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

نویسندگان

  • HANA ALGÜL
  • YUSUKE TANDO
  • MICHAEL BEIL
  • CHRISTOPH K. WEBER
  • Yusuke Tando
  • Michael Beil
  • Christoph K. Weber
  • Claus Von Weyhern
  • Günter Schneider
  • Guido Adler
چکیده

Algül, Hana, Yusuke Tando, Michael Beil, Christoph K. Weber, Claus Von Weyhern, Günter Schneider, Guido Adler, and Roland M. Schmid. Different modes of NFB/Rel activation in pancreatic lobules. Am J Physiol Gastrointest Liver Physiol 283: G270–G281, 2002; 10.1152/ajpgi.00407.2001.—The eukaryotic transcription factor nuclear factorB (NFB)/Rel is activated by a large variety of stimuli. It has been demonstrated that NFB/Rel is induced during the course of cerulein pancreatitis. Here, we show that NFB/Rel is differentially activated in pancreatic lobules. Cerulein induces NFB/Rel via activation of I B kinase (IKK), which causes degradation of I B but not I B . Tumor necrosis factor-mediated IKK activation leads to I B and I B degradation. In contrast, oxidative stress induced by H2O2 activates NFB/Rel independent of IKK activation and I B degradation; instead I B is phosphorylated on tyrosine. H2O2 but not cerulein-mediated NFB/Rel activation can be blocked by stabilizing microtubules with Taxol. Inhibition of tubulin polymerization with nocodazole causes NFB/Rel activation in pancreatic lobules. These results propose three different pathways of NFB/Rel activation in pancreatic acinar cells. Furthermore, these data demonstrate that microtubules play a key role in IKK-independent NFB/Rel activation following oxidative stress.

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تاریخ انتشار 2002