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首页> 外文期刊>Journal of Cellular Physiology >FGF‐2 promotes osteocyte differentiation through increased E11/podoplanin expression
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FGF‐2 promotes osteocyte differentiation through increased E11/podoplanin expression

机译：FGF 2应承担促进骨细胞分化增加E11 / podoplanin表达式

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摘要

E11/podoplanin is critical in the early stages of osteoblast‐to‐osteocyte transitions (osteocytogenesis), however, the upstream events which regulate E11 expression are unknown. The aim of this study was to examine the effects of FGF‐2 on E11‐mediated osteocytogenesis and to reveal the nature of the underlying signaling pathways regulating this process. Exposure of MC3T3 osteoblast‐like cells and murine primary osteoblasts to FGF‐2 (10?ng/ml) increased E11 mRNA and protein expression ( p ??0.05) after 4, 6, and 24?hr. FGF‐2 induced changes in E11 expression were also accompanied by significant ( p ??0.01) increases in Phex and Dmp1 (osteocyte markers) expression and decreases in Col1a1 , Postn , Bglap , and Alpl (osteoblast markers) expression. Immunofluorescent microscopy revealed that FGF‐2 stimulated E11 expression, facilitated the translocation of E11 toward the cell membrane, and subsequently promoted the formation of osteocyte‐like dendrites in MC3T3 and primary osteoblasts. siRNA knock down of E11 expression achieved 70% reduction of basal E11 mRNA expression ( p ??0.05) and effectively abrogated FGF‐2‐related changes in E11 expression and dendrite formation. FGF‐2 strongly activated the ERK signaling pathway in osteoblast‐like cells but inhibition of this pathway did not block the ability of FGF‐2 to enhance E11 expression or to promote acquisition of the osteocyte phenotype. The results of this study highlight a novel mechanism by which FGF‐2 can regulate osteoblast differentiation and osteocyte formation. Specifically, the data suggests that FGF‐2 promotes osteocytogenesis through increased E11 expression and further studies will identify if this regulatory pathway is essential for bone development and maintenance in health and disease.
机译：E11 / podoplanin的早期阶段是至关重要的然而,(osteocytogenesis)上游事件调节E11的表达是未知的。本研究的目的是检查的影响FGF 2 E11介导osteocytogenesis应承担的和揭示底层信号的本质通路调节这一过程。MC3T3成骨细胞细胞和小鼠初级成骨细胞地理FGF - 2 (10 ? ng / ml) E11增加信使rna和蛋白质表达(p & ? 0.05)4、6和24 ?人力资源。表达式也伴随着显著(0.01 p & ?)增加Phex Dmp1(骨细胞标记)表达和减少Col1a1、Postn Bglap, Alpl(成骨细胞标记)表达式。透露,FGF 2刺激E11应承担的表达式,促进E11向的易位随后细胞膜,促进了骨细胞形成的类在MC3T3树突和主造骨细胞。表达了在基底的减少70%E11 mRNA表达(p & ? 0.05)有效地废除FGF 2应承担的相关变化E11表达和树突的形成。强烈激活ERK信号通路但抑制成骨细胞的类细胞途径并没有阻止FGF 2应承担的能力加强E11表达式或促进收购骨细胞的表型。研究突出小说机制FGF 2可以调节成骨细胞分化和骨细胞的形成。表明FGF 2促进osteocytogenesis应承担的通过增加E11表达式,进一步研究将确定如果监管途径对骨骼发育和维护至关重要在健康和疾病。

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