NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

Li, Yanhui; Guo, Wei; Cai, Yiyong

doi:10.1515/med-2020-0007

Cited by 33 publications

(23 citation statements)

References 31 publications

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“…Silencing of circTLK1 attenuated myocardial ischaemia/reperfusion injury by sponging miR‐214 17 . Up‐regulation of miR‐17‐5p suppressed inflammation in sepsis, which was suggested as a therapeutic target for sepsis 53 . In the current study, the complementarity between circTLK1 and miR‐17‐5p was predicted by bioinformatics analysis.…”

Section: Discussionmentioning

confidence: 67%

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

Qiu

Qin

et al. 2021

J Cellular Molecular Medi

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Introduction Septic cardiomyopathy is a common complication of sepsis with high morbidity and mortality, but lacks specific therapy. This study aimed to reveal the role of circTLK1 and its potential mechanisms in septic cardiomyopathy. Materials and Methods The in vitro and in vivo models of septic cardiomyopathy were established. Cell viability and apoptosis were detected by CCK8, TUNEL and flow cytometry, respectively. LDH, CK, SOD, MDA, ATP, 8‐OHdG, NAD+/NADH ratio, ROS level, mitochondrial membrane potential and cytochrome C distribution were evaluated using commercial kits. qRT‐PCR and western blotting were performed to detect RNA and protein levels. Mitochondrial DNA (mtDNA) copy number and transcription were assessed by quantitative PCR. Dual‐luciferase assay, RNA immunoprecipitation and co‐immunoprecipitation were performed to verify the interaction between circTLK1/PARP1 and miR‐17‐5p. Results CircTLK1, PARP1 and HMGB1 were up‐regulated in the in vitro and in vivo models of septic cardiomyopathy. CircTLK1 inhibition restrained LPS‐induced up‐regulation of PARP1 and HMGB1. Moreover, circTLK1 knockdown repressed sepsis‐induced mtDNA oxidative damage, mitochondrial dysfunction and consequent cardiomyocyte apoptosis by inhibiting PARP1/HMGB1 axis in vitro and in vivo. In addition, circTLK1 enhanced PARP1 expression via sponging miR‐17‐5p. Inhibition of miR‐17‐5p abolished the protective effects of circTLK1 silencing on oxidative mtDNA damage and cardiomyocyte apoptosis. Conclusion CircTLK1 sponged miR‐17‐5p to aggravate mtDNA oxidative damage, mitochondrial dysfunction and cardiomyocyte apoptosis via activating PARP1/HMGB1 axis during sepsis, indicating that circTLK1 may be a putative therapeutic target for septic cardiomyopathy.

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Section: Discussionmentioning

confidence: 67%

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

Qiu

Qin

et al. 2021

J Cellular Molecular Medi

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“…These results demonstrated the therapeutic effects of noni fruit juice on acute gouty arthritis in mice. Furthermore, studies have shown that other four miRNAs (i.e., miR-122-5p, miR-146a-5p, miR-17-5p, and miR181c-5p) are involved in uric acid nephropathy, acute pneumonia, LPS-induced inflammatory injury, and poststroke inflammation, by combining with long noncoding RNAs of ANRIL, SNHG16, NEAT1, and Malat1, respectively [ 26 , 28 , 33 , 82 ]. Similarly, our results showed that these four miRNAs responded to the treatments of noni fruit juice and colchicine, showing up- and downregulated expressions in model mice and mice treated with both noni fruit juice and colchicine, respectively, indicating the therapeutic effects of noni fruit juice on acute gouty arthritis in mice.…”

Section: Resultsmentioning

confidence: 99%

MicroRNAs Involved in the Therapeutic Functions of Noni (Morinda citrifolia L.) Fruit Juice in the Treatment of Acute Gouty Arthritis in Mice Induced with Monosodium Urate

