Interaction of mitochondrial thioredoxin with glucocorticoid receptor and NF-κB modulates glucocorticoid receptor and NF-κB signalling in HEK-293 cells

摘要: Trx2 (mitochondrial thioredoxin) is an antioxidant and anti-apoptotic factor essential for cell viability. Trx1 (cytoplasmic a co-factor regulator of redox-sensitive transcription factors such as the GR (glucocorticoid receptor) NF-kappaB (nuclear kappaB). Both have been detected in mitochondria role mitochondrial regulation apoptosis has proposed. In present study, we show using SPR (surface plasmon resonance) immunoprecepitation that p65 subunit are Trx2-interacting proteins. The interaction with independent presence ligand redox conditions. can interact oxidized, but not reduced, form. Using HEK (human embryonic kidney)-293 lines increased or decreased expression Trx2, modulates reporter genes. Moreover, overexpression mRNA levels COX1 (cytochrome oxidase I) Cytb b), which known to be regulated by NF-kappaB. Increased differentially affects Cytb. glucocorticoid dexamethasone potentiates Cytb, whereas TNFalpha (tumour necrosis alpha) down-regulates it. These results suggest regulatory signalling pathways.