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—The transcriptional regulatory protein nuclear factor-κB (NF-κB) participates in the control of gene expression of many modulators of the inflammatory and immune responses, including the adhesion molecules E-selectin and intercellular adhesion molecule-1 (ICAM-1). NF-κB is found in the cytoplasm complexed with its inhibitory protein IκB. On activation, IκB is phosphorylated and degraded, thereby freeing NF-κB for translocation to the nucleus. We have generated populations of endothelial cells expressing wild-type and a proteolysis-resistant mutation of IκB that is lacking the 36 N-terminal amino acids (IκBΔN) in order to examine the effects of expression of the mutated IκB on tumor necrosis factor-α (TNF-α)–induced E-selectin and ICAM-1 expression. Wild-type and IκBΔN were introduced into primary endothelial cells using retrovirus infection followed by selection with G418. The IκBΔN protein remained at untreated control levels in endothelial cells treated with TNF-α and also remained complexed with the NF-κB family member p65. Furthermore, TNF-α–induced NF-κB DNA binding activity was inhibited in the population of endothelial cells expressing IκBΔN. That population of cells was also refractory to upregulation of E-selectin and ICAM-1 after treatment with TNF-α. The use of a truncated IκBα protein to prevent NF-κB–mediated gene expression provides a novel and specific approach for investigating the role of NF-κB in processes associated with adhesion molecule expression during inflammation.

Inhibition of Nuclear Factor-κB–Mediated Adhesion Molecule Expression in Human Endothelial Cells