Down-regulation of osteoprotegerin production in bone marrow macrophages by macrophage colony-stimulating factor.
Down-regulation of osteoprotegerin production in bone marrow macrophages by macrophage colony-stimulating factor.
复制标题
DOI：
10.1016/j.cyto.2005.03.009
复制
发表时间：
2005-08
期刊：
影响因子：
3.8
通讯作者：
N. Yamada;T. Tsujimura;H. Ueda;S. Hayashi;H. Ohyama;H. Okamura;N. Terada
中科院分区：
文献类型：
--
作者：
N. Yamada;T. Tsujimura;H. Ueda;S. Hayashi;H. Ohyama;H. Okamura;N. Terada
巨噬细胞集落刺激因子（M-CSF）和NF-κB配体受体激活因子（RANKL）诱导骨髓巨噬细胞（BMMs）向破骨细胞分化。为了描述相关机制，研究了M-CSF对骨髓瘤中骨保护素（OPG） （RANKL的诱饵受体）产生的影响。用M-CSF培养小鼠骨髓细胞4 d，形成的贴壁细胞作为骨髓基质。采用实时聚合酶链反应和酶联免疫吸附法分析OPG和NF-κB受体激活剂（RANK， RANKL受体）mrna的表达情况和OPG的分泌情况。BMMs表达巨噬细胞标志物CD115 （c-fms）、Mac-1和F4/80，并显示吞噬活性。此外，BMMs表达OPG mRNA，并将OPG分泌到培养基中。M-CSF对OPG mRNA表达和OPG分泌均有剂量依赖性和可逆抑制作用。M-CSF对RANK mRNA表达无显著影响。结果表明，M-CSF抑制BMMs中OPG的产生，这可能增加BMMs对RANKL的敏感性。
Macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL) induce the differentiation of bone marrow macrophages (BMMs) into osteoclasts. To delineate mechanisms involved, the effect of M-CSF on the production of osteoprotegerin (OPG), decoy receptor of RANKL, in BMMs was investigated. Mouse bone marrow cells were cultured with M-CSF for 4 days and adherent cells formed were used as BMMs. BMMs were cultured with or without M-CSF, and analyzed for expression of OPG and receptor activator of NF-κB (RANK; receptor for RANKL) mRNAs by real-time polymerase chain reaction and secretion of OPG by enzyme-linked immunosorbent assay. BMMs expressed macrophage markers, CD115 (c-fms), Mac-1 and F4/80, and showed phagocytotic activity. In addition, BMMs expressed OPG mRNA and secreted OPG into medium. M-CSF inhibited both the OPG mRNA expression and the OPG secretion dose-dependently and reversibly. The expression of RANK mRNA was not significantly affected by M-CSF. The results showed that M-CSF suppresses the OPG production in BMMs, which may increase the sensitivity of BMMs to RANKL.