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Matrix Protein Biglycan Induces Osteoblast Differentiation through Extracellular Signal-Regulated Kinase and Smad Pathways

机译:基质蛋白Biglycan通过细胞外信号调节的激酶和Smad途径诱导成骨细胞分化。

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摘要

Biglycan (Bgn) is a member of the small leucine-rich proteoglycan (SLRP) family found in bone extracellular matrix (ECM), and hence involved in regulating bone formation and matrix mineralization. It has been reported that Bgn facilitates osteoblast differentiation, and extracellular signal-regulated kinase (Erk) and Smad are two important pathways in regulating osteoblast differentiation. However, the underlying mechanism for Bgn facilitating osteoblast differentiation has not been fully elucidated. The present study demonstrated that the matrix protein Bgn activates Erk signaling pathway and therefore increases Runx2 transcriptional activity, in which glycosaminoglycans (GAGs) chains play an essential role. Additionally, Bgn also activated Smad pathway, another signaling pathway related with osteoblast differentiation. The activation of these two signaling pathways induced by Bgn facilitated the mineralization deposition in vitro. These results demonstrated the mechanism of Bgn promoting osteoblast differentiation and matrix mineralization.
机译:Biglycan(Bgn)是在骨细胞外基质(ECM)中发现的富含亮氨酸的小蛋白聚糖(SLRP)家族的成员,因此参与调节骨形成和基质矿化。据报道,Bgn促进成骨细胞分化,而细胞外信号调节激酶(Erk)和Smad是调节成骨细胞分化的两个重要途径。但是,尚未完全阐明Bgn促进成骨细胞分化的潜在机制。本研究表明,基质蛋白Bgn激活Erk信号传导途径,从而增加Runx2转录活性,其中糖胺聚糖(GAGs)链发挥重要作用。此外,Bgn还激活了Smad途径,这是另一个与成骨细胞分化有关的信号传导途径。 Bgn诱导的这两个信号通路的激活促进了体外矿化沉积。这些结果证明了Bgn促进成骨细胞分化和基质矿化的机制。

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