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Biochem Biophys Res Commun. 1994 Aug 30;203(1):149-55.

Interleukin-1 beta induced activation of NF-kappa B in insulin producing RINm5F cells is prevented by the protease inhibitor N alpha-p-tosyl-L-lysine chloromethylketone.

Author information

1
Department of Medical Cell Biology, Uppsala University, Sweden.

Abstract

The cytokine Interleukin-1 beta (IL-1 beta) is known to exert cytotoxic effects upon rodent beta-cells in vitro by inducing nitric oxide production and has therefore been suggested to play a role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). Using the insulin producing rat cell line RINm5F and an electrophoretic mobility shift assay (EMSA), it was presently found that IL-1 beta induced a rapid activation (5 min) of the transcription factor NF-kappa B and that this event was prevented by the protease inhibitor N alpha-p-tosyl-L-lysine chloromethylketone (TLCK). TLCK prevented also IL-1 beta induced nitric oxide production. It is concluded that NF-kappa B activation may be a necessary signal for IL-1 beta induced beta-cell damage and that this process can be modulated by specific protease and NF-kappa B inhibitors.

PMID:
8074648
DOI:
10.1006/bbrc.1994.2161
[Indexed for MEDLINE]

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