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首页> 外文期刊>Cell and Tissue Research >Dose-dependent mechanism of Notch action in promoting osteogenic differentiation of mesenchymal stem cells
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Dose-dependent mechanism of Notch action in promoting osteogenic differentiation of mesenchymal stem cells

机译：缺口作用促进间充质干细胞骨质发生分化的剂量依赖性机制

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Osteogenic differentiation is a tightly regulated process realized by progenitor cell osteoblasts. Notch signaling pathway plays a critical role in skeletal development and bone remodeling. Controversial data exist regarding the role of Notch activation in promoting or preventing osteogenic differentiation. This study aims to investigate the effect of several Notch components and their dosage on osteogenic differentiation of mesenchymal stem cells of adipose tissue. Osteogenic differentiation was induced in the presence of either of Notch components (NICD, Jag1, Dll1, Dll4) dosed by lentiviral transduction. We show that osteogenic differentiation was increased by NICD and Jag1 transduction in a dose-dependent manner; however, a high dosage of both NICD and Jag1 decreased the efficiency of osteogenic differentiation. NICD dose-dependently increased activity of the CSL luciferase reporter but a high dosage of NICD caused a decrease in the activity of the reporter. A high dosage of both Notch components NICD and Jag1 induced apoptosis. In co-culture experiments where only half of the cells were transduced with either NICD or Jag1, only NICD increased osteogenic differentiation according to the dosage, while Jag1-transduced cells differentiated almost equally independently on dosage. In conclusion, activation of Notch promotes osteogenic differentiation in a tissue-specific dose-dependent manner; both NICD and Jag1 are able to increase osteogenic potential but at moderate doses only and a high dosage of Notch activation is detrimental to osteogenic differentiation. This result might be especially important when considering possibilities of using Notch activation to promote osteogenesis in clinical applications to bone repair.
机译：成骨分化是由祖细胞成骨细胞实现的紧密调节过程。 Notch信号通路在骨骼发育和骨骼重塑中起着关键作用。存在有争议的数据，关于缺口激活在促进或预防骨质发生分化中的作用。本研究旨在探讨几种缺口组分及其剂量对脂肪组织间充质干细胞的成骨分化的影响。在慢病毒转导的缺口组分（NICD，JAG1，DLL1，DLL4）的存在下诱导骨质发生分化。我们表明，以剂量依赖性方式，NICD和JAG1转导增加了成骨分化;然而，NICD和JAG1的高剂量降低了成骨分化的效率。 NICD剂量依赖性增加了CSL荧光素酶报告的活性，但NICD的高剂量导致记者的活动减少。缺口组分NICD和JAG1诱导细胞凋亡的高剂量。在共培养实验中，仅通过NICD或JAG1转导细胞的一半，仅NICD根据剂量增加骨质发生分化，而JAG1转导细胞几乎同样地独立于剂量分化。总之，凹口的激活以组织特异性剂量依赖性方式促进成骨分化; NICD和JAG1都能够增加成骨潜力，但仅在中等剂量时，并且高剂量的凹口激活是对成骨分化有害的。当考虑使用缺口激活的可能性促进临床应用中的骨质发生到骨骼修复时，这种结果可能尤为重要。

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