AbstractAlveolar bone loss resulting from periodontal disease ultimately leads to tooth loss. Periodontal ligament mesenchymal stem cells (PDLMSCs) are the tissue-specific cells responsible for maintaining and repairing the periodontal ligament, cementum, and alveolar bone. In this study, we explored the role of aldehyde oxidase 1 (AOX1) in regulating the osteoinduction of human periodontal ligament stem cells (hPDLMSCs).

摘要牙周病引起的牙槽骨丢失最终导致牙齿脱落。牙周膜间充质干细胞（PDLMSCs）是负责维持和修复牙周膜，牙骨质和牙槽骨的组织特异性细胞。在这项研究中，我们探讨了醛氧化酶1（AOX1）在调节人牙周膜干细胞（hPDLMSCs）骨诱导中的作用。

hPDLMSCs were isolated from clinically healthy donors, and AOX1 expression was assessed by comparing inducted and non-inducted hPDLMSCs. Remarkably, we observed a significant upregulation of AOX1 expression during osteoinduction, while AOX1 silencing resulted in the enhanced osteogenic potential of hPDLMSCs.

从临床健康供体中分离hPDLMSC，并通过比较诱导的和未诱导的hPDLMSC来评估AOX1表达。值得注意的是，我们观察到在骨诱导过程中AOX1表达显着上调，而AOX1沉默导致hPDLMSC的成骨潜力增强。

Subsequent experiments and analysis unveiled the involvement of retinoid X receptor (RXR) signaling in the inhibition of osteogenesis in hPDLMSCs. Ligands targeting the RXR receptor mirrored the effects of AOX1 on osteogenesis, as evidenced by alterations in alkaline phosphatase (ALP) activity and bone formation levels.

随后的实验和分析揭示了类视黄醇X受体（RXR）信号传导参与抑制hPDLMSC中的成骨。靶向RXR受体的配体反映了AOX1对成骨的影响，碱性磷酸酶（ALP）活性和骨形成水平的改变证明了这一点。

Collectively, these findings underscore the potential regulatory role of AOX1 via RXR signaling in the osteogenesis of hPDLMSCs. This elucidation is pivotal for advancing hPDLMSC-based periodontal regeneration strategies and lays the groundwork for the development of targeted therapeutic interventions aimed at enhancing bone formation in the context of periodontal disease..

总的来说，这些发现强调了AOX1通过RXR信号传导在hPDLMSC成骨中的潜在调节作用。这一阐明对于推进基于hPDLMSC的牙周再生策略至关重要，并为开发旨在增强牙周病背景下骨形成的靶向治疗干预奠定了基础。。

IntroductionPeriodontitis is a chronic inflammatory disease affecting the supporting tissues of the teeth, including the gums, periodontal ligament, and alveolar bone. Traditional treatment approaches focus on controlling the infection and inflammation through mechanical debridement and antimicrobial therapy.

简介牙周炎是一种慢性炎症性疾病，影响牙齿的支持组织，包括牙龈，牙周韧带和牙槽骨。传统的治疗方法侧重于通过机械清创和抗菌治疗来控制感染和炎症。

However, these approaches may not always fully restore the damaged tissues1. Regenerative therapies aim to promote the regeneration of lost periodontal tissues, including the periodontal ligament, cementum, and alveolar bone. These approaches involve the use of various biomaterials, growth factors, and stem cells to stimulate tissue repair and regeneration.

。再生疗法旨在促进牙周组织（包括牙周膜，牙骨质和牙槽骨）的再生。这些方法涉及使用各种生物材料，生长因子和干细胞来刺激组织修复和再生。

Mesenchymal stem cells (MSCs) derived from sources such as the bone marrow, adipose tissue, or periodontal ligament have shown promise in periodontal regeneration due to their ability to differentiate into various cell types involved in tissue repair2,3.As a type of MSCs found within the periodontal ligament, PDLMSCs play a crucial role in maintaining the health and integrity of the periodontium, which includes the periodontal ligament, cementum, alveolar bone, and gingiva4,5,6.

