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Interaction of mitochondrial thioredoxin with glucocorticoid receptor and NF-κB modulates glucocorticoid receptor and NF-κB signalling in HEK-293 cells
Biomedical Research Foundation, Academy of Athens, Center of Basic Research, Athens, Greece.
Biomedical Research Foundation, Academy of Athens, Center of Basic Research, Athens, Greece.
Biomedical Sciences Research Center Alexander Fleming, Laboratory of Protein Chemistry, Vari, Greece.
Biomedical Research Foundation, Academy of Athens, Center of Basic Research, Athens, Greece.
2009 (Engelska)Ingår i: Biochemical Journal, ISSN 0264-6021, E-ISSN 1470-8728, Vol. 422, nr 3, s. 521-531Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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

Ort, förlag, år, upplaga, sidor
Portland Press, 2009. Vol. 422, nr 3, s. 521-531
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-98719DOI: 10.1042/BJ20090107PubMedID: 19570036OAI: oai:DiVA.org:liu-98719DiVA, id: diva2:655544
Tillgänglig från: 2013-10-11 Skapad: 2013-10-11 Senast uppdaterad: 2017-12-06

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