lncRNA RNA AC114812通过miR-181a-5p-SPP1轴调控牙周韧带细胞的炎症反应

IF 4.1 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-09-19 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S534691
Tong Tong, Fei Zhao, Ran Tao, Chunyan Liu, Bing Liu
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引用次数: 0

摘要

背景:长链非编码rna (lncRNAs)在牙周炎的发生和发展中起着重要作用。我们通过miR-181a-5p-SPP1轴研究了lncRNA AC114812在脂多糖(LPS)诱导的牙周韧带细胞(pdlc)增殖、迁移和炎症反应中的潜在作用。方法:对3对健康和牙周炎患者的牙龈组织进行生物信息学分析和全转录组测序分析,筛选牙周炎中差异表达的lncrna, LPS刺激构建牙周炎细胞模型。采用实时定量聚合酶链式反应(qRT-PCR)检测lncRNA AC114812在组织和细胞中的表达水平,采用荧光原位杂交(FISH)检测其表达定位。通过qRT-PCR、MTT法和创面愈合实验研究si-AC114812在牙周炎中的作用。通过数据库筛选结合测序结果,通过双荧光素酶基因报告实验验证lncRNA AC114812-miR-181a-5p-SPP1的竞争内源性RNA (ceRNA)机制。结果:LncRNA AC114812在牙周炎组织中高表达。lncRNA AC114812的敲低抑制炎症刺激的pdlc中炎症因子IL-1β (IL-1β)和IL-6 (IL-6)的表达,提高炎症影响的pdlc的增殖和迁移能力。FISH实验证实lncRNA AC114812主要在细胞质中表达,可能具有海绵效应。预测lncRNA AC114812-miR-181a-5p-SPP1的ceRNA机制。双荧光素酶基因报告试验证实了这三个基因之间存在结合位点以及它们之间的相互调控作用。结论:通过调节长链非编码RNA AC114812的表达,可以减轻炎症反应,从而影响细胞的增殖和迁移。这种作用可能通过miR-181a-5p-SPP1轴来实现。这为牙周病的防治提供了新的策略和干预目标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.

lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.

lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.

lncRNA RNA AC114812 Regulates the Inflammatory Response of Periodontal Ligament Cells via the miR-181a-5p-SPP1 Axis.

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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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: 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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