Lipoxin suppresses inflammation via the TLR4/MyD88/NF‐κB pathway in periodontal ligament cells

Ali, Muhanad; Yang, Fang; Jansen, John A.; Walboomers, X. Frank

doi:10.1111/odi.13250

Cited by 22 publications

(20 citation statements)

References 44 publications

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“…HPDLCs, the predominant cells of the periodontal ligament, have been reported to play a pivotal role in tooth support, collagen production, and tissue regeneration (Ali, Yang, Jansen, & Walboomers, 2020). Thus, as target cells of LPS, hPDLCs are commonly used to stimulate the periodontitis environment in vitro.…”

Section: Discussionmentioning

confidence: 99%

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

Huang

Sun

et al. 2020

Oral Diseases

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Aim This study was aimed to investigate the role of TUG1 in LPS‐stimulated hPDLCs and to evaluate the potential functions of TUG1 in the pathogenesis of periodontitis. Methods LPS‐stimulated hPDLCs were established as the cell model. CCK‐8 assay was performed to assess cell proliferation ability. Flow cytometry was performed to detect cell cycle distribution, and quantitative RT‐PCR and Western blotting were conducted to measure gene expressions. ELISA kits were used to evaluate the production of inflammatory cytokines. The putative binding site between TUG1 and miR‐498 was verified using luciferase reporter and RNA immunoprecipitation assays. Results TUG1 was downregulated upon LPS stimulation in hPDLCs. TUG1 overexpression promoted cell proliferation through regulating the cell cycle distribution, along with the decreased expression of p21 and increased expression of CDK2 and cyclin D1. Besides, TUG1 overexpression decreased the production of inflammatory cytokines. The effects were opposite upon TUG1 knockdown. TUG1 negatively regulated its target miR‐498, and influenced the expression of RORA, the direct target of miR‐498. Simultaneous TUG1 overexpression and miR‐498 reversed the effect of TUG1 overexpression alone on alleviating LPS‐induced cell injury and inhibition of Wnt/β‐catenin signaling, which was further changeover after co‐overexpression with RORA. Conclusion Therefore, TUG1 could protect against periodontitis via regulating miR‐498/RORA mediated Wnt/β‐catenin signaling.

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Section: Discussionmentioning

confidence: 99%

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

Huang

Sun

et al. 2020

Oral Diseases

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“…Notably, blocking TLR4 or NF-κB signaling could partly overturn the impact of LPS on the osteogenesis potential of human periodontal ligament stem cells [31]. Similarly, LPS challenge increased the expression levels of TNF-α, TLR4, myeloid differentiation primary response 88, and NF-κB, and reduced the expression of IL-4 in HPDLCs, indicating that TLR4-mediated NF-κB signaling was implicated in LPS-induced inflammatory injury of HPLDCs [32]. Therefore, inhibition of TLR4-mediated NF-κB signaling is considered as an effective therapeutic approach for treating periodontitis.…”

Section: Discussionmentioning

confidence: 97%

Knockdown of TRIM52 alleviates LPS-induced inflammatory injury in human periodontal ligament cells through the TLR4/NF-κB pathway

Liu

Cui²,

Shen

2020

Bioscience Reports

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Tripartite motif-containing 52 (TRIM52) is a vital regulator of inflammation. However, the function and mechanisms of TRIM52 in lipopolysaccharide (LPS)-induced inflammatory injury of human periodontal ligament cells (HPDLCs) in periodontitis remain undefined. In the present research, gene expression was determined using a quantitative polymerase chain reaction and western blot. The effect of TRIM52 on LPS-induced inflammatory injury was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and enyzme-linked immunosorbent assay. We found that TRIM52 expression was upregulated in LPS-treated HPDLCs. Knockdown of TRIM52 alleviated LPS-induced proliferative inhibition and apoptosis promotion in HPDLCs, as evidenced by a decrease in cleaved caspase-3 expression and caspase-3 activity. Silencing TRIM52 suppressed LPS-induced inflammatory response of HPDLCs, as indicated by the decrease in interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α) levels and increase in IL-10 levels. TRIM52 knockdown inhibited LPS-induced activation of TLR4/nuclear factor-kappa B (NF-κB) signaling pathway. Taken together, knockdown of TRIM52 mitigated LPS-induced inflammatory injury via the TLR4/NF-κB signaling pathway, providing an effective therapeutic target for periodontitis.

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“…The protective mechanism appears to lie in the inhibition of pro-inflammatory cytokines that modulate PMNs, hampering their recruitment and pro-inflammatory signaling thus preventing the onset of periodontal inflammation (149). In this sense, LXA 4 treatment has also been found to abolish NF-kB and TNFa signaling in periodontal ligament cells, which play a pivotal role exacerbating the inflammatory response (150). Furthermore, increased circulating ROS levels and blood aggregation caused by P. gingivalis infection were successfully reduced upon LXA 4 treatment, and this effect appears to be dependent on platelet-PMN interaction (151).…”

Section: Periodontal Diseasesmentioning

confidence: 99%

Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases

et al. 2021

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Inflammation is an a physiological response instead an essential response of the organism to injury and its adequate resolution is essential to restore homeostasis. However, defective resolution can be the precursor of severe forms of chronic inflammation and fibrosis. Nowadays, it is known that an excessive inflammatory response underlies the most prevalent human pathologies worldwide. Therefore, great biomedical research efforts have been driven toward discovering new strategies to promote the resolution of inflammation with fewer side-effects and more specificity than the available anti-inflammatory treatments. In this line, the use of endogenous specialized pro-resolving mediators (SPMs) has gained a prominent interest. Among the different SPMs described, lipoxins stand out as one of the most studied and their deficiency has been widely associated with a wide range of pathologies. In this review, we examined the current knowledge on the therapeutic potential of lipoxins to treat diseases characterized by a severe inflammatory background affecting main physiological systems, paying special attention to the signaling pathways involved. Altogether, we provide an updated overview of the evidence suggesting that increasing endogenously generated lipoxins may emerge as a new therapeutic approach to prevent and treat many of the most prevalent diseases underpinned by an increased inflammatory response.

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Lipoxin suppresses inflammation via the TLR4/MyD88/NF‐κB pathway in periodontal ligament cells

Cited by 22 publications

References 44 publications

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

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

Knockdown of TRIM52 alleviates LPS-induced inflammatory injury in human periodontal ligament cells through the TLR4/NF-κB pathway

Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases

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