Sp1 通过调节 noggin 促进牙髓干细胞成骨分化。
Sp1 promotes dental pulp stem cell osteoblastic differentiation through regulating noggin.
机构信息
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, 237 Luoyu Rd., Wuhan, 430079, China; Department of Stomatology, Liaocheng People's Hospital, Liaocheng University, 67 Dongchangxi Road, Liaocheng, 252000, China; Precision Biomedical Key Laboratory of Liaocheng, Liaocheng People's Hospital, 67 Dongchangxi Road, Liaocheng, 252000, China; Department of Orthodontics, School & Hospital of Stomatology, Wuhan University, 237 Luoyu Rd, Wuhan, 430079, China.
Department of Stomatology, Liaocheng People's Hospital, Liaocheng University, 67 Dongchangxi Road, Liaocheng, 252000, China.
出版信息
Mol Cell Probes. 2020 Apr;50:101504. doi: 10.1016/j.mcp.2019.101504. Epub 2020 Jan 2.
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.
基于牙髓干细胞（DPSCs）的高自我更新能力和成骨分化能力，它们被认为是成骨的有前途的细胞来源。因此，阐明 DPSCs 成骨分化的机制是必要的。本研究旨在阐明 Sp1 在调控 DPSCs 成骨分化中的作用和机制。在这项研究中，我们下调了 DPSCs 中的 Sp1，并通过 Western blot 分析和茜素红染色来评估 Runx2 和 OCN 的表达，以评估成骨分化。此外，我们通过萤火虫荧光素酶报告基因检测和 ChIP 检测研究了 Sp1 调控 noggin 的机制，并相应地评估了 noggin 在 Sp1 调控的 DPSCs 成骨分化中的功能。我们发现，Sp1 的下调抑制了 ALP、Runx2、COL1A1 和 OCN 的表达，并减少了 ALP 染色、茜素红染色。Sp1 结合 noggin 启动子并抑制 noggin 的表达，从而相应地调节 DPSCs 的成骨分化。总之，我们的研究表明，Sp1 通过 noggin 调节 DPSCs 的成骨分化，Sp1/noggin 可为增强 DPSCs 成骨提供新的视角。
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