G protein‐coupled receptor 84 controls osteoclastogenesis through inhibition of NF‐κB and MAPK signaling pathways

Park Ji‐Wan; Yoon Hye‐Jin; Kang Woo YoulCho SeungilSeong Sook JinLee Hae WonYoon Young‐RanKim Hyun‐Ju

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G protein‐coupled receptor 84 controls osteoclastogenesis through inhibition of NF‐κB and MAPK signaling pathways

机译：G蛋白耦合受体84控制通过抑制NF osteoclastogenesisκB和MAPK信号通路

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GPR84, a member of the G protein‐coupled receptor family, is found predominantly in immune cells, such as macrophages, and functions as a pivotal modulator of inflammatory responses. In this study, we investigated the role of GPR84 in receptor activator of nuclear factor‐κB ligand (RANKL)‐induced osteoclast differentiation. Our microarray data showed that GPR84 was significantly downregulated in osteoclasts compared to in their precursors, macrophages. The overexpression of GPR84 in bone marrow‐derived macrophages suppressed the formation of multinucleated osteoclasts without affecting precursor proliferation. In addition, GPR84 overexpression attenuated the induction of c‐Fos and nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), which are transcription factors that are critical for osteoclastogenesis. Furthermore, knockdown of GPR84 using a small hairpin RNA promoted RANKL‐mediated osteoclast differentiation and gene expression of osteoclastogenic markers. Mechanistically, GPR84 overexpression blocked RANKL‐stimulated phosphorylation of IκBα and three MAPKs, JNK, ERK, and p38. GPR84 also suppressed NF‐κB transcriptional activity mediated by RANKL. Conversely, GPR84 knockdown enhanced RANKL‐induced activation of IκBα and the three MAPKs. Collectively, our results revealed that GPR84 functions as a negative regulator of osteoclastogenesis, suggesting that it may be a potential therapeutic target for osteoclast‐mediated bone‐destructive diseases.

机译：成员GPR84 G蛋白耦合的受体家庭,主要发现在免疫细胞,如巨噬细胞和功能作为一个关键调制器的炎症反应。研究中,我们调查了GPR84的角色核因子受体激活κB配体(RANKL)诱导破骨细胞分化。微阵列数据显示GPR84在破骨细胞显著下调在前体相比,巨噬细胞。过度的GPR84骨髓衍生巨噬细胞抑制的形成多核破骨细胞而不影响前体增殖。过度减毒c的感应”丛书核转录因子激活T细胞,胞质1 (NFATc1)转录对osteoclastogenesis至关重要的因素。此外,击倒GPR84使用一个小的发夹RNA提升RANKL量破骨细胞介导的分化和基因表达osteoclastogenic标记。超表达了RANKL的刺激我三MAPKsκBα和磷酸化,物,ERK和p38。由RANKL转录活动。相反,GPR84击倒的增强RANKL必经我κBα诱导激活和3MAPKs。GPR84负调节的功能osteoclastogenesis,这表明它可能是一个潜在的治疗目标破骨细胞介导的骨破坏性疾病。

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来源
《Journal of Cellular Physiology》 |2018年第2期|1481-1489|共9页
作者
Park Ji‐Wan; Yoon Hye‐Jin; Kang Woo YoulCho SeungilSeong Sook JinLee Hae WonYoon Young‐RanKim Hyun‐Ju;
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Department of Biomedical Science, Cell and Matrix Research Institute, BK21 Plus KNU Biomedical;

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正文语种英语
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关键词
Osteoclast; Osteoclastogenesis; Nuclear Factor of Activated T-Cells, Cytoplasmic 1GPR84 gene;

机译：破骨细胞;Osteoclastogenesis;核因子激活t细胞,胞质1 gpr84基因;

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G protein‐coupled receptor 84 controls osteoclastogenesis through inhibition of NF‐κB and MAPK signaling pathways

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