Abstract
Purpose Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.
Highlights
Periodontitis is a common inflammatory disease, which is caused by the imbalance of periodontal microbiota, such as Porphyromonas gingivalis (P. gingivalis) [1]
LINC00687 expression is upregulated, whereas the expression of LBX2AS1 and LINC01566 is downregulated in periodontitis samples [9]. Long noncoding RNAs (lncRNAs) PTCSC3 expression is decreased in periodontal ligament stem cells (PDLSCs) of Chronic periodontitis (CP) patients, and its overexpression inhibits PDLSC proliferation [10]
metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression was increased in gingival tissues of patients with CP compared with gingival tissues of healthy controls (P < 0:01, Figure 1(a))
Summary
Periodontitis is a common inflammatory disease, which is caused by the imbalance of periodontal microbiota, such as Porphyromonas gingivalis (P. gingivalis) [1]. Long noncoding RNAs (lncRNAs) above 200 nt have been recognized to be involved in many human diseases [6]. Many researches showed that lncRNAs are aberrantly expressed in periodontitis and play essential roles in the development of periodontitis [7, 8]. LncRNA PTCSC3 expression is decreased in periodontal ligament stem cells (PDLSCs) of CP patients, and its overexpression inhibits PDLSC proliferation [10]. BioMed Research International metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is related to periodontitis progression [11]. MALAT1 expression is obviously increased in PDLSCs isolated from periodontitis patients, and its overexpression promotes cell proliferation [12]. MALAT1 is highly expressed in inflammatory gingival tissues of CP and promotes inflammatory cytokine secretion in human gingival fibroblast (HGF) cells [13]. The detailed molecular mechanism of MALAT1 in CP needs further study
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