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Am J Physiol Gastrointest Liver Physiol 283: G270-G281, 2002; doi:10.1152/ajpgi.00407.2001
0193-1857/02 $5.00
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Vol. 283, Issue 2, G270-G281, August 2002

INVITED REVIEW
Different modes of NF-kappa B/Rel activation in pancreatic lobules

Hana Algül, Yusuke Tando, Michael Beil, Christoph K. Weber, Claus Von Weyhern, Günter Schneider, Guido Adler, and Roland M. Schmid

Department of Internal Medicine I, University of Ulm, 89081 Ulm, Germany

The eukaryotic transcription factor nuclear factor-kappa B (NF-kappa B)/Rel is activated by a large variety of stimuli. It has been demonstrated that NF-kappa B/Rel is induced during the course of cerulein pancreatitis. Here, we show that NF-kappa B/Rel is differentially activated in pancreatic lobules. Cerulein induces NF-kappa B/Rel via activation of Ikappa B kinase (IKK), which causes degradation of Ikappa Balpha but not Ikappa Bbeta . Tumor necrosis factor-alpha -mediated IKK activation leads to Ikappa Balpha and Ikappa Bbeta degradation. In contrast, oxidative stress induced by H2O2 activates NF-kappa B/Rel independent of IKK activation and Ikappa Balpha degradation; instead Ikappa Balpha is phosphorylated on tyrosine. H2O2 but not cerulein-mediated NF-kappa B/Rel activation can be blocked by stabilizing microtubules with Taxol. Inhibition of tubulin polymerization with nocodazole causes NF-kappa B/Rel activation in pancreatic lobules. These results propose three different pathways of NF-kappa B/Rel activation in pancreatic acinar cells. Furthermore, these data demonstrate that microtubules play a key role in IKK-independent NF-kappa B/Rel activation following oxidative stress.

acute pancreatitis; inhibitor protein Ikappa B; Ikappa B kinase; inflammation; hydrogen peroxide; tyrosine phosphorylation; cytokines; cerulein


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[Abstract] [Full Text] [PDF]


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