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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Arachidonic acid influences proinflammatory gene induction by stabilizing the inhibitor-kappaBalpha/nuclear factor-kappaB (NF-kappaB) complex, thus suppressing the nuclear translocation of NF-kappaB.

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-kappaB (NF-kappaB) to the nucleus by blocking the degradation of the inhibitor of NF-kappaB (IkappaB) and thus stabilizing the IkappaB/NF-kappaB 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 IkappaBalpha. 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 IkappaBalpha. These findings establish a mechanism by which AA inhibits nuclear translocation of NF-kappaB and thereby explaining its modulatory role in the induction of proinflammatory genes.[1]


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