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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 >Adiponectin stimulates RANKL and inhibits OPG expression in human osteoblasts through the MAPK signaling pathway.
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Adiponectin stimulates RANKL and inhibits OPG expression in human osteoblasts through the MAPK signaling pathway.

机译：脂联素通过MAPK信号通路刺激人成骨细胞中的RANKL并抑制OPG表达。

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摘要

Our study indicates that recombinant adiponectin induced RANKL and inhibited OPG expression in human osteoblasts through the AdipoR1/p38 MAPK pathway, and these responses contributed to the adiponectin-induced osteoclasts formation in the co-culture of osteoblast and peripheral blood monocytes systems. These findings showed that adiponectin increased osteoclast formation indirectly through stimulating RANKL and inhibiting OPG production in osteoblasts. It also suggests the pharmacological nature of recombinant adiponectin that indirectly induces osteoclasts formation. INTRODUCTION: Recently, adiponectin has emerged as an element in the regulation of bone metabolism, but the mechanism remains. This study was undertaken to investigate the action of adiponectin on osteoclastogenesis through revealing RANKL and osteoprotegerin (OPG) expression in osteoblasts and osteoclast formation. MATERIALS AND METHODS: Real-time quantitative PCR and ELISA were used to detect RANKL and OPG mRNA and protein expression incultured human osteoblasts. The involved signal pathway was studied using mitogen-activated protein kinase (MAPK) inhibitor and adiponectin receptor 1 (AdipoR1) siRNA. The effects of recombinant adiponectin on osteoclasts formation also were examined in the co-culture systems of osteoblast and peripheral blood monocytes (PBMCs) systems or purified CD14 + PBMCs cultures. RESULTS: Our study showed that recombinant adiponectin induced RANKL and inhibited OPG mRNA expression in human osteoblasts in a dose- and time-dependent manner. Adiponectin also increased soluble RANKL and decreased OPG secretion in osteoblasts conditioned media. Suppression of AdipoR1 with siRNA abolished the adiponectin-regulated RANKL and OPG mRNA expression in osteoblasts. Furthermore, pretreatment of osteoblasts with the MAPK inhibitor SB203580 abolished adiponectin-regulated RANKL and OPG mRNA expression. Adiponectin induced osteoclast formation in the co-culture systems of osteoblast and PBMCs systems, and OPG entirely blocked this response. However, adiponectin had no direct effect on the differentiation of osteoclast precursor purified CD14 + PBMCs. CONCLUSIONS: These data indicate that recombinant adiponectin induced RANKL and inhibited OPG expression in human osteoblasts through the AdipoR1/p38 MAPK pathway, and these responses contributed to the adiponectin-induced osteoclast formation in the co-culture of osteoblast and PBMCs systems. These findings showed that adiponectin increased osteoclast formation indirectly through stimulating RANKL and inhibiting OPG production in osteoblasts. It suggests the pharmacological nature of recombinant adiponectin that indirectly induces osteoclasts formation.
机译：我们的研究表明重组脂连蛋白通过AdipoR1 / p38 MAPK途径诱导人成骨细胞中的RANKL并抑制OPG表达，并且这些应答在成骨细胞和外周血单核细胞系统的共培养中促进了脂连蛋白诱导的破骨细胞形成。这些发现表明，脂联素通过刺激RANKL和抑制成骨细胞中OPG的产生间接增加了破骨细胞的形成。它还暗示了间接诱导破骨细胞形成的重组脂联素的药理性质。引言：近年来，脂联素已成为调节骨代谢的一种成分，但其​​机制仍然存在。这项研究旨在通过揭示成骨细胞和破骨细胞形成中的RANKL和骨保护素（OPG）表达来研究脂联素对破骨细胞的作用。材料与方法：采用实时定量PCR和ELISA法检测培养的人成骨细胞中的RANKL和OPG mRNA及蛋白表达。使用有丝分裂原激活的蛋白激酶（MAPK）抑制剂和脂联素受体1（AdipoR1）siRNA研究了参与的信号途径。在成骨细胞和外周血单核细胞（PBMC）系统或纯化的CD14 + PBMC培养物的共培养系统中，还检查了重组脂联素对破骨细胞形成的影响。结果：我们的研究表明重组脂联素诱导人成骨细胞中的RANKL并抑制OPG mRNA的表达，呈剂量和时间依赖性。脂联素还增加了成骨细胞条件培养基中的可溶性RANKL和OPG分泌。用siRNA抑制AdipoR1消除了脂联素调节的成骨细胞中RANKL和OPG mRNA的表达。此外，用MAPK抑制剂SB203580预处理成骨细胞可消除脂联素调节的RANKL和OPG mRNA表达。脂联素在成骨细胞和PBMCs系统的共培养系统中诱导破骨细胞形成，而OPG完全阻断了这种反应。然而，脂联素对破骨细胞前体纯化的CD14 + PBMC的分化没有直接影响。结论：这些数据表明重组脂连蛋白通过AdipoR1 / p38 MAPK途径诱导人成骨细胞中的RANKL并抑制OPG表达，并且这些应答有助于在成骨细胞和PBMCs系统的共培养中脂联素诱导的破骨细胞形成。这些发现表明，脂联素通过刺激RANKL和抑制成骨细胞中OPG的产生间接增加了破骨细胞的形成。它暗示了间接诱导破骨细胞形成的重组脂联素的药理性质。

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