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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Regulation of osteoclast differentiation by fibroblast growth factor 2: stimulation of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor expression in osteoblasts and inhibition of macrophage colony-stimulating fact
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Regulation of osteoclast differentiation by fibroblast growth factor 2: stimulation of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor expression in osteoblasts and inhibition of macrophage colony-stimulating fact

机译：成纤维细胞生长因子2对破骨细胞分化的调节：刺激成核细胞中核因子kappaB配体/破骨细胞分化因子受体激活剂的表达并抑制巨噬细胞集落的形成

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This study investigated the mechanism of direct and indirect actions of fibroblast growth factor 2 (FGF-2) on osteoclast differentiation using two mouse cell culture systems. In the coculture system of osteoblasts and bone marrow cells, FGF-2 stimulated osteoclast formation. This effect was decreased markedly by osteoprotegerin (OPG) or NS-398, a selective cyclo-oxygenase 2 (COX-2) inhibitor. FGF-2 (> or = 10(-9) M) stimulated receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor (RANKL/ODF) messenger RNA (mRNA) expression from 2 h to 7 days in cultured osteoblasts. NS-398 did not affect the early induction but decreased the later one, indicating that the later effect is mediated by COX-2 induction in osteoblasts. To study the direct action of FGF-2 on osteoclast precursors, we used mouse macrophage-like cell line C7 cells that can differentiate into osteoclasts in the presence of soluble RANKL/ODF (sRANKL/ODF) and macrophage colony-stimulating factor (M-CSF). Although osteoblasts expressed all FGF receptors (FGFR-1 to -4), only FGFR-1 was detected in C7 cells at various differentiation stages. FGF-2 alone or in combination with sRANKL/ODF did not induce osteoclastogenesis from C7 cells; however, FGF-2 from lower concentrations (> or = 10(-11) M) significantly decreased osteoclast formation induced by M-CSF in the presence of sRANKL/ODF. FGF-2 did not alter mRNA levels of M-CSF receptor (Fms) or RANK in C7 cells. Immunoprecipitation/ immunoblotting analyses revealed that tyrosine phosphorylation of several cellular proteins including Fms in C7 cells induced by M-CSF was inhibited by FGF-2 in the presence of sRANKL/ODF. We conclude that FGF-2 regulates osteoclast differentiation through two different mechanisms: (1) an indirect stimulatory action via osteoblasts to induce RANKL/ODF partly through COX-2 induction and prostaglandin production and (2) a direct inhibitory action on osteoclast precursors by counteracting M-CSF signaling.
机译：本研究使用两种小鼠细胞培养系统研究了成纤维细胞生长因子2（FGF-2）对破骨细胞分化的直接和间接作用机制。在成骨细胞和骨髓细胞的共培养系统中，FGF-2刺激破骨细胞形成。骨保护素（OPG）或选择性环加氧酶2（COX-2）抑制剂NS-398显着降低了该作用。在培养的成骨细胞中，从2小时到7天，FGF-2（>或= 10（-9）M）刺激了核因子kappaB配体/破骨细胞分化因子（RANKL / ODF）信使RNA（mRNA）表达的受体激活剂。 NS-398不会影响早期诱导，但会降低后一诱导，表明后者的作用是由成骨细胞中的COX-2诱导介导的。为了研究FGF-2对破骨细胞前体的直接作用，我们使用了小鼠巨噬细胞样细胞系C7细胞，该细胞可在可溶性RANKL / ODF（sRANKL / ODF）和巨噬细胞集落刺激因子（M- CSF）。尽管成骨细胞表达所有FGF受体（FGFR-1至-4），但在各个分化阶段的C7细胞中仅检测到FGFR-1。单独的FGF-2或与sRANKL / ODF组合使用，都不能诱导C7细胞破骨细胞的形成。然而，在存在sRANKL / ODF的情况下，来自较低浓度（>或= 10（-11）M）的FGF-2显着降低了M-CSF诱导的破骨细胞形成。 FGF-2不会改变C7细胞中M-CSF受体（Fms）或RANK的mRNA水平。免疫沉淀/免疫印迹分析显示，在sRANKL / ODF存在的情况下，FGF-2抑制了M-CSF诱导的C7细胞中包括Fms在内的几种细胞蛋白的酪氨酸磷酸化。我们得出结论，FGF-2通过两种不同的机制调节破骨细胞分化：（1）通过成骨细胞的间接刺激作用，部分地通过COX-2诱导和前列腺素的产生来诱导RANKL / ODF;（2）通过抵消而对破骨细胞前体的直接抑制作用M-CSF信令。

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