The Institute of Stomatology, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518000, China.
Guangdong Provincial High-level Clinical Key Specialty, Shenzhen, Guangdong, 518000, China.
Cell Mol Life Sci. 2024 Aug 9;81(1):338. doi: 10.1007/s00018-024-05356-3.
Alveolar bone loss is a main manifestation of periodontitis. Human periodontal ligament stem cells (PDLSCs) are considered as optimal seed cells for alveolar bone regeneration due to its mesenchymal stem cell like properties. Osteogenic potential is the premise for PDLSCs to repair alveolar bone loss. However, the mechanism regulating osteogenic differentiation of PDLSCs remain elusive. In this study, we identified Neuron-derived orphan receptor 1 (NOR1), was particularly expressed in PDL tissue in vivo and gradually increased during osteogenic differentiation of PDLSCs in vitro. Knockdown of NOR1 in hPDLSCs inhibited their osteogenic potential while NOR1 overexpression reversed this effect. In order to elucidate the downstream regulatory network of NOR1, RNA-sequencing was used. We found that downregulated genes were mainly enriched in TGF-β, Hippo, Wnt signaling pathway. Further, by western blot analysis, we verified that the expression level of phosphorylated-SMAD2/3 and phosphorylated-SMAD4 were all decreased after NOR1 knockdown. Additionally, ChIP-qPCR and dual luciferase reporter assay indicated that NOR1 could bind to the promoter of TGFBR1 and regulate its activity. Moreover, overexpression of TGFBR1 in PDLSCs could rescue the damaged osteogenic potential after NOR1 knockdown. Taken together, our results demonstrated that NOR1 could activate TGF-β/SMAD signaling pathway and positively regulates the commitment of osteoblast lineages of PDLSCs by targeting TGFBR1 directly.
牙槽骨丧失是牙周炎的主要表现。人牙周韧带干细胞(PDLSCs)因其具有间充质干细胞特性而被认为是牙槽骨再生的最佳种子细胞。成骨潜能是 PDLSCs 修复牙槽骨丢失的前提。然而,调节 PDLSCs 成骨分化的机制仍不清楚。在本研究中,我们鉴定了神经元衍生孤儿受体 1(NOR1),它在体内 PDL 组织中特异性表达,并在体外 PDLSCs 的成骨分化过程中逐渐增加。在 hPDLSCs 中敲低 NOR1 抑制其成骨潜能,而 NOR1 过表达则逆转了这种效应。为了阐明 NOR1 的下游调控网络,我们进行了 RNA 测序。我们发现下调的基因主要富集在 TGF-β、Hippo、Wnt 信号通路中。进一步通过 Western blot 分析,我们验证了 NOR1 敲低后磷酸化-SMAD2/3 和磷酸化-SMAD4 的表达水平均降低。此外,ChIP-qPCR 和双荧光素酶报告基因检测表明,NOR1 可以结合 TGFBR1 的启动子并调节其活性。此外,在 PDLSCs 中转染 TGFBR1 过表达可以挽救 NOR1 敲低后受损的成骨潜能。综上所述,我们的研究结果表明,NOR1 可以通过直接靶向 TGFBR1 激活 TGF-β/SMAD 信号通路,并正向调节 PDLSCs 成骨谱系的分化。