The long noncoding <scp>RNA MALAT</scp>1 regulates the lipopolysaccharide‐induced inflammatory response through its interaction with <scp>NF</scp>‐κB

Gui, Zhao; Su, Zhenyi; Song, Dan; Mao, Yimin; Mao, Xiaohua

doi:10.1002/1873-3468.12315

Cited by 190 publications

(194 citation statements)

References 41 publications

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“…15 In consistent with the previous study, we also found that MALAT1 was upregulated in LPS-stimulated ATDC5 cells. 15 In consistent with the previous study, we also found that MALAT1 was upregulated in LPS-stimulated ATDC5 cells.…”

Section: 4 | Discussionsupporting

confidence: 93%

“…Puthanveetil et al 13 suggested that MALAT1 participated in the hyperglycemia-induced endothelial cell inflammatory injury. The experimental study from Zhao et al 15 proved that MALAT1 modulated the lipopolysaccharide (LPS)-stimulated inflammatory response by interacting NF-κB pathway. The experimental study from Zhao et al 15 proved that MALAT1 modulated the lipopolysaccharide (LPS)-stimulated inflammatory response by interacting NF-κB pathway.…”

Section: Introductionmentioning

confidence: 99%

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Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Lin

Liu

Zhao

et al. 2018

J of Cellular Biochemistry

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Osteoarthritis is the most frequent chronic bone-joint disease in middle-aged and older people worldwide. This study investigated the effects of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on lipopolysaccharide (LPS)-induced murine chondrogenic ATDC5 cell inflammatory injury. Cell viability and apoptosis were assessed using cell counting kit-8 assay and annexin V-phycoerythrin (PE) staining, respectively. The expression levels of interleukin-1β (IL)-1β, IL-6, IL-8, tumor necrosis factor α (TNF-α), MALAT1, and microRNA-19b (miR)-19b were measured using quantitative reverse-transcription polymerase chain reaction. Enzyme-linked immunosorbent assay was conducted to detect the concentrations of IL-1β, IL-6, IL-8, and TNF-α in culture supernatant of ATDC5 cells. Expressions of key factors involved in cell apoptosis, proinflammatory response, Wnt/β-catenin, and nuclear factor κB (NF-κB) pathways were analyzed using Western blot analysis. We found that LPS treatment remarkably induced ATDC5 cell apoptosis and inflammatory injury. MALAT1 was upregulated in LPS-stimulated ATDC5 cells. Overexpression of MALAT1 significantly reversed the LPS-induced ATDC5 cell inflammatory injury, while suppression of MALAT1 had opposite effects. Further results showed that MALAT1 positively regulated the expression of miR-19b in ATDC5 cells. Knockdown of miR-19b reversed the protective effect of MALAT1 on LPS-induced ATDC5 cells. In addition, MALAT1 reduced LPS-induced Wnt/β-catenin and NF-κB pathways activation in ATDC5 cells by upregulating miR-19. To conclude, our research verified that MALAT1 alleviated LPS-induced ATDC5 cell inflammatory injury by upregulating miR-19b and inactivating Wnt/β-catenin and NF-κB pathways. This finding will be helpful for further understanding the critical roles of MALAT1 and miR-19b in osteoarthritis and may provide possible targets for osteoarthritis diagnosis and treatment.

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Section: 4 | Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Lin

Liu

Zhao

et al. 2018

J of Cellular Biochemistry

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“…An independent group of researchers revealed that this miRNA additionally interferes in vitro with Th1 cell differentiation of human CD4 + T lymphocytes via PRKC [154]. Other miRNAs, including miR-124, miR-142-3p, and miR-195, have also been demonstrated to be useful in preventing hyperinflammation, apoptosis, and multiple organ injury in murine sepsis models [8, 140, 155, 156]. Similarly, indirect induction of miR-126 expression in vitro by CTEC-0214, a stromal cell-derived factor 1 alpha analog, preserved endothelial cell barrier integrity and attenuated pulmonary vascular leak [157].…”

