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• W2093785223 endingPage "97" @default.
• W2093785223 startingPage "91" @default.
• W2093785223 abstract "Interleukin (IL)-6 is a causative agent of systemic juvenile idiopathic arthritis (sJIA), a chronic inflammatory disease complicated with severe growth impairment. Recent trials of anti-IL-6 receptor monoclonal antibody, tocilizumab, indicated that tocilizumab blocks IL-6/IL-6 receptor-mediated inflammation, and induces catch-up growth in children with sJIA. This study evaluates the effects of IL-6 on chondrogenesis by ATDC5 cells, a clonal murine chondrogenic cell line that provides an excellent model for studying endochondral ossification at growth plate. ATDC5 cells were examined for the expression of IL-6 receptor and gp130 by fluorescence-activated cell sorting analysis. Recombinant murine IL-6 was added to ATDC5 cultures to observe cell differentiation, using a quantitative RT-PCR for the chondrogenic differentiation markers type II collagen, aggrecan, and type X collagen. To block IL-6, the anti-mouse IL-6 receptor monoclonal antibody MR16-1 was added. As a result, the cells expressed IL-6 receptor and gp130. The expression of chondrogenic differentiation marker gene was reduced by IL-6, but this was abrogated by MR16-1. We conclude that IL-6 inhibits early chondrogenesis of ATDC5 cells suggesting that IL-6 may affect committed stem cells at a cellular level during chondrogenic differentiation of growth plate chondrocytes, and that IL-6 may be a cellular-level factor in growth impairment in sJIA." @default.
• W2093785223 created "2016-06-24" @default.
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• W2093785223 date "2009-08-01" @default.
• W2093785223 modified "2023-10-16" @default.
• W2093785223 title "Interleukin-6 inhibits early differentiation of ATDC5 chondrogenic progenitor cells" @default.
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• W2093785223 doi "https://doi.org/10.1016/j.cyto.2009.05.002" @default.
• W2093785223 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19535264" @default.
• W2093785223 hasPublicationYear "2009" @default.
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