Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

Cui, Huachun; Banerjee, Sami; Guo, Sijia; Xie, Na; Ge, Jing; Jiang, Dechun; Zörnig, Martin; Thannickal, Victor J.; Liu, Gang

doi:10.1172/jci.insight.124522

Cited by 116 publications

(100 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Isolation of primary mouse AMs, AECs, and lung Fbs. Mouse AMs were purified as previously described (41). Briefly, cells within BALF were collected by centrifugation (500 g for 5 minutes).…”

Section: Methodsmentioning

confidence: 99%

Monocyte-derived alveolar macrophage apolipoprotein E participates in pulmonary fibrosis resolution

Jiang¹,

Banerjee²,

Xie³

et al. 2020

JCI Insight

Self Cite

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Monocyte-derived alveolar macrophage apolipoprotein E participates in pulmonary fibrosis resolution

Jiang¹,

Banerjee²,

Xie³

et al. 2020

JCI Insight

Self Cite

View full text Add to dashboard Cite

“…Recently, more and more studies had explored its function in inflammatory progression. A study reported that MALAT1 regulated polarization of macrophage and response to lung injury [52]. Another study revealed MALAT1 regulated T-cell differentiation towards a Tregs phenotype, played an anti-inflammatory role in autoimmune neuroinflammation [53].…”

Section: Discussionmentioning

confidence: 99%

Construction of asthma related competing endogenous RNA network revealed novel long non-coding RNAs and potential new drugs

Liao

Wang

et al. 2020

Respir Res

View full text Add to dashboard Cite

Background: Asthma is a heterogeneous disease characterized by chronic airway inflammation. Long non-coding RNA can act as competing endogenous RNA to mRNA, and play significant role in many diseases. However, there is little known about the profiles of long non-coding RNA and the long non-coding RNA related competing endogenous RNA network in asthma. In current study, we aimed to explore the long non-coding RNA-microRNA-mRNA competing endogenous RNA network in asthma and their potential implications for therapy and prognosis. Methods: Asthma-related gene expression profiles were downloaded from the Gene Expression Omnibus database, re-annotated with these genes and identified for asthma-associated differentially expressed mRNAs and long noncoding RNAs. The long non-coding RNA-miRNA interaction data and mRNA-miRNA interaction data were downloaded using the starBase database to construct a long non-coding RNA-miRNA-mRNA global competing endogenous RNA network and extract asthma-related differentially expressed competing endogenous RNA network. Finally, functional enrichment analysis and drug repositioning of asthma-associated differentially expressed competing endogenous RNA networks were performed to further identify key long non-coding RNAs and potential therapeutics associated with asthma. Results: This study constructed an asthma-associated competing endogenous RNA network, determined 5 key long non-coding RNAs (MALAT1, MIR17HG, CASC2, MAGI2-AS3, DAPK1-IT1) and identified 8 potential new drugs (Tamoxifen, Ruxolitinib, Tretinoin, Quercetin, Dasatinib, Levocarnitine, Niflumic Acid, Glyburide). Conclusions: The results suggested that long non-coding RNA played an important role in asthma, and these novel long non-coding RNAs could be potential therapeutic target and prognostic biomarkers. At the same time, potential new drugs for asthma treatment have been discovered through drug repositioning techniques, providing a new direction for the treatment of asthma.

show abstract

“…Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (LncRNA MALAT1), a highly abundant and evolutionary conserved lncRNA, locates on chromosomal 11, which is essential in the regulation of various pathology-physiological processes such as inflammation and immunity. [1][2][3][4] For instance, lncRNA MALAT1 evokes and intensifies inflammation via activating p38 mitogen-activated protein kinase (MAPK)/nuclear factor kappa-light-chain enhancer of activated B-cell (NF-κB) signaling pathway in sepsis. 4 Another study reveals that lncRNA MALAT1 knockdown inhibits inflammatory responses in lipopolysaccharide (LPS)-induced acute lung injury.…”

Section: Introductionmentioning

confidence: 99%

The clinical value of lncRNA MALAT1 and its targets miR‐125b, miR‐133, miR‐146a, and miR‐203 for predicting disease progression in chronic obstructive pulmonary disease patients

Liu

Dong

2020

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Objective The study aimed to explore the correlations of long non‐coding RNA MALAT1 (lncRNA MALAT1) and its targets microRNA (miR)‐125b, miR‐133, miR‐146a, and miR‐203 with acute exacerbation risk, inflammation, and disease severity of chronic obstructive pulmonary disease (COPD). Methods Plasma samples were obtained from 120 acute exacerbation COPD (AECOPD) patients, 120 stable COPD patients, and 120 healthy controls (HCs). RT‐qPCR was conducted to detect lncRNA MALAT1 expression and its target miRNAs, and ELISA was performed to detect the inflammatory cytokines. Results LncRNA MALAT1 was highest in AECOPD patients followed by stable COPD patients and then HCs, which distinguished AECOPD patients from HCs (AUC: 0.969, 95% CI: 0.951‐0.987) and stable COPD patients (AUC: 0.846, 95% CI: 0.798‐0.894). Furthermore, lncRNA MALAT1 positively correlated with GOLD stage in both AECOPD and stable COPD patients. Regarding inflammatory cytokines, lncRNA MALAT1 positively correlated with tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, IL‐8, IL‐17, and IL‐23 in both AECOPD and stable COPD patients. Besides, lncRNA MALAT1 negatively correlated with miR‐125b, miR‐146a, and miR‐203 in AECOPD patients and reversely correlated with miR‐125b and miR‐146a in stable COPD patients. Notably, miR‐125b, miR‐133, miR‐146a, and miR‐203 were the lowest in AECOPD patients, followed by stable COPD patients, and then HCs; miR‐125b, miR‐133, miR‐146a, and miR‐203 negatively correlated with inflammation and GOLD stage in AECOPD and stable COPD patients. Conclusion LncRNA MALAT1 exhibits clinical implications in acute exacerbation risk prediction and management of COPD via the inner‐correlation with its targets miR‐125b, miR‐146a, and miR‐203.

show abstract

Long noncoding RNA Malat1 regulates differential activation of macrophages and response to lung injury

Cited by 116 publications

References 56 publications

Monocyte-derived alveolar macrophage apolipoprotein E participates in pulmonary fibrosis resolution

Monocyte-derived alveolar macrophage apolipoprotein E participates in pulmonary fibrosis resolution

Construction of asthma related competing endogenous RNA network revealed novel long non-coding RNAs and potential new drugs

The clinical value of lncRNA MALAT1 and its targets miR‐125b, miR‐133, miR‐146a, and miR‐203 for predicting disease progression in chronic obstructive pulmonary disease patients

Contact Info

Product

Resources

About