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Biochem Biophys Res Commun. 1997 May 19;234(2):424-31.

Cyclosporin A-sensitive calcium signaling represses NFkappaB activation in human bronchial epithelial cells and enhances NFkappaB activation in Jurkat T-cells.

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  • 1Pulmonary and Critical Care Medicine, Stanford University Medical Center, California 94305-5236, USA.


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.

[PubMed - indexed for MEDLINE]
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