Islam Shamima, Hassan Ferdaus, Tumurkhuu Gantsetseg, Dagvadorj Jargalsaikhan, Koide Naoki, Naiki Yoshikazu, Yoshida Tomoaki, Yokochi Takashi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
Microbiol Immunol. 2008 Dec;52(12):585-90. doi: 10.1111/j.1348-0421.2008.00076.x.
RAW 264.7 macrophage cells differentiate into osteoclast-like cells in the presence of RANKL. Participation of M-CSF in RANKL-induced osteoclast formation of RAW 264.7 cells was examined. TRAP-positive osteoclast-like cells appeared in RAW 264.7 cells cultured in the presence of RANKL. RANKL-induced osteoclast formation was markedly inhibited by anti-M-CSF antibody. RANKL augmented M-CSF mRNA expression and M-CSF production in RAW 264.7 cells. Further, anti-M-CSF antibody inhibited the expression of RANK, c-fms, c-fos and TRAP mRNA in RANKL-stimulated RAW 264.7 cells. However, anti-M-CSF antibody did not affect the expression of DC-STAMP in the stimulated cells. Therefore, RANKL was suggested to induce osteoclast formation in RAW 264.7 cells via augmented production of M-CSF. The putative role of M-CSF in RANKL-induced osteoclast formation of RAW 264.7 cells is discussed.
在RANKL存在的情况下，RAW 264.7巨噬细胞可分化为破骨细胞样细胞。研究了M-CSF在RANKL诱导的RAW 264.7细胞破骨细胞形成中的作用。在存在RANKL的情况下培养的RAW 264.7细胞中出现了抗酒石酸酸性磷酸酶（TRAP）阳性的破骨细胞样细胞。抗M-CSF抗体显著抑制了RANKL诱导的破骨细胞形成。RANKL增加了RAW 264.7细胞中M-CSF mRNA的表达和M-CSF的产生。此外，抗M-CSF抗体抑制了RANKL刺激的RAW 264.7细胞中RANK、c-fms、c-fos和TRAP mRNA的表达。然而，抗M-CSF抗体并不影响受刺激细胞中DC-STAMP的表达。因此，提示RANKL通过增加M-CSF的产生来诱导RAW 264.7细胞中的破骨细胞形成。本文讨论了M-CSF在RANKL诱导的RAW 264.7细胞破骨细胞形成中的假定作用。
