Static magnetic field contributes to osteogenic differentiation of hPDLSCs through the H19/Wnt/β-catenin axis

被引:0
|
作者
Yang, Yanling [1 ,2 ,3 ]
Gao, Na [4 ]
Ji, Guang [4 ]
Hu, Wenzhu [4 ]
Bi, Rong [5 ]
Liang, Jiangli [4 ]
Liu, Yali [1 ,2 ]
机构
[1] Kunming Med Univ, Sch & Hosp Stomatol, Dept Orthodont, 1088 Haiyuan Middle Rd, Kunming 650106, Yunnan, Peoples R China
[2] Kunming Med Univ, Yunnan Key Lab Stomatol, 1168 Chunrong West Rd, Kunming 650500, Yunnan, Peoples R China
[3] Yunnan Univ, Affiliated Hosp, Ctr Stomatol, 176 Qingnian Rd, Kunming 650021, Yunnan, Peoples R China
[4] Chinese Acad Med Sci, Inst Med Biol, Peking Union Med Coll, Lab Vaccine Dev, 935 Jiaoling Rd, Kunming 650118, Yunnan, Peoples R China
[5] Chinese Acad Med Sci, Inst Med Biol, Peking Union Med Coll, Genet Engn & Vaccine Res Ctr, 935 Jiaoling Rd, Kunming 650118, Yunnan, Peoples R China
基金
中国国家自然科学基金;
关键词
Periodontitis; Static magnetic field; Periodontal ligament stem cells; Osteogenic differentiation; Non-coding RNA; Wnt/(3-catenin pathway; MESENCHYMAL STEM-CELLS; PROMOTES; IMPLANTS; DISEASES;
D O I
10.1016/j.gene.2024.148967
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Background: Static magnetic field (SMF) as an effective physical stimulus is capable of osteogenic differentiation for multiple mesenchymal stem cells, including human periodontal ligament stem cells (hPDLSCs). However, the exact molecular mechanism is still unknown. Therefore, this study intends to excavate molecular mechanisms related to SMF in hPDLSCs using functional experiments. Methods: hPDLSCs were treated with different intensities of SMF, H19 lentivirus, and Wnt/(3-catenin pathway inhibitor (XAV939). Changes in osteogenic markers (Runx2, Col I, and BMP2), Wnt/(3-catenin markers ((3-catenin and GSK-3(3), and calcified nodules were examined using RT-qPCR, western blotting, and alizarin red staining in hPDLSCs. Results: SMF upregulated the expression of H19, and SMF and overexpressing H19 facilitated the expression of osteogenic markers (Runx2, Col I, and BMP2), activation of the Wnt/(3-catenin pathway, and mineralized sediment in hPDLSCs. Knockdown of H19 alleviated SMF function, and treatment with XAV939 limited SMF- and H19-mediated osteogenic differentiation of hPDLSCs. Notably, the expression of hsa-miR-532-3p, hsa-miR-3703p, hsa-miR-18a-5p, and hsa-miR-483-3p in hPDLSCs was regulated by SMF, and may form an endogenous competitive RNA mechanism with H19 and (3-catenin. Conclusion: SMF contributes to the osteogenic differentiation of hPDLSCs by mediating the H19/Wnt/(3-catenin pathway, and hsa-miR-532-3p, hsa-miR-370-3p, hsa-miR-18a-5p, and hsa-miR-483-3p may be the key factors in it.
引用
收藏
页数:10
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