口腔颌面外科杂志2025，Vol.35Issue(2)：116-122,7.DOI:10.12439/kqhm.1005-4979.2025.02.005
EGR1通过激活lnc-HCG11/Wnt/β-catenin通路促进牙周膜细胞的成骨分化
EGR1 promotes osteogenic differentiation of periodontal ligament cells by activating the lnc-HCG11/Wnt/β-catenin pathway
摘要
Abstract
Objective:To investigate the effect of early growth response gene 1(EGR1)on osteogenic differentiation of human periodontal ligament stem cells(hPDLSCs)by regulating long non-coding RNA human leukocyte antigen complex group 11(lnc-HCG11)and wingless/β-catenin(Wnt/β-catenin)pathway.Methods:The expression levels of EGR1 and lnc-HCG11 were changed in hPDLSCs through gene overexpression and interference assays,while the activation level of the Wnt/β-catenin pathway was altered by the β-catenin inhibitor IWR-1.Subsequently,real-time quantitative polymerase chain reaction(RT-qPCR)and Western blotting experiments were conducted to validate the intervention effect.After osteogenic induction,RT-qPCR was used to detect the expression levels of osteogenic genes runt-related transcription factor 2(RUNX2),collagen typeⅠα 1(COL1A1),osteopontin(OPN),osteocalcin(OCN),and alizarin red staining was used to detect the mineralization level of cells.Results:The overexpression of EGR1 was observed to promote the expression of lnc-HCG11 in hPDLSCs,while the overexpression of lnc-HCG11 promoted the expression levels of RUNX2,COL1A1,OPN,OCN,and mineralization in hPDLSCs.The pro-osteogenic effect of EGR1 was inhibited by silencing lnc-HCG11,while treatment with IWR-1 suppressed the expression of active β-catenin and weakened the pro-osteogenic effect of lnc-HCG11 on hPDLSCs.Conclusion:EGR1 promotes osteogenic differentiation of hPDLSCs by activating the lnc-HCG11/Wnt/β-catenin pathway.关键词
牙周炎/人牙周膜干细胞/早期生长应答因子1/lncRNA HCG11/成骨分化Key words
periodontitis/human periodontal ligament stem cells/early growth response gene 1/lncRNA HCG11/osteogenic differentiation分类
医药卫生引用本文复制引用
李成,隆湘凤,周琴,徐方方,黄学成,毛加团..EGR1通过激活lnc-HCG11/Wnt/β-catenin通路促进牙周膜细胞的成骨分化[J].口腔颌面外科杂志,2025,35(2):116-122,7.基金项目
2022年静安区医学科研课题(2022MS18) （2022MS18）
