{"title":"Role of Long Non-Coding RNA GUSBP11 in Chronic Periodontitis Through Regulation of miR-185-5p: A Retrospective Cohort Study.","authors":"Xiaowen Zhang, Xiang Shen","doi":"10.2147/JIR.S496143","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Previous studies have shown that long non-coding RNA GUSBP11 is abnormally expressed in patients with periodontitis, but the specific mechanism remains to be investigated. The purpose of this study was to explore the role of GUSBP11/miR-185-5p in chronic periodontitis (CP) and its potential mechanism, so as to provide a basis for elucidating the pathogenesis of CP.</p><p><strong>Patients and methods: </strong>The expression trends of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients and control group were analyzed by RT-qPCR. Human gingival fibroblasts (HGF) induced by 10μg/mL LPS were used to construct CP cell models in vitro. The level of intracellular gene expression is regulated by cell transfection. The cell viability of HGF was evaluated by CCK-8 method, and the expression of HGF inflammatory factors was evaluated by ELISA. The targeting relationship between GUSBP11 and miR-185-5p was confirmed by luciferase reporter gene. The target genes of miR-185-5p were predicted using an online database, and the intersection target genes were obtained by constructing Venn diagram. Then GO analysis and KEGG pathway enrichment analysis were performed.</p><p><strong>Results: </strong>Compared with the control group, the expression levels of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients were up-regulated and down-regulated, respectively (<i>P</i> < 0.001). The levels of GUSBP11 and miR-185-5p increased and decreased with the severity of CP, respectively (<i>P</i> < 0.01). LPS induces the decrease of HGF activity and the activation of inflammatory response, and the decrease of GUSBP11 may prevent the adverse effect of LPS on HGF (<i>P</i> < 0.001). Dual luciferase reporter genes showed that miR-185-5p interacts with GUSBP11. The increase of miR-185-5p also significantly improved the negative effect of LPS induction on HGF (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>GUSBP11 promotes the inflammatory response and proliferation inhibition of human gingival fibroblasts induced by LPS by down-regulating miR-185-5p, thus promoting the development of CP.</p>","PeriodicalId":16107,"journal":{"name":"Journal of Inflammation Research","volume":"18 ","pages":"655-665"},"PeriodicalIF":4.2000,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745139/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Inflammation Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2147/JIR.S496143","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: Previous studies have shown that long non-coding RNA GUSBP11 is abnormally expressed in patients with periodontitis, but the specific mechanism remains to be investigated. The purpose of this study was to explore the role of GUSBP11/miR-185-5p in chronic periodontitis (CP) and its potential mechanism, so as to provide a basis for elucidating the pathogenesis of CP.
Patients and methods: The expression trends of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients and control group were analyzed by RT-qPCR. Human gingival fibroblasts (HGF) induced by 10μg/mL LPS were used to construct CP cell models in vitro. The level of intracellular gene expression is regulated by cell transfection. The cell viability of HGF was evaluated by CCK-8 method, and the expression of HGF inflammatory factors was evaluated by ELISA. The targeting relationship between GUSBP11 and miR-185-5p was confirmed by luciferase reporter gene. The target genes of miR-185-5p were predicted using an online database, and the intersection target genes were obtained by constructing Venn diagram. Then GO analysis and KEGG pathway enrichment analysis were performed.
Results: Compared with the control group, the expression levels of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients were up-regulated and down-regulated, respectively (P < 0.001). The levels of GUSBP11 and miR-185-5p increased and decreased with the severity of CP, respectively (P < 0.01). LPS induces the decrease of HGF activity and the activation of inflammatory response, and the decrease of GUSBP11 may prevent the adverse effect of LPS on HGF (P < 0.001). Dual luciferase reporter genes showed that miR-185-5p interacts with GUSBP11. The increase of miR-185-5p also significantly improved the negative effect of LPS induction on HGF (P < 0.001).
Conclusion: GUSBP11 promotes the inflammatory response and proliferation inhibition of human gingival fibroblasts induced by LPS by down-regulating miR-185-5p, thus promoting the development of CP.
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An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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