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J. Biol. Chem., Vol. 277, Issue 33, 29662-29668, August 16, 2002

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Norepinephrine Increases IB Expression in Astrocytes^*

Vitaliy Gavrilyuk, Cinzia Dello Russo^§, Michael T. Heneka^¶, Dale Pelligrino, Guy Weinberg, and Douglas L. Feinstein^**

From the  Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois 60612, ^¶ Department of Neurology, University of Bonn, Bonn 50236, Germany, and  Veterans Affairs Chicago Health Care System West Side Division, Chicago, Illinois 60680

The neurotransmitter norepinephrine (NE) can inhibit inflammatory gene expression in glial cells; however, the mechanisms involved are not clear. In primary astrocytes, NE dose-dependently increased the expression of inhibitory IB protein accompanied by an increase in steady state levels of IB mRNA. Maximal increases were observed at 30-60 min for the mRNA and at 4 h for protein, and these effects were mediated by NE binding to -adrenergic receptors. NE activated a 1.3-kilobase IB promoter transfected into astrocytes or C6 glioma cells, and this activation was prevented by a -antagonist and by protein kinase A inhibitors but not by an NFB inhibitor. NE increased IB protein in both the cytosolic and the nuclear fractions, suggesting an increase in nuclear uptake of IB. IB was detected in the frontal cortex of normal adult rats, and its levels were reduced if central NE levels were depleted by lesion of the locus ceruleus. The reduction of brain IB levels was paralleled by increased inflammatory responses to lipopolysaccharide. These results demonstrate that IB expression is regulated by NE at both transcriptional and post-transcriptional levels, which could contribute to the observed anti-inflammatory properties of NE in vitro and in vivo.

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