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  • Title: Rapid activation of NF-kappaB and AP-1 and target gene expression in postischemic rat intestine.
    Author: Yeh KY, Yeh M, Glass J, Granger DN.
    Journal: Gastroenterology; 2000 Mar; 118(3):525-34. PubMed ID: 10702203.
    Abstract:
    BACKGROUND & AIMS: The molecular mechanisms underlying intestinal mucosal damage-repair processes induced by ischemia-reperfusion (IR) remain unknown. We determined nuclear factor-kappaB (NF-kappaB) and activator protein 1 (AP-1) activities and the expression of potential target genes relevant to damage-repair events. METHODS: Rat jejunal segment was subjected to ischemia for 30 minutes followed by reperfusion for defined times. NF-kappaB and AP-1 activities; mucosal p105, p50, and inhibitor kappaB-alpha (IkappaB-alpha) levels; and c-fos, neurotensin, and ferritin H expression were determined by electrophoretic mobility shift assay and Western and Northern analyses, respectively. RESULTS: NF-kappaB and AP-1 activities were significantly elevated from 1 to 12 hours after reperfusion. The activated NF-kappaB in the nuclear extract consisted of solely p50 homodimers. Activation of p50 was associated with a decrease of p105, generation of p50, and increased phosphorylation and degradation of IkappaB-alpha. The activated AP-1 contained c-fos but not c-jun, fosB, and Fra-1. Reperfusion induced a transient elevation of c-fos, prolonged increase of neurotensin, and early reduction followed by recovery of ferritin H messenger RNA. CONCLUSIONS: The intestine shows organ-specific responses to IR, characterized by prolonged NF-kappaB and AP-1 activation involving NF-kappaB p50 dimers and excluding AP-1 c-jun protein. Degradation of the IkappaB-gamma component of p105 and partial reduction IkappaB-alpha selectively activate p50/p50 dimers. Temporal patterns of target gene expression reflect functional relevance to mucosal damage-repair processes after IR.
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