High Constitutive NF-κB Activity Mediates Resistance to Oxidative Stress in Neuronal Cells

摘要: Selected clones of the sympathetic precursor-like cell line PC12 (rCl8) are resistant to oxidative death induced by Alzheimer’s disease-associated amyloid β protein (Aβ) and hydrogen peroxide (H2O2). Here, we show that transcriptional activity DNA binding redox-sensitive transcription factor NF-κB its nuclear expression constitutively increased in rCl8 cells compared with their nonresistant parental (PC12p) counterpart. Suppression synthetic glucocorticoid dexamethasone or direct overexpression a super-repressor mutant form IκBα, specific inhibitor NF-κB, reversed stress resistance phenotype these ultimately led after challenge H2O2. Dexamethasone treatment also caused an increase level IκBα. Our data baseline may mediate neuronal origin stress. Therefore, presented model help identify possible target genes further elucidate molecular basis differential sensitivity neurons neurodegenerative conditions associated burden, such as disease.