源自骨髓，脂肪组织或牙周膜等来源的间充质干细胞（MSCs）由于能够分化为参与组织修复的各种细胞类型，因此在牙周再生中显示出前景2,3。作为一种在牙周膜内发现的MSCs，PDLMSCs在维持牙周组织的健康和完整性方面起着至关重要的作用，牙周组织包括牙周膜，牙骨质，牙槽骨和牙龈4,5,6。

One of the key functions of PDLMSCs is their potential for osteogenesis, which is the process of forming bone tissue. PDLMSCs have the capacity to differentiate into osteoblasts, the cells responsible for bone formation by secreting collagen and other proteins that form the organic matrix of bone, subsequently facilitating the mineralization process7.

PDLMSCs的关键功能之一是它们的成骨潜力，这是形成骨组织的过程。PDLMSCs具有分化成成骨细胞的能力，成骨细胞是通过分泌胶原蛋白和其他形成骨有机基质的蛋白质来负责骨形成的细胞，随后促进矿化过程7。

These functions of PDLMSCs indicate their roles in maintaining periodontal homeostasis or managing periodontal disease. And this differentiation process is regulated by various signaling pathways and molecular factors8,9. This prompts researchers to investigate potential pathways that can b.

PDLMSCs的这些功能表明它们在维持牙周稳态或管理牙周疾病中的作用。这种分化过程受各种信号通路和分子因素的调节8,9。这促使研究人员调查可能导致b的潜在途径。

Data availability

数据可用性

Data and materials supporting the findings of this study are available in the article and its Supplementary Figures. The RNA-seq datasets mentioned in this study have been deposited in the DNA Data Bank of Japan (DDBJ) Sequence Read Archive (DRA) under accession number DRA003917.

。本研究中提到的RNA-seq数据集已保存在日本DNA数据库（DDBJ）序列读取档案（DRA）中，登录号为DRA003917。

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Download referencesAcknowledgementsThis study was supported by the Japan Society for the Promotion of Science, KAKENHI (grant number 23K24531 to Takanori Iwata). We thank Dr. Kazuki Morita and Dr. Jiacheng Wang at Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University for their kind supports.Author informationAuthors and AffiliationsDepartment of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8549, JapanShiwei Sun & Takanori IwataAuthorsShiwei SunView author publicationsYou can also search for this author in.

下载参考文献致谢本研究得到了日本科学促进会KAKENHI的支持（岩田隆的批准号为23K24531）。我们感谢东京医科牙科大学医学与牙科科学研究生院牙周学系的Kazuki Morita博士和Jiacheng Wang博士的大力支持。作者信息作者和附属机构东京医科牙科大学医学与牙科研究生院牙周病学系，东京文kyo ku Yushima 1-5-45，113-8549，JapanShiwei Sun＆Takanori IwataAuthorsShiwei Sun View作者出版物您也可以在中搜索这位作者。

PubMed Google ScholarTakanori IwataView author publicationsYou can also search for this author in

PubMed Google ScholarTakanori IwataView作者出版物您也可以在

PubMed Google ScholarContributionsS.S. performed the experiments, analyzed the data and drafted the manuscript. T.I. designed and supervised the study. All authors reviewed and approved the final manuscript.Corresponding authorCorrespondence to

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Reprints and permissionsAbout this articleCite this articleSun, S., Iwata, T. Role of AOX1 on RXR signaling regulates osteoblastogenesis in hPDLMSCs.

转载和许可本文引用本文Sun，S.，Iwata，T。AOX1在RXR信号传导中的作用调节hPDLMSC中的成骨细胞生成。

Sci Rep 14, 16767 (2024). https://doi.org/10.1038/s41598-024-68009-2Download citationReceived: 20 May 2024Accepted: 18 July 2024Published: 22 July 2024DOI: https://doi.org/10.1038/s41598-024-68009-2Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

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