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首页> 外文期刊>Journal of Cellular Physiology >DGK Downregulation Enhances Osteoclast Differentiation and Bone Resorption Activity Under Inflammatory Conditions
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DGK Downregulation Enhances Osteoclast Differentiation and Bone Resorption Activity Under Inflammatory Conditions

机译：提高差别DGK对这些破骨细胞分化和骨吸收活动在炎症条件下

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Bone homeostasis is maintained by a balance between resorption of the bone matrix and its replacement by new bone. Osteoclasts play a crucially important role in bone metabolism. They are responsible for bone resorption under pathophysiological conditions. Differentiation of these cells, which are derived from bone marrow cells, depends on receptor activator of NF-B ligand (RANKL). RANKL-induced osteoclastogenesis is regulated by the phosphoinositide (PI) signaling pathway, in which diacylglycerol (DG) serves as a second messenger in signal transduction. In this study, we examined the functional implications of DG kinase (DGK), an enzyme family responsible for DG metabolism, for osteoclast differentiation and activity. Of DGKs, DGK is most abundantly expressed in osteoclast precursors such as bone marrow-derived monocytes/macrophages. During osteoclast differentiation from precursor cells, DGK is downregulated at the protein level. In this regard, we found that DGK deletion enhances osteoclast differentiation and bone resorption activity under inflammatory conditions in an animal model of osteolysis. Furthermore, DGK deficiency upregulates RANKL expression in response to TNF stimulation. Collectively, results suggest that DGK is silent under normal conditions, but it serves as a negative regulator in osteoclast function under inflammatory conditions. Downregulation of DGK might be one factor predisposing a person to osteolytic bone destruction in pathological conditions. J. Cell. Physiol. 232: 617-624, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：骨内稳态维持的平衡吸收骨基质及其之间的关系被新骨取代。在骨代谢至关重要的作用。负责骨吸收下吗病理生理条件。这些细胞来源于骨髓细胞,取决于NF-B受体激活配体(RANKL)。是由磷酸肌醇(PI)信号通路中,甘油二酯(DG)作为第二信使信号转导。DG激酶(DGK)功能的影响酶家族负责DG新陈代谢,破骨细胞分化和活动。DGK最破骨细胞中大量表达前兆如骨骨髓来源单核细胞/巨噬细胞。分化的前体细胞,DGK在蛋白质水平表达下调。方面,我们发现DGK删除了破骨细胞分化和骨吸收在一个活动在炎症条件下骨质溶解的动物模型。缺乏上调RANKL表达肿瘤坏死因子刺激。结果表明,在正常DGK是沉默条件,但它作为消极的监管机构在破骨细胞功能受到炎症条件。因素诱发一个人溶骨的骨在病理条件下的破坏。杂志。232:617 - 624年,2017年。期刊、公司。

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