Liu

Shan

et al. 2021

Foods

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We investigated the functions of microRNAs in the therapeutic effects of noni (Morinda citrifolia L.) fruit juice on mouse models of acute gouty arthritis induced with monosodium urate (MSU). Compared with the model group (treated with MSU), mice in both the positive control group (treated with both MSU and colchicine) and noni fruit juice group (treated with MSU and noni fruit juice) showed a significantly decreased degree of paw swelling in 5 days, as well as the contents of two types of proinflammatory cytokines (i.e., NALP3 and TNF-α). Based on the next-generation sequencing technology, a total of 3896 microRNAs (234 known and 3662 novel) were identified in mice treated with noni fruit juice. A large amount of differentially expressed miRNAs were identified in the noni fruit juice group, suggesting the significant effects of noni fruit juice on the mice with acute gouty arthritis, while the different patterns of change in the numbers of both upregulated and downregulated miRNAs in both noni fruit juice and positive control groups indicated that the mice of acute gouty arthritis may be regulated by differential mechanisms between the treatments of noni fruit juice and colchicine. The target genes of microRNAs involved in the pathogenesis and pathology of acute gouty arthritis in mice were identified and further annotated by both Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Our results revealed the therapeutic effects of noni fruit juice on acute gouty arthritis in mice with a group of microRNAs involved in the pharmacological mechanisms of noni fruit juice, providing scientific evidence to support both the agricultural cultivation and pharmacological significance of noni plants.

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“…Furthermore, NEAT1 is not only im-plicated in cancer, but may also affect the inflammatory response. Li et al (35) reported that NEAT1 may promote LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4. In addition, downregulation of NEAT1 promoted cell proliferation and inhibited the apoptosis of rat cardiac muscle cells (36).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NEAT1 contributes to lipopolysaccharide‑induced inflammation and apoptosis of human middle ear epithelial cells via regulating the miR‑301b‑3p/TLR4 axis

et al. 2021

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Acute otitis media (AOM) is a common infectious disease in children that is accompanied by signs and symptoms of middle ear inflammation and infection. Previous studies have shown that the long non-coding (lnc)RNA nuclear-enriched abundant transcript 1(NEAT1) participates in various inflammatory conditions and plays an important regulatory role. The focus of the present study was the biological function of NEAT1 and underlying molecular mechanism in lipopolysaccharide (LPS)-induced human middle ear epithelial cells (HMEECs). The expression of NEAT1, miR-301b-3p and toll-like receptor 4 (TLR4) protein were determined by reverse transcription-quantitative PCR and western blot assays, respectively. Dual-luciferase reporter assay was performed to investigate the combination of miR-301b-3p and NEAT1 or TLR4. In addition, cell viability, apoptosis and the levels of pro-inflammatory factors (IL-1β, TNF-α and IL-6) were measured by Cell Counting Kit-8 assay, flow cytometry and ELISA, respectively. Cell viability was significantly decreased, whereas apoptosis and inflammation were increased in LPS-stimulated HMEECs. Functional analyses demonstrated that NEAT1 was upregulated following LPS treatment, whereas knockdown of NEAT1 significantly increased cell viability and alleviated apoptosis and inflammation. Mechanistically, NEAT1 directly bound to and negatively regulated miR-301b-3p expression, whereas miR-301b-3p inhibitors abolished the inhibitory effect of NEAT1 knockdown on cell apoptosis and inflammation. As a target of miR-301b-3p, TLR4 was regulated by NEAT1 and miR-301b-3p. TLR4 overexpression alleviated NEAT1 silencing-induced inflammatory suppression. Rescue experiments demonstrated that NEAT1 promoted TLR4 expression by inhibiting miR-301b-3p. Collectively, the results of the present study suggested that NEAT1 may attenuate LPS-induced inflammation and apoptosis in HMEECs by modulating the miR-301b-3p/TLR4 axis, and may provide a new therapeutic target for the clinical treatment of AOM.

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NEAT1 promotes LPS-induced inflammatory injury in macrophages by regulating miR-17-5p/TLR4

Cited by 33 publications

References 31 publications

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

MicroRNAs Involved in the Therapeutic Functions of Noni (Morinda citrifolia L.) Fruit Juice in the Treatment of Acute Gouty Arthritis in Mice Induced with Monosodium Urate

Long non‑coding RNA NEAT1 contributes to lipopolysaccharide‑induced inflammation and apoptosis of human middle ear epithelial cells via regulating the miR‑301b‑3p/TLR4 axis

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