Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Huang, Nannan; Li, Chanxiu; Sun, Wenjuan; Wu, Jian; Xiao, Feng

doi:10.1111/odi.13590

Cited by 16 publications

(13 citation statements)

References 41 publications

(42 reference statements)

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“…Table 3 presents 18 studies that investigated the role of lncRNAs in regulating cellular processes in PDL cells in the presence or absence of stimuli, including studies that compared H-PDL and P-PDL cells [ 60 , 61 , 62 , 63 , 64 , 65 ]. These studies also explored the role of lncRNAs in lipopolysaccharide (LPS)-induced inflammation [ 66 , 67 , 68 , 69 , 70 , 71 ], tumor necrosis factor-alpha (TNF-α)-induced inflammation [ 72 ], mechanical stress [ 73 , 74 , 75 ], hypoxia [ 76 ], and oxidative stress [ 77 ]. To review the outcomes of lncRNA involvement, cell proliferation, apoptosis, inflammatory responses, autophagy, migration, and root resorption were examined.…”

Section: Resultsmentioning

confidence: 99%

“…Inflammation-stimulating factors released by bacteria, such as LPS and TNF-α, activate the immune response in PDL cells, thereby aggravating the destruction of alveolar bone. Among the 18 studies that investigated the regulatory role of lncRNAs in PDL cells in response to inflammation and other stimuli, 6 studies compared the inflammatory responses of H-PDL and P-PDL cells [ 66 , 67 , 68 , 69 , 70 , 71 ], 7 studies stimulated PDL cells with LPS or/and TNF-α to mimic periodontal inflammation [ 66 , 68 , 69 , 70 , 71 , 72 , 74 ], 3 studies stimulated PDL cells with mechanical stress [ 73 , 74 , 75 ], 1 study subjected PDL cells to hypoxia [ 76 ], and 1 study subjected cells to oxidative stress [ 77 ]. Under these stimuli, the biological activities of PDL cells, including cell proliferation, apoptosis, inflammatory responses, osteogenic differentiation, and autophagy, were explored.…”

Section: Discussionmentioning

confidence: 99%

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The Expression and Regulatory Roles of Long Non-Coding RNAs in Periodontal Ligament Cells: A Systematic Review

et al. 2022

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Periodontal ligament (PDL) cells play a pivotal role in periodontal and bone homeostasis and have promising potential for regenerative medicine and tissue engineering. There is compelling evidence that long non-coding RNAs (lncRNAs) are differentially expressed in PDL cells compared to other cell types and that these lncRNAs are involved in a variety of biological processes. This study systematically reviews the current evidence regarding the expression and regulatory functions of lncRNAs in PDL cells during various biological processes. A systematic search was conducted on PubMed, the Web of Science, Embase, and Google Scholar to include articles published up to 1 July 2021. Original research articles that investigated the expression or regulation of lncRNAs in PDL cells were selected and evaluated for a systematic review. Fifty studies were ultimately included, based on our eligibility criteria. Thirteen of these studies broadly explored the expression profiles of lncRNAs in PDL cells using microarray or RNA sequencing. Nineteen studies investigated the mechanisms by which lncRNAs regulate osteogenic differentiation in PDL cells. The remaining 18 studies investigated the mechanism by which lncRNAs regulate the responses of PDL cells to various stimuli, namely, lipopolysaccharide-induced inflammation, tumor necrosis factor alpha-induced inflammation, mechanical stress, oxidative stress, or hypoxia. We systematically reviewed studies on the expression and regulatory roles of lncRNAs in diverse biological processes in PDL cells, including osteogenic differentiation and cellular responses to inflammation, mechanical stress, and other stimuli. These results provide new insights that may guide the development of lncRNA-based therapeutics for periodontal and bone regeneration.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Expression and Regulatory Roles of Long Non-Coding RNAs in Periodontal Ligament Cells: A Systematic Review

et al. 2022

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“…Huang et al . reported that TUG1 could decrease the production of inflammatory cytokines to protect against periodontitis via regulating miR‐498/RORA mediated Wnt/beta‐catenin signaling 74 . PTCSC3 could downregulate TLR‐4 to exert anti‐inflammatory effects in periodontitis 57 …”

Section: The Role Of Lncrnas In the Pathophysiology Of Periodontitismentioning

confidence: 99%

Long non‐coding RNAs: Emerging roles in periodontitis

Yin

Lin

et al. 2021

J of Periodontal Research

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Periodontitis is a major burden of public health, affecting 20%–50% of the global population. It is a complex inflammatory disease characterized by the destruction of supporting structures of the teeth, leading to tooth loss and the emergence or worsening of systematic diseases. Understanding the molecular mechanisms underlying the physiopathology of periodontitis is beneficial for targeted therapeutics. Long non‐coding RNAs (lncRNAs), transcripts made up of more than 200 nucleotides, have emerged as novel regulators of many biological and pathological processes. Recently, an increasing number of dysregulated lncRNAs have been found to be implicated in periodontitis. In this review, an overview of lncRNAs, including their biogenesis, characteristics, function mechanisms and research approaches, is provided. And we summarize recent research reports on the emerging roles of lncRNAs in regulating proliferation, apoptosis, inflammatory responses, and osteogenesis of periodontal cells to elucidate lncRNAs related physiopathology of periodontitis. Furthermore, we have highlighted the underlying mechanisms of lncRNAs in periodontitis pathology by interacting with microRNAs. Finally, the potential clinical applications, current challenges, and prospects of lncRNAs as diagnostic and prognostic biomarkers and therapeutic targets for periodontitis disease are discussed.

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“…Previous studies suggested that the roles of miRNAs in periodontitis are regulated by lncRNAs. For example, lncRNA TUG1 mitigates cell injury and cytokine production by regulating miR-498 in LPS-treated PDLCs [ 20 ]. The inhibition effects of miR-20a on secretion of inflammatory cytokines are regulated by MALAT1 in LPS-treated HGF cells [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis

Chen

Cao

2021

BioMed Research International

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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.

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Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Cited by 16 publications

References 41 publications

The Expression and Regulatory Roles of Long Non-Coding RNAs in Periodontal Ligament Cells: A Systematic Review

The Expression and Regulatory Roles of Long Non-Coding RNAs in Periodontal Ligament Cells: A Systematic Review

Long non‐coding RNAs: Emerging roles in periodontitis

Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis

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