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dc.contributor.authorGonzález-Rey, Elena-
dc.contributor.authorMartínez-Romero, Rubén-
dc.contributor.authorO'Valle, Francisco-
dc.contributor.authorAguilar-Quesada, Rocío-
dc.contributor.authorConde, Carmen-
dc.contributor.authorDelgado, M.-
dc.contributor.authorOliver, Francisco Javier-
dc.identifier.citationPLoS ONE 2(10): e1071en_US
dc.identifier.issn1932-6203 (Online)-
dc.description6 páginas, 3 figuras.-- PMID: 17971849 [PubMed].-- PMCID: PMC2034533.en_US
dc.description.abstractPoly(ADP-ribose) polymerase-1 (PARP-1) synthesizes and transfers ADP ribose polymers to target proteins, and regulates DNA repair and genomic integrity maintenance. PARP-1 also plays a crucial role in the progression of the inflammatory response, and its inhibition confers protection in several models of inflammatory disorders. Here, we investigate the impact of a selective PARP-1 inhibitor in experimental arthritis. PARP-1 inhibition with 5-aminoisoquinolinone (AIQ) significantly reduces incidence and severity of established collagen-induced arthritis, completely abrogating joint swelling and destruction of cartilage and bone. The therapeutic effect of AIQ is associated with a striking reduction of the two deleterious components of the disease, i.e. the Th1-driven autoimmune and inflammatory responses. AIQ downregulates the production of various inflammatory cytokines and chemokines, decreases the antigen-specific Th1-cell expansion, and induces the production of the anti-inflammatory cytokine IL-10. Our results provide evidence of the contribution of PARP-1 to the progression of arthritis and identify this protein as a potential therapeutic target for the treatment of rheumatoid arthritis.en_US
dc.description.sponsorshipThis work has been supported by grants CTS870 from Junta de Andalucía to MD, SAF 2003-01217, RNIHG c03/02, PI050972, SAF2006-01089 and FIS G03/152 to FJO.en_US
dc.format.extent326045 bytes-
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofPublisher’s version-
dc.titleTherapeutic effect of a poly(ADP-ribose) polymerase-1 inhibitor on experimental arthritis by downregulating inflammation and Th1 responseen_US
dc.description.peerreviewedPeer revieweden_US
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