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首页> 外文期刊>Journal of Cellular Physiology >Characterization of Notch Signaling During Osteogenic Differentiation in Human Osteosarcoma Cell Line MG63
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Characterization of Notch Signaling During Osteogenic Differentiation in Human Osteosarcoma Cell Line MG63

机译：描述中Notch信号人类骨肉瘤成骨分化细胞系MG63

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Osteogenic differentiation is a multi-step process controlled by a complex molecular framework. Notch is an evolutionarily conserved intercellular signaling pathway playing a prominent role in cell fate and differentiation, although the mechanisms by which this pathway regulates osteogenesis remain controversial. This study aimed to investigate, in vitro, the involvement of Notch pathway during all the developmental stages of osteogenic differentiation in human osteosarcoma cell line MG63. Cells were cultured in basal condition (control) and in osteoinductive medium (OM). Notch inhibitors were also added in OM to block Notch pathway. During osteogenic differentiation, early (alkaline phosphatase activity and collagen type I) and late osteogenic markers (osteocalcin levels and matrix mineralization), as well as the gene expression of the main osteogenic transcription factors (Runx2, Osterix, and Dlx5) increased. Time dependent changes in the expression of specific Notch receptors were identified in OM versus control with a significant reduction in the expression of Notch1 and Notch3 receptors in the early phase of differentiation, and an increase of Notch2 and Notch4 receptors in the late phase. Among Notch nuclear target genes, Hey1 expression was significantly higher in OM than control, while Hes5 expression decreased. Osteogenic markers were reduced and Hey1 was significantly inhibited by Notch inhibitors, suggesting a role for Notch through the canonical pathway. In conclusion, Notch pathway might be involved with a dual role in osteogenesis of MG63, through the activation of Notch2, Notch4, and Hey1, inducing osteoblast differentiation and the depression of Notch1, Notch3, and Hes5, maintaining an undifferentiated status. (C) 2016 Wiley Periodicals, Inc.
机译：成骨分化是一个多步骤的过程由一个复杂的分子框架。缺口是一种进化保守细胞间信号通路发挥突出的作用在细胞命运和分化,尽管这条通路的机制调节骨仍有争议。研究旨在探讨体外,在所有的切口的参与途径成骨的发展阶段人类骨肉瘤细胞系分化MG63。(控制)和论述媒介(OM)。切口抑制剂也加入了OM阻止Notch通路。早期(碱性磷酸酶活性和胶原蛋白I型)和晚期成骨的标记(骨钙素水平和基质矿化),以及基因表达的主要阻力转录因子(Runx2 Osterix和Dlx5)增加了。特定切口受体的表达确定在OM和控制显著减少Notch1的表达和Notch3受体的早期阶段分化,增加Notch2和新的高度受体后期阶段。核目标基因,Hey1表达式OM的显著高于控制Hes5表达减少。减少和Hey1明显抑制通过切口抑制剂,暗示角色等级通过规范化的途径。切口途径可能参与双重角色在MG63骨生成,通过激活Notch2,新的高度,Hey1诱导成骨细胞分化和Notch1的抑郁症,Notch3 Hes5,维护一个未分化的地位。

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