Longnon‐coding RNA NEAT1 overexpression associates with increased exacerbation risk, severity, and inflammation, as well as decreased lung function through the interaction with microRNA‐124 in asthma

Li, Xueying; Ye, Shenglan; Lü, Yang

doi:10.1002/jcla.23023

Cited by 41 publications

(44 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Jin et al ( 29 ) found that NEAT1 promoted liver fibrosis by mediating miR-506 and transcriptional activator GLI3. In addition, NEAT1 has been found to impair lung function through the interaction with miR-124 ( 30 ). Understanding the crosstalk between lncRNA, miRNA and mRNA, and their regulatory pattern could provide a novel perspective for the therapy of pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Liu

Wang

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. In this study, the mRNA expression levels of NEAT1, miR-455-3p and SMAD3 in the HPAEpiC alveolar and BEAS-2B bronchial epithelial cell lines were determined using reverse transcription-quantitative PCR, while the markers of epithelial-mesenchymal transformation (EMT) and collagen production were determined using western blot analysis. A wound healing assay was performed to evaluate the migratory ability of the HPAEpiC and BEAS-2B cell lines. The interactions between NEAT1 and miR-455-3p or SMAD3 and miR-455-3p were validated using a luciferase reporter gene assay. The results showed that the mRNA expression levels of NEAT1 and SMAD3 were upregulated in the TGF-β1-treated HPAEpiC and BEAS-2B cell lines, while the mRNA expression level of miR-455-3p was significantly decreased. In addition, silencing NEAT1 effectively alleviated the migratory ability, EMT and collagen generation of the epithelial cells. Following these experiments, NEAT1 was identified as a sponge for miR-455-3p, and SMAD3 was a target gene of miR-455-3p. NEAT1 downregulation or miR-455-3p mimic inhibited the migratory ability, EMT and collagen production of the epithelial cells; however, the effects were reversed by the overexpression of SMAD3. Furthermore, NEAT1 knockdown reduced the expression level of SMAD3 by increasing the expression level of miR-455-3p to further inhibit the migratory ability, EMT and collagen production of epithelial cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Liu

Wang

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…Several lncRNAs have been revealed to act as a modulator of Th1 and Th2 inflammation in asthma. Li et al (2020) confirmed that lncRNA NEAT1 was upregulated and were negatively correlated with miR-124. Also, it was positively correlated with Th1-associated TNF-α, IL-1β and Th17-associated IL-17 to enhance the exacerbation risk of asthma, which showed its potential to regulate Th1 inflammation in asthma.…”

Section: Lncrnas Associated With Inflammation In Asthma Pathogenesismentioning

confidence: 64%

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

2020

View full text Add to dashboard Cite

Asthma is a chronic airway inflammatory disorder related to variable expiratory airflow limitation, leading to wheeze, shortness of breath, chest tightness, and cough. Its characteristic features include airway inflammation, airway remodeling and airway hyperresponsiveness. The pathogenesis of asthma remains extremely complicated and the detailed mechanisms are not clarified. Long noncoding RNAs (lncRNAs) have been reported to play a prominent role in asthma and function as modulators of various aspects in pathological progress of asthma. Here, we summarize recent advances of lncRNAs in asthma pathogenesis to guide future researches, clinical treatment and drug development, including their regulatory functions in the T helper (Th) 1/Th2 imbalance, Th17/T regulatory (Treg) imbalance, eosinophils dysfunction, macrophage polarization, airway smooth muscle cells proliferation, and glucocorticoid insensitivity.

show abstract

“…To determine the role of lncRNAs in autophagy, we tested six candidate lncRNAs (FER1L4, HIF1A-AS1, MIR22HG, NEAT1, H19, and MIAT) supposed to be involved in the process of inflammation. 19,[33][34][35][36][37] Among them, H19, a conserved lncRNA, was the most differentially expressed. H19 has been reported to regulate autophagy in various types of cancer, and its aberrant expression was associated with tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy

Guo

Huang

Líu

et al. 2020

JIR

View full text Add to dashboard Cite

Purpose: Periodontitis is the leading cause of tooth loss. The role of long non-coding RNA (lncRNA) in periodontal inflammation remains unclear. The aim of this study was to investigate the role of lncRNA H19 in periodontitis and its possible regulation of autophagy in periodontitis. Material and Methods: Inflammation level was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) in periodontal ligament cells (PDLCs). Western blotting, flow cytometric analysis, and immunofluorescence staining were used to detect the autophagy flux. Overexpression or knockdown of H19 was used to confirm its function. Ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue were used in vivo. RNA sequencing was performed to determine the differentially expressed genes. Results: Autophagy was significantly increased in PDLCs after inflammatory stimulation as well as in a ligature-induced periodontitis model in mice and periodontitis-affected human gingival tissue. During the inflammatory process, H19 expression was also significantly upregulated. Further, the levels of autophagic markers were significantly upregulated after overexpressing H19 in PDLCs, and the increased autophagic activity induced by inflammatory stimulation was reversed by H19 knockdown. RNA sequencing showed that the expression profiles of mRNAs were significantly altered after H19 overexpression, and the differentially expressed genes were enriched in the PI3K/AKT signaling pathway, which was confirmed by the decreased p-AKT protein expression in the H19 overexpression group. Conclusion: Periodontal inflammation activates autophagy flux, and H19 mediates the activation of autophagy via AKT pathway in periodontitis. This study expands our understanding of molecular regulation in periodontitis.

show abstract

Longnon‐coding RNA NEAT1 overexpression associates with increased exacerbation risk, severity, and inflammation, as well as decreased lung function through the interaction with microRNA‐124 in asthma

Cited by 41 publications

References 24 publications

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis

Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications

<p>Long Non-Coding RNA H19 Participates in Periodontal Inflammation via Activation of Autophagy</p>

Contact Info

Product

Resources

About