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首页> 外文期刊>Journal of Cellular Physiology >G Protein-Coupled Receptor 120 Signaling Negatively Regulates Osteoclast Differentiation, Survival, and Function
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G Protein-Coupled Receptor 120 Signaling Negatively Regulates Osteoclast Differentiation, Survival, and Function

机译：120 G Protein-Coupled受体信号负调节破骨细胞分化,生存和功能

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摘要

G protein-coupled receptor 120 (GPR120) plays an important role in the regulation of inflammation and lipid metabolism. In this study, we investigated the role of GPR120 in osteoclast development and found that GPR120 regulates osteoclast differentiation, survival and function. We observed that GPR120 was highly expressed in osteoclasts compared to their precursors, bone marrow-derived macrophages (BMMs). Activation of GPR120 by its ligand GW9508 suppressed receptor activator of NF-kappa B ligand (RANKL)-induced osteoclast differentiation and the expression of nuclear factor of activated T cells c1 (NFATc1), a key modulator of osteoclastogenesis. GPR120 activation further inhibited the RANKL-stimulated phosphorylation of I kappa B alpha and JNK. In addition to osteoclast differentiation, GPR120 activation increased the apoptosis of mature osteoclasts by inducing caspase-3 and Bim expression. Activation of GPR120 also interfered with cell spreading and actin cytoskeletal organization mediated by M-CSF but not by RANKL. Coincident with the impaired cytoskeletal organization, GPR120 activation blocked osteoclast bone resorbing activity. Furthermore, knockdown of GPR120 using small hairpin RNA abrogated all these inhibitory effects on osteoclast differentiation, survival, and function. Together, our findings identify GPR120 as a negative modulator of osteoclast development that may be an attractive therapeutic target for bone-destructive diseases. (C) 2015 Wiley Periodicals, Inc.
机译：120 G protein-coupled受体(GPR120)扮演重要的作用在调节炎症和脂质代谢。调查GPR120在破骨细胞的作用开发和发现GPR120调节破骨细胞分化、存活和函数。破骨细胞表达与他们相比前兆,骨骨髓来源的巨噬细胞(桥梁养护管理系统)。抑制nf -κB受体激活配体(RANKL)全身的破骨细胞分化核转录因子的表达和激活T细胞c1 (NFATc1),一个关键的调制器osteoclastogenesis。RANKL-stimulated磷酸化的抑制我κα和物。破骨细胞分化、GPR120激活成熟破骨细胞的凋亡增加诱导caspase-3,女子的表情。GPR120也干扰细胞扩散肌动蛋白细胞骨架组织由csf但不是由RANKL。细胞骨架组织,GPR120激活阻止破骨细胞骨突起的活动。此外,击倒GPR120使用小发夹RNA废除这些抑制对破骨细胞分化的影响,生存,和功能。GPR120 -调制器的破骨细胞这可能是一个有吸引力的治疗发展bone-destructive疾病的目标。威利期刊公司。

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