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Título

Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

AutorMaicas, Nuria; Cuadrado, Antonio CSIC ORCID
Fecha de publicación1-ago-2011
EditorMary Ann Liebert
CitaciónAntioxidants and Redox Signalling 15(4): 899-901 (2011)
Resumen[Aims]: Although oxidative stress participates in the etiopathogenesis of rheumatoid arthritis, its importance in this inflammatory disease has not been fully elucidated. In this study, we analyzed the relevance of the transcription factor Nrf2, master regulator of redox homeostasis, in the effector phase of an animal model of rheumatoid arthritis, using the transfer of serum from K/BxN transgenic mice to Nrf2(-/-) mice. [Results]: Nrf2 deficiency accelerated the incidence of arthritis, and animals showed a widespread disease affecting both front and hind paws. Therefore, the inflammatory response was enhanced, with increased migration of leukocytes and joint destruction in front paws. We observed an increased production of tumor necrosis factor-alpha, interleukin-6, and CXCL-1 in the joint, with small changes in eicosanoid levels. Serum levels of CXCL-1 and receptor activator for nuclear factor kappa B ligand were enhanced and osteocalcin decreased in arthritic Nrf2(-/-) mice. The expression of cyclooxygenase-2, inducible nitric oxide synthase, and peroxynitrite in the joints was higher in Nrf2 deficiency, whereas heme oxygenase-1 was downregulated. Innovation: Nrf2 may be a therapeutic target for arthritis. [Conclusion]: Our results support a protective role of Nrf2 against joint inflammation and degeneration in arthritis.
Descripción14 páginas, 8 figuras, 1 tabla.-- et al.
Versión del editorhttp://dx.doi.org/10.1089/ars.2010.3835
URIhttp://hdl.handle.net/10261/40094
DOI10.1089/ars.2010.3835
ISSN1523-0864
E-ISSN1557-7716
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