ArticleJournal of inflammation research2025
lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Non-Coding RNAs in Oral Diseases: From Pathogenesis to Clinical Translation.International journal of molecular sciences · 2026Review
- Epigenetic memory in periodontal healing: mechanisms, evidence, and emerging therapeutic perspectives.Odontology · 2026Review
- Downregulation of UNC5B-AS1 in Preterm Infants with Bronchopulmonary Dysplasia and Its Protective Mechanism via the miR-134-5p/IGF1 Axis.Journal of inflammation research · 2026Article
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Authors and funding
5 authors.
Funding
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Abstract
Background: Long noncoding RNAs (lncRNAs) play a significant role in the occurrence and development of periodontitis. We investigate the potential role of the lncRNA AC114812 in the lipopolysaccharide (LPS) induced proliferation, migration and inflammatory response of periodontal ligament cells (PDLCs) via the miR-181a-5p-SPP1 axis. Methods: Bioinformatics analysis and whole transcriptome sequencing analysis were conducted on the gingival tissues of three pairs of healthy and periodontitis patients to screen out lncRNAs with differential expression in periodontitis and a periodontitis cell model was constructed via stimulation with LPS. The expression levels of the lncRNA AC114812 in tissues and cells were detected via real-time quantitative polymerase chain reaction (qRT-PCR), and the expression localization was detected via fluorescence in situ hybridization (FISH). The role of si-AC114812 in periodontitis was investigated through qRT-PCR, MTT assay and wound healing experiments. Through database screening combined with sequencing results, the competitive endogenous RNA (ceRNA) mechanism of lncRNA AC114812-miR-181a-5p-SPP1 was verified via a dual-luciferase gene reporter assay. Results: LncRNA AC114812 was highly expressed in periodontitis tissues. Knockdown of lncRNA AC114812 inhibited the expression of inflammatory factors interleukin-1β (IL-1β) and interleukin-6 (IL-6) in PDLCs stimulated by inflammation and improved the proliferation and migration abilities of PDLCs affected by inflammation. FISH assays confirmed that the lncRNA AC114812 was expressed mainly in cytoplasm and may have a sponge effect. The ceRNA mechanism of the lncRNA AC114812-miR-181a-5p-SPP1 was predicted. The dual-luciferase gene reporter assay verified the existence of binding sites among the three genes and their mutual regulatory effects. Conclusion: By regulating the expression of long non-coding RNA AC114812, the inflammatory response can be alleviated, thereby affecting cell proliferation and migration. The effect may be achieved through the miR-181a-5p-SPP1 axis. These can provide new strategies and intervention targets for the prevention and treatment of periodontal diseases.
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