LncRNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) regulates the proliferation of human periodontal ligament stem cells and toll-like receptor 4 (TLR4) expression to improve periodontitis

Liu, Wei; Zheng, Yongyang; Chen, Ben; Tang, Ke; Shi, Zhenxiang

doi:10.1186/s12903-019-0802-9

Cited by 16 publications

(16 citation statements)

References 23 publications

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“…Besides protein‐coding genes, differentially expressed lncRNAs have also been identified in periodontitis 16 . Certain differentially expressed lncRNAs have been reported to be critical players in periodontitis 17,18 . In this study, we observed reduced expression levels of DCST1‐AS1 in periodontitis and its enhancing effects on PDLCs’ proliferation, suggesting that DCST1‐AS1 might participate in the pathogenesis of periodontitis through regulating PDLCs proliferation.…”

Section: Discussionsupporting

confidence: 50%

LncRNA DCST1‐AS1 inhibits PDLCs’ proliferation in periodontitis and may bind with miR‐21 precursor to upregulate PLAP‐1

Wang

2021

J of Periodontal Research

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Objective This study aimed to investigate the potential interactions among long noncoding RNA domain containing 1‐antisense (lncRNA DCST1‐AS1), miR‐21, and periodontal ligament–associated protein‐1 (PLAP‐1) in periodontitis. Background data discussing the present state of the field It has been verified that miR‐21 can target PLAP‐1 to regulate the osteogenic differentiation of periodontal ligament cells (PDLCs). Methods Differential expression of DCST1‐AS1 and miR‐21 in PDLCs derived from periodontitis patients and healthy controls was determined by qPCR and unpaired t test. QPCR and Western blots were conducted to evaluate the effects of overexpression of DCST1‐AS1 and miR‐21 on the expression of PLAP‐1. CCK‐8 assay was applied to evaluate the effect of DCST1‐ASI, miR‐21, or PLAP‐1 on PDLCs’ proliferation. Western blotting was conducted to detect the expression levels of CKD family (CDK4, CDK6, and CCND1). Results DCST1‐AS1 was downregulated in PDLCs derived from periodontitis patients, and its expression was inversely correlated with the expression of miR‐2 but positively correlated with PLAP‐1. Bioinformatics analysis showed that DCST1‐AS1 might bind with miR‐21 precursor but not mature miR‐21. Transfection experiments showed that overexpression of DCST1‐AS1 led to decreased expression levels of miR‐21 and significantly increased the expression levels of PLAP‐1 at both mRNA and protein levels, while overexpression of miR‐21 resulted in a dramatic lower level of PLAP‐1. CCK‐8 assay indicated that overexpression of DCST1‐AS1 or PLAP‐1 prohibited PDLCs’ proliferation. However, elevation of miR‐21 had a contrary effect on the proliferation of PDLCs. And increased expression levels of DCST1‐AS1 could significantly inhibit the expression of CDK4, CDK6, and CCND‐1, while overexpression of miR‐21 inversed the effects of DCST1‐AS1. Conclusion Therefore, the expression levels of DCST1‐AS1 are much lower in periodontitis patients compared to that in healthy controls, and overexpression of DCST1‐AS1 can significantly elevate the expression of PLAP‐1 by inhibiting miR‐21 in PDLCs.

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Section: Discussionsupporting

confidence: 50%

LncRNA DCST1‐AS1 inhibits PDLCs’ proliferation in periodontitis and may bind with miR‐21 precursor to upregulate PLAP‐1

Wang

2021

J of Periodontal Research

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“…Gram-negative bacteria are the major pathogen involved in periodontitis, and their main pathogenic component is the lipopolysaccharide (LPS) that is primarily recognized by TLR4 ( Janssens and Beyaert, 2003 ; Sun et al, 2008 ). A large body of evidence has proven the involvement of TLR4 in periodontitis ( Renn et al, 2018 ; Liu et al, 2019a ). Researchers have revealed that TLR4 can be activated by LPS to regulate NF-κB pathway of PDLSCs to subsequently decrease their osteogenic potential ( Li et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

CircMAP3K11 Contributes to Proliferation, Apoptosis and Migration of Human Periodontal Ligament Stem Cells in Inflammatory Microenvironment by Regulating TLR4 via miR-511 Sponging

et al. 2021

Front. Pharmacol.

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Growing number of studies regarding the role of circRNAs in the development of various diseases have emerged in recent years, but the role of circRNAs in periodontitis pathogenesis remains obscure. Human periodontal ligament stem cells (hPDLSCs) play a critical role in periodontal remodeling, regeneration and repair processes, and their regenerative capacity could be prohibited in local periodontal inflammatory microenvironment. Herein, we sought to uncover the molecular mechanisms of periodontitis pathogenesis by investigating the role of circMAP3K11 (hsa_circ_002284) for regenerative capacity of hPDLSCs under an inflammatory condition. The hPDLSCs isolated from periodontitis patients were used as a cell model of inflammatory microenvironment to study the effect of the circMAP3K11/miR-511-3p/TLR4 axis on the proliferation, apoptosis and migration of hPDLSCs under inflammatory conditions. Compared to the periodontal tissues from normal subjects, those from periodontitis patients exhibited higher expression levels of circMAP3K11 and TLR4, and lower expression level of miR-511-3p. Both the expressions of circMAP3K11 and TLR4 were negatively correlated with the expressions of miR-511-3p in periodontitis. In vitro studies demonstrated that circMAP3K11 is capable of enhancing hPDLSCs proliferation and migration, and reducing the apoptosis of hPDLSCs. We also found that circMAP3K11 could up-regulate the expression of transcription factors that are closely related to periodontal regeneration (Runx2, OSX, ATF4, and BSP). RT-PCR and western blot showed that the inhibitory role of miR-511-3p on TLR4 expression could be reversed by circMAP3K11, which was in line with the results of bioinformatics tools and luciferase reporter assay. Meanwhile, both in vitro and in vivo studies indicated that circMAP3K11 could reverse the effects of miR-511-3p in periodontitis, which further confirmed that circMAP3K11 functioned as a ‘sponge’ of miR-511-3p to positively regulate the expression of TLR4. Taken together, our study preliminarily uncovered a circMAP3K11/miR-511-3p/TLR4 axis that regulates the function of hPDLSCs in periodontitis, providing novel insight and scientific base in the treatment of periodontal tissue regeneration based on stem cells.

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“…Periodontitis is characterized by an imbalance between proliferation and apoptosis of periodontal ligament cells (PDLCs) 55 . Accumulating evidence has demonstrated that various lncRNAs exert vital roles in the proliferation and apoptosis of periodontitis PDLCs (pPDLCs) 17,56‐63 . Fibroblast growth factor‐2 (FGF2) is a pivotal promoter of PDLSCs proliferation 64 .…”

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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LncRNA papillary thyroid carcinoma susceptibility candidate 3 (PTCSC3) regulates the proliferation of human periodontal ligament stem cells and toll-like receptor 4 (TLR4) expression to improve periodontitis

Cited by 16 publications

References 23 publications

LncRNA DCST1‐AS1 inhibits PDLCs’ proliferation in periodontitis and may bind with miR‐21 precursor to upregulate PLAP‐1

LncRNA DCST1‐AS1 inhibits PDLCs’ proliferation in periodontitis and may bind with miR‐21 precursor to upregulate PLAP‐1

CircMAP3K11 Contributes to Proliferation, Apoptosis and Migration of Human Periodontal Ligament Stem Cells in Inflammatory Microenvironment by Regulating TLR4 via miR-511 Sponging

Long non‐coding RNAs: Emerging roles in periodontitis

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