Influence of METTL3 knockdown on PDLSC osteogenesis in E. coli LPS-induced inflammation

作者全名："Chen, Hang; Peng, Limin; Wang, Zhenxiang; He, Yujuan; Zhang, Xiaonan"

作者地址："[Chen, Hang; Peng, Limin; Wang, Zhenxiang; Zhang, Xiaonan] Chongqing Med Univ, Coll Stomatol, Chongqing, Peoples R China; [Chen, Hang; Peng, Limin; Wang, Zhenxiang; Zhang, Xiaonan] Chongqing Med Univ, Chongqing Municipal Key Lab Oral Biomed Engn Highe, Chongqing, Peoples R China; [Chen, Hang; Peng, Limin; Wang, Zhenxiang; Zhang, Xiaonan] Chongqing Med Univ, Chongqing Key Lab Oral Dis & Biomed Sci, Chongqing, Peoples R China; [He, Yujuan] Chongqing Med Univ, Dept Lab Med, Key Lab Diagnost Med, Minist Educ, Chongqing, Peoples R China; [Zhang, Xiaonan] Chongqing Med Univ, Coll Stomatol, 426 Songshi North Rd, Chongqing, Peoples R China"

通信作者："Zhang, XN (通讯作者)，Chongqing Med Univ, Coll Stomatol, 426 Songshi North Rd, Chongqing, Peoples R China."

来源：ORAL DISEASES

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:001080997500001

JCR分区：Q1

影响因子：2.9

年份：2023

卷号：　

期号：　

开始页：　

结束页：　

文献类型：Article; Early Access

关键词：bioinformatics; METTL3; osteogenesis; periodontitis; PI3K/Akt signaling pathway

摘要："Objective: This study aimed to investigate the effect of METTL3 knockdown on osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) in the weak inflammation microenvironments, as well as the underlying mechanisms.Materials and Methods: PDLSCs were stimulated by lipopolysaccharide from Escherichia coli (E. coli LPS), followed by quantification of METTL3. METTL3 expression was assessed using RT-qPCR and Western blot analysis in periodontitis. METTL3 knockdown PDLSCs were stimulated with or without E. coli LPS. The evaluation included proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules. Bioinformatics analysis and Western blot determined the association between METTL3 and the PI3K/Akt pathway.Results: METTL3 was overexpressed in periodontitis. METTL3 knockdown in PDLSCs reduced proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules in both environments. Bioinformatics analysis suggested a link between METTL3 and the PI3K/Akt pathway. METTL3 knockdown inhibited PI3K/Akt signaling pathway activation.Conclusion: METTL3 knockdown might inhibit osteogenesis in PDLSCs through the inactivation of PI3K/Akt signaling pathway. Concomitant findings might shed novel light on the roles and potential mechanisms of METTL3 in the LPS-stimulated inflammatory microenvironments of PDLSCs."

基金机构："This work was financially supported by National Natural Science Foundation of China (81700982), the Natural Science Foundation Project of Chongqing, China (CSTB2022NSCQ-MSX0084), and the Chongqing Medical Reserve Talent Studio for Young People (ZQNYXGDRCGZ [81700982]; National Natural Science Foundation of China [CSTB2022NSCQ-MSX0084]; Natural Science Foundation Project of Chongqing, China [ZQNYXGDRCGZS2019004]; Chongqing Medical Reserve Talent Studio for Young People"

基金资助正文："This work was financially supported by National Natural Science Foundation of China (81700982), the Natural Science Foundation Project of Chongqing, China (CSTB2022NSCQ-MSX0084), and the Chongqing Medical Reserve Talent Studio for Young People (ZQNYXGDRCGZS2019004)."