Peter Kao

Publication Details

  • Cyclosporin A-sensitive calcium signaling represses NF kappa B activation in human bronchial epithelial cells and enhances NF kappa B activation in Jurkat T-cells BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Aoki, Y., Kao, P. N. 1997; 234 (2): 424-431


    Activation of the NFkappaB transcription factor in 16HBE human bronchial epithelial cells was compared with activation of NFkappaB in Jurkat T-cells. An NFkappaB-luciferase reporter gene was activated by phorbol myristyl acetate (PMA) in both cell types. Ionomycin added to PMA (P/I) inhibited NFkappaB activation in epithelial cells and enhanced PMA activation in T-cells. Cyclosporin A (CsA) inhibited calcium signaling in both cell types. Nuclear NFkappaB DNA-binding stimulated with PMA was inhibited with ionomycin in epithelial cells and was enhanced with ionomycin in T-cells; CsA reversed both effects of ionomycin. Cytosolic IkappaB-alpha was regulated identically in both cell types. Thus, calcium activated opposing nuclear signaling pathways in epithelial cells and T-cells. Calcium-mediated repression of NFkappaB in epithelial cells was derepressed by CsA, and this establishes a mechanism through which CsA may exert proinflammatory effects in nonlymphoid cells.

    View details for Web of Science ID A1997XB33100028

    View details for PubMedID 9177287

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