The Long Non-coding RNAs: Paramount Regulators of the NLRP3 Inflammasome

Menon, Mridula P.; Hua, Kuo-Feng

doi:10.3389/fimmu.2020.569524

Cited by 36 publications

(31 citation statements)

References 209 publications

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“…Serological tests show that the inflammatory cytokine storm response (ICSR) is associated with COVID-19 severity and mortality as a result of an uncontrolled systemic inflammatory response in the host (4,(64)(65)(66). IL-6 and NLRP3 inflammasome complexes are the main immune components of the immune response after pathogen infection, and their function and expression are significantly affected by ncRNAs, including lncRNAs (44,67,68). IL-6, which is a typical proinflammatory factor causing cytokine storm, seems have a direct association with a worsened patient condition, is particularly affected (69,70).…”

Section: Inflammatory Responsementioning

confidence: 99%

Long Noncoding RNAs as Emerging Regulators of COVID-19

et al. 2021

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Coronavirus disease 2019 (COVID-19), which has high incidence rates with rapid rate of transmission, is a pandemic that spread across the world, resulting in more than 3,000,000 deaths globally. Currently, several drugs have been used for the clinical treatment of COVID-19, such as antivirals (radecivir, baritinib), monoclonal antibodies (tocilizumab), and glucocorticoids (dexamethasone). Accumulating evidence indicates that long noncoding RNAs (lncRNAs) are essential regulators of virus infections and antiviral immune responses including biological processes that are involved in the regulation of COVID-19 and subsequent disease states. Upon viral infections, cellular lncRNAs directly regulate viral genes and influence viral replication and pathology through virus-mediated changes in the host transcriptome. Additionally, several host lncRNAs could help the occurrence of viral immune escape by inhibiting type I interferons (IFN-1), while others could up-regulate IFN-1 production to play an antiviral role. Consequently, understanding the expression and function of lncRNAs during severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection will provide insights into the development of lncRNA-based methods. In this review, we summarized the current findings of lncRNAs in the regulation of the strong inflammatory response, immune dysfunction and thrombosis induced by SARS-CoV-2 infection, discussed the underlying mechanisms, and highlighted the therapeutic challenges of COVID-19 treatment and its future research directions.

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Section: Inflammatory Responsementioning

confidence: 99%

Long Noncoding RNAs as Emerging Regulators of COVID-19

et al. 2021

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“…MALAT1 also exerts various immunological effects including the mediation of NLRP3 inflammasome activation. ( Menon and Hua, 2020 ; Yu et al, 2018 ) MALAT1 has been linked to M1-like activity in macrophages, promoting inflammation. ( Cui et al, 2019 ) Our finding that MALAT1 is overexpressed in BAL MoMa of severe versus mild patients suggests that it might be involved in precipitating a shift towards M1 macrophages that exacerbates inflammation.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNAs (lncRNAs) NEAT1 and MALAT1 are differentially expressed in severe COVID-19 patients: An integrated single cell analysis

Kai

Wang

Vagts

et al. 2021

Preprint

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Hyperactive and damaging inflammation is a hallmark of severe rather than mild COVID-19 syndrome. To uncover key inflammatory differentiators between severe and mild COVID-19 disease, we applied an unbiased single-cell transcriptomic analysis. We integrated a bronchoalveolar lavage (BAL) dataset with a peripheral blood mononuclear cell dataset (PBMC) and analyzed the combined cell population, focusing on genes associated with disease severity. Distinct cell populations were detected in both BAL and PBMC where the immunomodulatory long non-coding RNAs (lncRNAs) NEAT1 and MALAT1 were highly differentially expressed between mild and severe patients. The detection of other severity associated genes involved in cellular stress response and apoptosis regulation suggests that the pro-inflammatory functions of these lncRNAs may foster cell stress and damage. The lncRNAs NEAT1 and MALAT1 are potential components of immune dysregulation in COVID-19 that may provide targets for severity related diagnostic measures or therapy.

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“…LncRNAs have been shown to regulate the occurrence and development of in ammatory diseases 35,36 . Maninjay K et al found that LINC-EPS regulated in ammatory response at the transcriptional level, inhibiting in ammation progression 37 .…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Tang¹,

Li²,

Yu³

et al. 2021

Preprint

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Background Periodontitis is a serious threat to oral quality of life and overall health. Although our previous studies confirmed that long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues, there are few reports on the pathogenesis of LINC01126 in periodontitis. Our study investigated the biological functions of LINC01126 in periodontitis and the potential mechanism. Results An inflammatory model of human gingival fibroblasts (HGFs) was successfully established. LINC01126 silencing can alleviate lipopolysaccharide (LPS) induced cell inflammation, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. qRT- PCR, WB, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK/STAT3 was abnormally activated in periodontitis tissues. Conclusions Our results indicate that LINC01126, as an endogenous competitive RNA (ceRNA) of miR-655-3p, can promote IL-6/JAK3/STAT3 pathway activation, thereby promoting periodontitis pathogenesis. And this is the first study of miR-655-3p in inflammatory periodontal diseases. Our study reveales a new pathogenesis of periodontitis, and provides a new strategy for preventing and treating periodontitis.

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The Long Non-coding RNAs: Paramount Regulators of the NLRP3 Inflammasome

Cited by 36 publications

References 209 publications

Long Noncoding RNAs as Emerging Regulators of COVID-19

Long Noncoding RNAs as Emerging Regulators of COVID-19

Long non-coding RNAs (lncRNAs) NEAT1 and MALAT1 are differentially expressed in severe COVID-19 patients: An integrated single cell analysis

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

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