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20639492

Source:http://linkedlifedata.com/resource/pubmed/id/20639492

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pubmed-article:20639492pubmed:abstractTextThe ATP-gated P2X(7) receptor (P2X(7)R) is a promising therapeutic target in chronic inflammatory diseases with highly specific antagonists currently under clinical trials for rheumatoid arthritis. Anti-inflammatory actions of P2X(7)R antagonists are considered to result from inhibition of P2X(7)R-induced release of proinflammatory cytokines from activated macrophages. However, P2X(7)Rs are also expressed in resting macrophages, suggesting that P2X(7)R may also signal via cytokine-independent mechanisms involved in joint disease. In this study, we examined P2X(7)R function in resting human lung macrophages and mouse bone marrow-derived macrophages and found that ATP induced rapid release of the lysosomal cysteine proteases cathepsin B, K, L, and S and that was independent of the presence of the proinflammatory cytokines IL-1beta and IL-18. Cathepsins released into the medium were effective to degrade collagen extracellular matrix. ATP-induced cathepsin release was abolished by P2X(7)R antagonists, absent from P2X(7)R(-/-) mouse macrophages, and not associated with cell death. Our results suggest P2X(7)R activation may play a novel and direct role in tissue damage through release of cathepsins independently of its proinflammatory actions via IL-1 cytokines.lld:pubmed
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pubmed-article:20639492pubmed:articleTitleP2X(7) receptor-mediated release of cathepsins from macrophages is a cytokine-independent mechanism potentially involved in joint diseases.lld:pubmed
pubmed-article:20639492pubmed:affiliationFaculty of Life Sciences, University of Manchester, Manchester, United Kingdom. gloria.lopez-castejon@manchester.ac.uklld:pubmed
pubmed-article:20639492pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20639492pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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