Please use this identifier to cite or link to this item: https://doi.org/10.1042/BJ20120888
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dc.titleComplement C1q production by osteoclasts and its regulation of osteoclast development
dc.contributor.authorTeo, B.H.D.
dc.contributor.authorBobryshev, Y.V.
dc.contributor.authorTeh, B.K.
dc.contributor.authorWong, S.H.
dc.contributor.authorLu, J.
dc.date.accessioned2014-11-26T07:43:45Z
dc.date.available2014-11-26T07:43:45Z
dc.date.issued2012-10-15
dc.identifier.citationTeo, B.H.D., Bobryshev, Y.V., Teh, B.K., Wong, S.H., Lu, J. (2012-10-15). Complement C1q production by osteoclasts and its regulation of osteoclast development. Biochemical Journal 447 (2) : 229-237. ScholarBank@NUS Repository. https://doi.org/10.1042/BJ20120888
dc.identifier.issn02646021
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/109262
dc.description.abstractC1q deficiency is the strongest known risk factor for SLE (systemic lupus erythematosus) but its endogenous cellular origin remains limitedly understood. In the present study we investigate the production of C1q by both cultured and endogenous bone osteoclasts. Blood monocytes were cultured with RANKL (receptor activator of nuclear factor κB ligand) and M-CSF (macrophage colony-stimulating factor) to generate osteoclasts and these cells expressed C1Q mRNA and also secreted C1q protein. IntracellularC1qwas detectable in developing osteoclasts at day 3 by Western blotting and was also detectable by flow cytometry. By immunofluorescence microscopy, C1q was preferentially detected in immature osteoclasts. By multiple detection methods, C1q expression was markedly increased after IFNγ (interferon γ) treatment. By immunohistochemistry, C1q was also detected in endogenous bone osteoclasts. When osteoclasts were cultured on immobilized C1q, these cells exhibited 2-7-fold increases in the expression of signature osteoclast genes [TRAP (tartrate-resistant acid phosphatase), cathepsin K, calcitonin receptor, carbonic anhydrase II and NFATc1 (nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1)], suggesting an osteoclastogenic capability. This is the first report of C1q production by osteoclasts. Its ability to enhance osteoclast development implies reduced osteoclastogenesis in patients with SLE as they often experience decreased C1q levels. This is consistent with the non-erosive nature of lupus arthritis. © The Authors Journal compilation © 2012 Biochemical Society.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1042/BJ20120888
dc.sourceScopus
dc.subjectBone
dc.subjectC1q
dc.subjectDendritic cell
dc.subjectLupus
dc.subjectMonocyte
dc.subjectOsteoclast
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1042/BJ20120888
dc.description.sourcetitleBiochemical Journal
dc.description.volume447
dc.description.issue2
dc.description.page229-237
dc.description.codenBIJOA
dc.identifier.isiut000310100700005
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