ArticleJournal of inflammation research2020
Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy.
Article in Journal of inflammation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Expression and Regulatory Roles of Long Non-Coding RNAs in Periodontal Ligament Cells: A Systematic Review.Biomolecules · 2022Pooled it
- Long Non-coding RNA TLX1NB Regulates Inflammatory Response in Periodontitis by Interacting With Matrix Metalloproteinase 8.Inflammation · 2026Article
- Melatonin ameliorates inflammation-induced mitochondrial dysfunction and cementoblastic differentiation in cells by regulating the METTL3/LINC01444/HSPD1 axis.Fundamental research · 2026Article
- LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy.Chinese medical journal · 2026Article
- Potential Roles of Long Non-coding RNAs in the Pathogenesis of Periodontitis: Inflammation Response, Immune Infiltration, Collagen Fibers Synthesis, and Bone Remodeling.Current medicinal chemistry · 2025Article
- hsa_circ_0095812 accelerates periodontitis progression by adsorbing miR-485-3p-mediated THBS1 expression.Clinics (Sao Paulo, Brazil) · 2025Article
- Regulating the regulators: long non-coding RNAs as autophagic controllers in chronic disease management.Journal of biomedical science · 2024Review
- Non-coding RNAs Function in Periodontal Ligament Stem Cells.Stem cell reviews and reports · 2024Review
- The Expression Patterns of Non-Coding RNAs in Periodontal Disease.Dentistry journal · 2024Review
- Identification and assessment of differentially expressed necroptosis long non-coding RNAs associated with periodontitis in human.BMC oral health · 2023Article
- Psychological stress: neuroimmune roles in periodontal disease.Odontology · 2023Review
- Long non-coding RNA ZFY-AS1 represses periodontitis tissue inflammation and oxidative damage via modulating microRNA-129-5p/DEAD-Box helicase 3 X-linked axis.Bioengineered · 2022Article
- Long non-coding RNA SNHG5 promotes the osteogenic differentiation of bone marrow mesenchymal stem cells via the miR-212-3p/GDF5/SMAD pathway.Stem cell research & therapy · 2022Article
- Dysregulation of lncRNAs in circulation of patients with periodontitis: results of a pilot study.BMC oral health · 2021Article
- Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease.International journal of molecular sciences · 2021Review
- Identification and integrated analysis of differentially expressed long non-coding RNAs associated with periodontitis in humans.Journal of periodontal research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePeriodontitis is the leading cause of tooth loss. The role of long non-coding RNA (lncRNA) in periodontal inflammation remains unclear. The aim of this study was to investigate the role of lncRNA H19 in periodontitis and its possible regulation of autophagy in periodontitis. MATERIAL AND
methodsInflammation level was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) in periodontal ligament cells (PDLCs). Western blotting, flow cytometric analysis, and immunofluorescence staining were used to detect the autophagy flux. Overexpression or knockdown of H19 was used to confirm its function. Ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue were used in vivo. RNA sequencing was performed to determine the differentially expressed genes.
resultsAutophagy was significantly increased in PDLCs after inflammatory stimulation as well as in a ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue. During the inflammatory process, H19 expression was also significantly upregulated. Further, the levels of autophagic markers were significantly upregulated after overexpressing H19 in PDLCs, and the increased autophagic activity induced by inflammatory stimulation was reversed by H19 knockdown. RNA sequencing showed that the expression profiles of mRNAs were significantly altered after H19 overexpression, and the differentially expressed genes were enriched in the PI3K/AKT signaling pathway, which was confirmed by the decreased p-AKT protein expression in the H19 overexpression group.
conclusionPeriodontal inflammation activates autophagy flux, and H19 mediates the activation of autophagy via AKT pathway in periodontitis. This study expands our understanding of molecular regulation in periodontitis.
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