AbstractFibroblast growth factor 2 (FGF2) is a crucial factor in odontoblast differentiation and dentin matrix deposition, which facilitates pulpodentin repair and regeneration. Nevertheless, the specific biological function of FGF2 in odontoblastic differentiation remains unclear because it is controlled by complex signalling pathways.

摘要成纤维细胞生长因子2（FGF2）是成牙本质细胞分化和牙本质基质沉积的关键因素，有助于牙髓修复和再生。。

This study aimed to investigate the mechanism underlying the effect of FGF2 on osteo/odontogenic differentiation of stem cells from the apical papilla (SCAP). SCAP were pretreated with conditioned media containing FGF2 for 1 week, followed by culturing in induced differentiation medium for another week.

。用含有FGF2的条件培养基预处理SCAP 1周，然后在诱导分化培养基中再培养一周。

RNA sequencing (RNA-seq) combined with quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to evaluate the pathways affected by FGF2 in SCAP. Osteo/odontogenic differentiation of SCAP was determined using Alizarin red S staining, alkaline phosphatase staining, RT-qPCR, and western blotting.

RNA测序（RNA-seq）结合定量逆转录聚合酶链反应（RT-qPCR）用于评估SCAP中受FGF2影响的途径。使用茜素红S染色，碱性磷酸酶染色，RT-qPCR和蛋白质印迹法测定SCAP的骨/牙源性分化。

Pretreatment with FGF2 for 1 week increased the osteo/odontogenic differentiation ability of SCAP. RNA-seq and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that phosphatidylinositol 3-kinase (PI3K)/AKT signalling is involved in the osteogenic function of FGF2. RT-qPCR results indicated that SCAP expressed FGF receptors, and western blotting showed that p-AKT was reduced in FGF2-pretreated SCAP.

用FGF2预处理1周增加了SCAP的骨/牙源性分化能力。RNA-seq和京都基因和基因组百科全书途径分析显示磷脂酰肌醇3-激酶（PI3K）/AKT信号传导参与FGF2的成骨功能。RT-qPCR结果表明SCAP表达FGF受体，蛋白质印迹显示FGF2预处理的SCAP中p-AKT降低。

The activation of the PI3K/AKT pathway partially reversed the stimulatory effect of FGF2 on osteo/odontogenic differentiation of SCAP. Our findings suggest that pretreatment with FGF2 enhances the osteo/odontogenic differentiation ability of SCAP by inhibiting the PI3K/AKT pathway..

PI3K/AKT途径的激活部分逆转了FGF2对SCAP的骨/牙源性分化的刺激作用。我们的研究结果表明，用FGF2预处理可通过抑制PI3K/AKT途径增强SCAP的骨/牙源性分化能力。。

IntroductionStem cells from the apical papilla (SCAP) are a type of mesenchymal stem cells (MSCs) that hold great potential for dental regeneration because of their high proliferation, migration, and dental differentiation abilities1,2,3. However, the number of SCAP is limited because they exist only during root development, before the tooth erupts into the oral cavity4,5.

引言根尖乳头干细胞（SCAP）是一种间充质干细胞（MSCs），由于其高增殖，迁移和牙齿分化能力，具有巨大的牙齿再生潜力1,2,3。然而，SCAP的数量是有限的，因为它们只存在于牙根发育过程中，在牙齿爆发进入口腔之前4,5。

Therefore, for their formative functions, it is important to efficiently induce SCAP to proliferate and differentiate into odontoblast-like cells6.Fibroblast growth factor 2 (FGF2) plays a crucial role in wound healing and tissue formation7,8,9. At the cellular level, FGF2 regulates various cellular functions by activating FGF receptors (FGFR) on the cell membrane10.

因此，对于它们的形成功能，有效诱导SCAP增殖并分化为成牙本质细胞样细胞6是重要的。成纤维细胞生长因子2（FGF2）在伤口愈合和组织形成中起着至关重要的作用7,8,9。在细胞水平上，FGF2通过激活细胞膜上的FGF受体（FGFR）来调节各种细胞功能10。

This activation leads to the dimerisation and activation of intracellular signalling pathways, such as mitogen-activated protein kinase and phosphoinositide three kinase (PI3K)/AKT, which in turn regulate the proliferation, differentiation, and migration of different types of cells11,12.However, the role of FGF2 in the biological functions of SCAP has not yet been thoroughly investigated.

这种激活导致细胞内信号传导途径的二聚化和激活，例如丝裂原活化蛋白激酶和磷酸肌醇三激酶（PI3K）/AKT，其反过来调节不同类型细胞的增殖，分化和迁移11,12。然而，FGF2在SCAP生物学功能中的作用尚未得到彻底研究。

It was reported that FGF2 maintains the expression of stemness markers such as Oct4, Sox2, and Nanog by activating specific signalling pathways, including the ERK1/2 and PI3K/AKT pathways, and subsequently promotes the self-renewal ability of MSCs13. Although the effect of FGF2 on cell proliferation is well established, its effects on mineralisation and osteogenic differentiation are still being debated.

