher Site

Abstract

Combinations of cytokines and/or phorbol ester induce expression of Type II nitric oxide synthase (NOS) mRNA in astrocyte cultures via protein kinase mediated pathways (Simmons and Murphy: GLIA 11:227, 1994; Feinstein et al.: J Neurochem 62:811,1994). Agonists that activate receptors linked to protein kinases did not reproduce this effect of cytokines in astrocytes. On the contrary, ATP and glutamate treatment of astrocytes prior to a combination of interleukin‐1ß and interferon‐γ markedly reduced (30–50%) subsequent NOS mRNA expression. The effect was not seen if treatment coincided with or followed cytokine activation, suggesting that ATP and glutamate were not destabilizing NOS mRNA. The effects of ATP and glutamate were additive and could be mimicked by selective receptor agonists, but were insensitive to a specific inhibitor of protein kinase C. The inhibition of cytokine‐induced NOS mRNA expression caused by these agents was not the result of interference with the activation/translocation of nuclear factor‐ϰB by interleukin‐1ß. These results suggest that exposure of astrocytes to ATP and glutamate, both of which increase markedly in a variety of neuropathologies, could modulate the subsequent responsiveness of these cells to NOS‐inducing stimuli. As such, this may be an important regulatory mechanism in the expression of Type II NOS in vivo. © 1995 Wiley‐Liss, Inc.

Journal

GliaWiley

Published: Sep 1, 1995

References

  • Induction of nitric oxide synthase in demyelinating regions of multiple sclerosis brains
    Bo, Bo; Dawson, Dawson; Wesselingh, Wesselingh; Mork, Mork; Choi, Choi; King, King; Hanley, Hanley; Trapp, Trapp
  • ATP‐evoked arachidonic acid mobilization in astrocytes is via a P 2Y ‐purinergic receptor
    Bruner, Bruner; Murphy, Murphy
  • Electrophysiological behavior of microglia
    Kettenmann, Kettenmann; Banati, Banati; Walz, Walz
  • Duration of expression of inducible nitric oxide synthase in glial cells
    Park, Park; Murphy, Murphy
  • Cytokines regulate L‐arginine‐dependent cyclic GMP production in rat glial cells
    Simmons, Simmons; Murphy, Murphy

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