Based on the high self-renewal ability and osteoblastic differentiation capacity, dental pulp stem cells (DPSCs) are suggested to be promising cell source for osteogenesis. Therefore, illustrating the mechanism of osteoblastic differentiation of DPSCs is required. This current study aims to illustrate the role and mechanism of Sp1 in regulating osteoblastic differentiation of DPSCs. In this study, we downregulated Sp1 in DPSCs and evaluated the osteoblastic differentiation by measuring Runx2 and OCN expression with Western blot analysis and by Alizarin red staining. Furthermore, we investigated the mechanism of Sp1 regulating noggin with Firefly luciferase reporter gene assay and ChIP assay, and correspondingly evaluated the function of noggin in Sp1-regulated osteoblastic differentiation of DPSCs. We found that knockdown of Sp1 inhibits the expression of ALP, Runx2, COL1A1 and OCN, and decreases ALP staining, Alizarin red staining. Sp1 binds to noggin promoter and inhibits noggin expression, thus correspondingly regulates DPSCs osteoblastic differentiation. In conclusion, our study revealed that Sp1 regulates DPSCs osteoblastic differentiation through noggin and that Sp1/noggin can provide new perspective for enhancing DPSCs osteogenesis.

中文翻译：

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Sp1通过调节头蛋白促进牙髓干细胞成骨细胞分化。

基于高的自我更新能力和成骨细胞分化能力，牙髓干细胞（DPSCs）被认为是成骨细胞的有前途的细胞来源。因此，需要阐明DPSC的成骨细胞分化的机制。这项当前的研究旨在说明Sp1在调节DPSC的成骨细胞分化中的作用和机制。在这项研究中，我们下调了DPSC中Sp1的表达，并通过Western blot分析和茜素红染色测量Runx2和OCN的表达来评估成骨细胞的分化。此外，我们用萤火虫荧光素酶报道基因和ChIP法研究了Sp1调节头蛋白的机制，并相应地评估了头蛋白在Sp1调节DPSCs成骨细胞分化中的功能。我们发现，敲低Sp1会抑制ALP，Runx2，COL1A1和OCN的表达，并降低ALP染色，茜素红染色。Sp1结合头蛋白启动子并抑制头蛋白表达，从而相应地调节DPSC的成骨细胞分化。总之，我们的研究表明Sp1通过头蛋白调节DPSC的成骨细胞分化，而Sp1 / noggin可以为增强DPSC的成骨作用提供新的视角。