据报道，FGF2通过激活特定的信号通路（包括ERK1/2和PI3K/AKT通路）来维持干细胞标志物如Oct4，Sox2和Nanog的表达，并随后促进MSCs13的自我更新能力。尽管FGF2对细胞增殖的影响已经确立，但其对矿化和成骨分化的影响仍在争论中。

Previous studies have shown that the effect of FGF2 on the differentiation of dental MSCs depends on both the cellular phase and duration of FGF2 exposure14,15. In other words, different durations of FGF treatment or pretreatment may either inhibit or en.

先前的研究表明，FGF2对牙科MSCs分化的影响取决于FGF2暴露的细胞期和持续时间14,15。换句话说，FGF治疗或预处理的不同持续时间可能会抑制或抑制。

Data availability

数据可用性

The authors confirm that the data supporting the findings of this study are available within the article and supplementary materials. More data will be made available (Jiayuan Wu, Email address: wujiayuan@zmu.edu.cn) on reasonable request.

作者证实，文章和补充材料中提供了支持本研究结果的数据。将提供更多数据（Jiayuan Wu，电子邮件地址：wujiayuan@zmu.edu.cn)应合理要求。

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Download referencesFundingThis study was supported by grants from Guizhou Provincial Health Commission Science and Technology Fund Project (No. gzwjkj2020-1-163), Science and Technology Plan Project of Guizhou Province (QKH- Foundation-ZK (2022) General 638), The Etiology and Prevention Team Project of Oral Infectious and Malignant Diseases in the Affiliated Stomatological Hospital of Zunyi Medical University (No.

下载参考文献资助本研究得到了贵州省卫生委员会科学技术基金项目（编号gzwjkj2020-1-163），贵州省科学技术计划项目（QKH-基金ZK（2022）General 638），遵义医科大学附属口腔医院口腔传染病和恶性疾病病因学和预防团队项目（No。

(2020)293).Author informationAuthor notesThese authors contributed equally: Zijie Wang and Chuying Chen.Authors and AffiliationsHospital of Stomatology, Zunyi Medical University, Zunyi, 563000, Guizhou, ChinaZijie Wang, Liying Sun, Mei He, Ting Huang, Jiji Zheng & Jiayuan WuSchool of Stomatology, Southern Medical University, Guangzhou, 510000, Guangdong, ChinaChuying ChenDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510000, ChinaChuying ChenAuthorsZijie WangView author publicationsYou can also search for this author in.

（2020）293）。作者信息作者注意到这些作者做出了同样的贡献：王子杰和陈楚英。作者和附属机构遵义医科大学口腔医学院，遵义，563000，贵州，中国王子杰，孙丽英，梅荷，黄婷，郑季吉，吴佳元南方医科大学口腔医学院，广州，510000，广东，中国陈楚英南方医科大学南方医院口腔科，广州，510000，中国陈楚英作者王子杰作者出版物您也可以在中搜索这位作者。

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PubMed Google ScholarContributionsZijie Wang: Conceptualisation, methodology, formal analysis, data curation, writing—original draft, writing—review and editing, visualisation. Chuying Chen: Writing—original draft, writing—review and editing, formal analysis. Liying Sun: Acquisition of data, or analysis and interpretation of data.

PubMed谷歌学术贡献王：概念化，方法论，形式分析，数据管理，撰写原稿，撰写评论和编辑，可视化。陈楚英：撰写原稿，撰写评论和编辑，形式分析。孙立英：获取数据，或分析和解释数据。

Mei He: Acquisition of data, or analysis and interpretation of data. Ting Huang: Acquisition of data, or analysis and interpretation of data. Jiji Zheng: Acquisition of data, or analysis and interpretation of data. Jiayuan Wu: Conceptualisation, methodology, formal analysis. The final manuscript was reviewed and approved by all the authors.Corresponding authorCorrespondence to.

。黄婷：获取数据，或分析和解释数据。Jiji Zheng：获取数据，或分析和解释数据。吴佳元：概念化，方法论，形式分析。所有作者都审查并批准了最终稿件。对应作者对应。

Jiayuan Wu.Ethics declarations

吴佳元。道德宣言

Competing interests

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The authors declare no competing interests.

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Reprints and permissionsAbout this articleCite this articleWang, Z., Chen, C., Sun, L. et al. Fibroblast growth factor 2 promotes osteo/odontogenic differentiation in stem cells from the apical papilla by inhibiting PI3K/AKT pathway.

转载和许可本文引用本文Wang，Z.，Chen，C.，Sun，L。等人。成纤维细胞生长因子2通过抑制PI3K/AKT途径促进干细胞从顶端乳头的骨/牙源性分化。

Sci Rep 14, 19354 (2024). https://doi.org/10.1038/s41598-024-70123-0Download citationReceived: 29 January 2024Accepted: 13 August 2024Published: 21 August 2024DOI: https://doi.org/10.1038/s41598-024-70123-0Share 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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