Abstract

Members of the nuclear factor kappa-B (NF-κB) family of transcription factors are activated by tissue damaging stimuli that cause oxidative stress. The regulation of NF-κB activity in rat dorsal root ganglia (DRG) and the neural-crest derived pheochromocytoma cell line PC12 was examined. Electrophoretic mobility shift assays show that specific κB binding activities are present in DRG extracts and PC12 cells. These activities can be supershifted with antisera directed against p50, p52 and p65. South-western blots show the presence of a single NF-κB binding protein with picomolar affinity, co-migrating with NF-κB2 ( p49 p52 ) immunoreactive material in dorsal root ganglia. Intraplantar injection of tumour necrosis factor but not nerve growth factor (NGF) induces NF-κB activity in the DRG of adult rats 6 h later. NGF has no effect on NF-κB activity in PC12 cells after 6 h, but elevates NF-κB activity more than 5-fold after 24 h treatment. These data suggest a role for NF-κB in delayed rather than immediate-early responses of the peripheral nervous system and related cell lines to inflammatory cytokines.

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