Section: Discussionmentioning

confidence: 99%

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

Chan

Wong

et al. 2016

Crit Care

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BackgroundSepsis coincides with altered gene expression in different tissues. Accumulating evidence has suggested that microRNAs, long non-coding RNAs, and circular RNAs are important molecules involved in the crosstalk with various pathways pertinent to innate immunity, mitochondrial functions, and apoptosis.MethodsWe searched articles indexed in PubMed (MEDLINE), EMBASE and Europe PubMed Central databases using the Medical Subject Heading (MeSH) or Title/Abstract words (“microRNA”, “long non-coding RNA”, “circular RNA”, “sepsis” and/or “septic shock”) from inception to Sep 2016. Studies investigating the role of host-derived microRNA, long non-coding RNA, and circular RNA in the pathogenesis of and as biomarkers or therapeutics in sepsis were included. Data were extracted in terms of the role of non-coding RNAs in pathogenesis, and their applicability for use as biomarkers or therapeutics in sepsis. Two independent researchers assessed the quality of studies using a modified guideline from the Systematic Review Center for Laboratory animal Experimentation (SYRCLE), a tool based on the Cochrane Collaboration Risk of Bias tool.ResultsObservational studies revealed dysregulation of non-coding RNAs in septic patients. Experimental studies confirmed their crosstalk with JNK/NF-κB and other cellular pathways pertinent to innate immunity, mitochondrial function, and apoptosis. Of the included studies, the SYRCLE scores ranged from 3 to 7 (average score of 4.55). This suggests a moderate risk of bias. Of the 10 articles investigating non-coding RNAs as biomarkers, none of them included a validation cohort. Selective reporting of sensitivity, specificity, and receiver operating curve was common.ConclusionsAlthough non-coding RNAs appear to be good candidates as biomarkers and therapeutics for sepsis, their differential expression across tissues complicated the process. Further investigation on organ-specific delivery of these regulatory molecules may be useful.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1555-3) contains supplementary material, which is available to authorized users.

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“…lncRNAs metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is firstly discovered in non‐small cell lung cancer, which can promote the proliferation, metastasis, and invasion of tumor cells, and participate in epigenetic processes and cell cycle . Recent studies have found that MALAT1 is involved in the development of immune inflammatory diseases . Puthanveetil et al found that MALAT1 can increase high glucose‐induced inflammatory cytokines tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) expression.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 regulates inflammatory cytokine production in lipopolysaccharide‐stimulated human gingival fibroblasts through sponging miR‐20a and activating TLR4 pathway

Wang

Song

et al. 2019

J of Periodontal Research

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Background and Objective It has been reported that long non‐coding RNAs (lncRNAs), such as metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1), act as key regulators of the development of inflammatory diseases. However, it is unclear whether MALAT1 regulates the function of human gingival fibroblasts (HGFs) in periodontitis. This study is to explore the role of MALAT1 on inflammatory cytokine production of HGFs. Material and Methods Primary HGFs were harvested from human gingiva. MALAT1 was detected in inflammatory and healthy gingival tissues via quantitative real‐time PCR (qRT‐PCR). Bioinformatics analysis, dual‐luciferase reporter assay, and RNA‐binding protein immunoprecipitation (RIP) were used to detect the relationship among MALAT1, toll‐like receptor 4 (TLR4), and microRNA (miR) ‐20a. After transfection LPS‐treated HGFs with MALAT1 siRNA (si‐MALAT1), miR‐20a mimic or overexpression MALAT1 plasmid (sno‐MALAT1), the levels of MALAT1, miR‐20a, TLR4, IL‐6 and IL‐8 were analyzed by qRT‐PCR, enzyme‐linked immunosorbent assay, or western blot assay. Results MALAT1 up‐regulated in inflammatory gingival tissues of chronic periodontitis. MiR‐20a was bound with MALAT1 and TLR4 3′‐UTR in RNA‐protein complex with Ago2, respectively. Moreover, MALAT1, TLR4, IL‐6, and IL‐8 increased while miR‐20a decreased after 1 μg/mL Porphyromonas gingivalis lipopolysaccharide (LPS) or Escherichia coli LPS stimulation. MiR‐20a inhibited the expression of proinflammatory cytokines via binding to TLR4 3′‐UTR. In addition, MALAT1 increased TLR4 level and the secretion of inflammatory cytokines. Conclusion MALAT1 enhances inflammatory cytokine production through sponging miR‐20a and releasing TLR4, indicating a regulatory role of MALAT1 in periodontal inflammation.

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The long noncoding RNA MALAT1 regulates the lipopolysaccharide‐induced inflammatory response through its interaction with NF‐κB

Cited by 190 publications

References 41 publications

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

The involvement of regulatory non-coding RNAs in sepsis: a systematic review

LncRNA MALAT1 regulates inflammatory cytokine production in lipopolysaccharide‐stimulated human gingival fibroblasts through sponging miR‐20a and activating TLR4 pathway

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