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首页> 外文期刊>Journal of Cellular Physiology >FAM20C regulates osteoblast behaviors and intracellular signaling pathways in a cell‐autonomous manner
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FAM20C regulates osteoblast behaviors and intracellular signaling pathways in a cell‐autonomous manner

机译：FAM20C调节成骨细胞行为细胞内信号通路细胞量自治的方式

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Recent studies indicate that Family with sequence similarity 20 member C (FAM20C) catalyzes the phosphorylation of secreted proteins, and participates in a variety of biological processes, including cell proliferation, migration, mineralization, and phosphate homeostasis. To explore the local influences of FAM20C on osteoblast, Fam20c ‐deficient osteoblasts were generated by treating the immortalized Fam20c f/f osteoblasts with CMV‐Cre‐IRES‐EGFP lentivirus. Compared with the normal Fam20c f/f osteoblasts, the expression of Bone sialoprotein ( Bsp) , Osteocalcin ( Ocn) , Fibroblast growth factor 23 ( Fgf23) , and transcription factors that promote osteoblast maturation were up‐regulated in the Fam20c ‐deficient osteoblasts. In contrast, the expression of Dental matrix protein 1 (Dmp1), Dentin sialophosphoprotein (Dspp), Osteopontin (Opn), type I Collagen a 1 (Col1a1), and Alkine phosphatase (Alp) were down‐regulated in the Fam20c ‐deficient cells. These alterations disclosed the primary regulation of Fam20c on gene expression. The Fam20c ‐deficient osteoblasts showed a remarkable reduction in the ability of forming mineralized nodules. However, supplements of extracellular matrix proteins extracted from the normal bone failed to rescue the reduced mineralization, suggesting that FAM20C may affect the biomineralization by the means more than local phosphorylation of extracellular matrix proteins and systemic phosphorus homeostasis. Moreover, although Fam20c deficiency had little impact on cell proliferation, it significantly reduced cell migration and lowered the levels of p‐Smad1/5/8, p‐Erk and p‐p38, suggesting that the kinase activity of FAM20C might be essential to cell mobility and the activity of BMP ligands. In summary, these findings provide evidences that FAM20C may regulate osteoblast maturation, migration, mineralization, and BMP signaling pathways in a cell‐autonomous manner.
机译：最近的研究表明,家庭使用序列相似性20 C (FAM20C)催化分泌蛋白的磷酸化参与各种各样的生物过程,包括细胞增殖、迁移、矿化和磷酸盐体内平衡。成骨细胞生成的治疗不灭的Fam20c / f成骨细胞巨细胞病毒检测Cre必经IRES EGFP应承担的慢病毒。正常Fam20c f / f成骨细胞的表达骨涎蛋白(Bsp)、骨钙素(Ocn),成纤维细胞生长因子23 (Fgf23),促进成骨细胞的转录因子成熟了还是Fam20c监管缺乏成骨细胞。牙基质蛋白- 1的表达(Dmp1),牙质sialophosphoprotein (Dspp),骨桥蛋白(Opn)、I型胶原蛋白1 (Col1a1)和炔烃磷酸酶(Alp)下降的监管Fam20c缺乏细胞。披露的主要监管Fam20c基因的表达。成骨细胞表现出显著的减少形成矿化结节的能力。细胞外基质蛋白质的补充从正常的骨头中提取失败的救援减少矿化,说明FAM20C可能影响的生物矿化不仅仅是当地的磷酸化细胞外基质蛋白和系统性磷体内平衡。缺乏对细胞影响不大扩散,细胞显著减少迁移和降低p Smad1/5/8应承担的水平,p的Erk和p38应承担的,这表明激酶活动FAM20C细胞可能是必要的流动性和骨形态发生蛋白配体的活性。总结,这些发现提供证据FAM20C可能调节成骨细胞的成熟,迁移、矿化和BMP信号以一个细胞自治的方式途径。

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