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Originally published In Press as doi:10.1074/jbc.M101315200 on April 17, 2001

J. Biol. Chem., Vol. 276, Issue 25, 22461-22467, June 22, 2001
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Endoplasmic Reticulum D-myo-Inositol 1,4,5-Trisphosphate-sensitive Stores Regulate Nuclear Factor-kappa B Binding Activity in a Calcium-independent Manner*

Gordon W. GlaznerDagger §, Simonetta CamandolaDagger , Jonathan D. Geiger§, and Mark P. MattsonDagger ||**

From the Dagger  Laboratory of Neurosciences, NIA Gerontology Research Center, National Institutes of Health, Baltimore, Maryland 21224, the § Department of Pharmacology and Therapeutics, University of Manitoba Faculty of Medicine, Winnipeg, Manitoba R3E 0T6, Canada, and the || Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

The transcription factor nuclear factor-kappa B (NF-kappa B) plays critical roles in neuronal survival and plasticity and in activation of immune responses. The activation of NF-kappa B has been closely associated with changes in intracellular calcium levels, but the relationship between the two remains unclear. Here we report that inhibition of endoplasmic reticulum (ER) D-myo-inositol 1,4,5-trisphosphate (IP3)-gated calcium release caused decreased basal NF-kappa B DNA-binding activity in cultured rat cortical neurons. Activation of NF-kappa B in response to tumor necrosis factor-alpha and glutamate was completely abolished when IP3 receptors were blocked, and NF-kappa B activation in response to depletion of ER calcium by thapsigargin treatment was also decreased by IP3 receptor blockade. We further investigated the relationship between IP3 receptor activation and NF-kappa B activity using a cell-free system. Microsomes enriched in the ER were isolated from adult rat cerebral cortex, resuspended, and treated with agents that induce or inhibit ER calcium release. They were then recentrifuged, and the supernatant was added to cytoplasmic extract isolated from the same source tissue. We found that microsomes released an NF-kappa B-stimulating signal in response to activation of IP3 receptors or inhibition of the ER Ca2+-ATPase, but not in response to ryanodine. Studies of intact cells and cell-free preparations indicated that the signal released from the ER was not calcium and was heat- and trypsin-sensitive. Our data suggest that activation of IP3 receptors is required for a major component of both constitutive and inducible NF-kappa B binding activity in neurons and that decreasing ER intraluminal calcium levels triggers release of a diffusible NF-kappa B-activating signal from the ER.

* This work was supported by National Institutes of Health Grants NRSA467305 (to G. W. G.) and NS39184 (to J. D. G.) and by NIA, National Institutes of Health.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These two authors contributed equally to this work.

** To whom correspondence should be addressed: Lab. of Neurosciences, NIA, GRC 4F02, 5600 Nathan Shock Dr., Baltimore, MD 21224. Tel.: 410-558-8463; Fax: 410-558-8465; E-mail: mattsonm@grc.nia.nih.gov.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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