期刊
LIFE-BASEL
卷 12, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/life12060789
关键词
monocyte chemotactic protein 1 (MCP-1); osteoclast; macrophage colony stimulating factor (M-CSF); granulocyte macrophage colony stimulating factor (GM-CSF); receptor activator of NF-kappa B ligand (RANKL); human CD14+mononuclear cells
资金
- National Health and Medical Research Council of Australia [481946]
- Queensland Cancer Fund [481928]
In this study, the effects of different cytokines on the expression of chemokines in human CD14(+) cells in culture were investigated. It was found that M-CSF treatment promoted MCP1 expression, while GM-CSF suppressed MCP1 expression. Furthermore, addition of MCP1 significantly increased osteoclast formation and overcame the suppression caused by GM-CSF.
In vitro osteoclast methods require constant treatment with macrophage colony stimulating factor (M-CSF) to support precursor survival and addition of the differentiation agent receptor activator of NF-kappa B ligand (RANKL). Constant exposure to granulocyte macrophage colony stimulating factor (GM-CSF) suppresses human osteoclast formation in vitro. Addition of the chemokine monocyte chemotactic protein-1 (MCP1) to such cultures dramatically increases osteoclast formation and overcomes GM-CSF mediated suppression. We investigated the effect of M-CSF, GM-CSF and the combination of M-CSF and GM-CSF treatment on the expression of chemokines in human CD14(+) cells in culture. Of assayed chemokines, MCP1 was the most abundant in terms of mRNA transcript and protein in M-CSF treated cultures and was suppressed by GM-CSF. MCP1 protein accumulated up to 50 ng/mL in culture medium, greatly exceeding other assayed chemokines. C-C chemokine receptor-2 (CCR2) is the receptor for MCP1: the formation of osteoclast-like cells was inhibited by constant exposure to the CCR2 antagonist RS102895, in part by decreasing expression of RANK, the receptor for RANKL.
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