JBC INTERFERin siRNA transfection reagent

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Volume 272, Number 39, Issue of September 26, 1997 pp. 24679-24683
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Arachidonic Acid Influences Proinflammatory Gene Induction by Stabilizing the Inhibitor-kappa Balpha /Nuclear Factor-kappa B (NF-kappa B) Complex, thus Suppressing the Nuclear Translocation of NF-kappa B

(Received for publication, May 15, 1997, and in revised form, July 8, 1997)

Karl M. Stuhlmeier , Janet J. Kao and Fritz H. Bach

From the Sandoz Center for Immunobiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215

Arachidonic acid (AA), through its myriad metabolites, is involved in inflammation in a number of ways. AA is produced and released by several cell types, including endothelial cells (EC), and acts on a variety of cells. EC activation plays a key role in inflammation presumably by modulating the immune response through up- or down-regulation of several genes. We have previously shown that AA and its nonmetabolizable analogue, 5,8,11,14-eicosatetraynoic acid (ETYA), inhibit up-regulation of proinflammatory genes in EC. In the present study we identify a mechanism to explain the inhibitory effects: AA and ETYA both inhibit the translocation of nuclear factor-kappa B (NF-kappa B) to the nucleus by blocking the degradation of the inhibitor of NF-kappa B (Ikappa B) and thus stabilizing the Ikappa B/NF-kappa B complex. To investigate the mechanism whereby AA inhibits up-regulation of genes encoding proinflammatory mediators, we examined the ability of ETYA to inhibit tumor necrosis factor-alpha (TNF-alpha ) mediated phosphorylation and degradation of Ikappa Balpha . Western blot analysis revealed that preincubation of EC with ETYA for 40 min prior to stimulation with TNF-alpha inhibits the phosphorylation and degradation of Ikappa Balpha . These findings establish a mechanism by which AA inhibits nuclear translocation of NF-kappa B and thereby explaining its modulatory role in the induction of proinflammatory genes.


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Copyright © 1997 by the American Society for Biochemistry and Molecular Biology.