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首页> 外文期刊>Cytokine >Primary human bone marrow adipocytes support TNF-alpha-induced osteoclast differentiation and function through RANKL expression.
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Primary human bone marrow adipocytes support TNF-alpha-induced osteoclast differentiation and function through RANKL expression.

机译：主要的人类骨髓脂肪细胞通过RANKL表达来支持TNF-α诱导的破骨细胞分化和功能。

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摘要

PURPOSE: In previous reports, it was demonstrated that bone marrow adipocytes were related to steroid osteoporosis through osteoclastogenesis induced by Receptor Activator of Nuclear factor kappa-B Ligand (RANKL) expression. The purpose of this study was to evaluate the effect of Tumor necrosis factor-alpha (TNF-alpha) on RANKL expression in bone marrow adipocytes, and osteoclast differentiation supported by human bone marrow adipocytes. METHODS: RANKL, osteoprotegerin (OPG), and macrophage-colony stimulating factor (M-CSF) mRNA expression in bone marrow adipocytes and their regulation by TNF-alpha treatment were measured by real-time RT-PCR. Co-cultures of bone marrow adipocytes and osteoclast precursors were performed with or without TNF-alpha, and osteoclast differentiation was evaluated morphologically and functionally. RESULTS: RANKL expression and an increase in the RANKL/OPG ratio in bone marrow adipocytes were stimulated by TNF-alpha treatment. In co-culture of bone marrow adipocytes and osteoclast precursors with TNF-alpha, the number of TRAP-positive multinuclear cells and resorption cavity formations of calcium phosphate film were increased. Osteoclast differentiation was suppressed by anti-RANKL antibody treatment. In co-culture with non-cell-contact conditions, no TRAP-positive cells or resorption cavity formations were observed. CONCLUSIONS: TNF-alpha increased RANKL expression in primary human bone marrow adipocytes. TNF-alpha induced the ability of bone marrow adipocytes to promote osteoclast differentiation and activity in a manner directly related to RANKL expression.
机译：目的：在以前的报道中，已证明骨髓脂肪细胞通过核因子κB配体受体激活剂（RANKL）表达诱导的破骨细胞生成与类固醇骨质疏松症相关。这项研究的目的是评估肿瘤坏死因子-α（TNF-alpha）对骨髓脂肪细胞中RANKL表达以及人骨髓脂肪细胞支持的破骨细胞分化的影响。方法：采用实时RT-PCR技术检测骨髓脂肪细胞中RANKL，骨保护素（OPG）和巨噬细胞集落刺激因子（M-CSF）mRNA的表达及其对TNF-α的调节作用。在有或没有TNF-α的情况下，进行骨髓脂肪细胞和破骨细胞前体的共培养，并从形态和功能上评估破骨细胞的分化。结果：TNF-α处理刺激了骨髓脂肪细胞中RANKL的表达和RANKL / OPG比的增加。在将骨髓脂肪细胞和破骨细胞前体与TNF-α共培养时，TRAP阳性多核细胞数量增加，磷酸钙膜的吸收腔形成增加。抗RANKL抗体处理抑制了破骨细胞的分化。在非细胞接触条件下共培养时，未观察到TRAP阳性细胞或吸收腔形成。结论：TNF-α增加了人原代骨髓脂肪细胞中RANKL的表达。 TNF-α以与RANKL表达直接相关的方式诱导骨髓脂肪细胞促进破骨细胞分化和活性的能力。

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