Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Zhu, Ke; Zhou, Sijing; Xu, Aiqun; Lee, Sun; Li, Min; Jiang, Huihui; Zhang, Binbin; Zeng, Daxiong; Fei, Guanghe; Wang, Ran

doi:10.1016/j.omtn.2020.09.017

Cited by 21 publications

(13 citation statements)

References 42 publications

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“…Importantly, we further observed a 5-fold decrease in the expression of miR-122-5p on comparing miRNA population from lung-derived exosomes from COPD patients versus healthy smokers. Our results are in accordance with previous literature (50-52). For instance, Zhu et al (2020) demonstrated the downregulation of miR-122-5p in the sputum and plasma of COPD patients and proved that it functions as a negative regulator of IL-17A production (50).…”

Section: Discussionsupporting

confidence: 94%

“…Our results are in accordance with previous literature (50-52). For instance, Zhu et al (2020) demonstrated the downregulation of miR-122-5p in the sputum and plasma of COPD patients and proved that it functions as a negative regulator of IL-17A production (50). It is pertinent to mention here that though we did not find any commonly altered miRNAs in the exosomes from BALF or lung tissues of COPD patients, we found links that associate miRNA-mediated modulation of IL17-signalling amongst the diseased individual.…”

Section: Discussionsupporting

confidence: 94%

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Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

Kaur

Maremanda

Campos

et al. 2021

Preprint

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BackgroundChronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) are chronic, progressive lung ailments which are characterized by distinct pathologies. Early detection biomarkers and disease mechanisms for these debilitating diseases are lacking. Exosomes are small extracellular vesicles attributed to carry proteins, mRNA, miRNA and sncRNA to facilitate cell-to-cell communication under normal and diseased conditions. Exosomal miRNAs have been studied in relation to many diseases. However, there is little to no knowledge regarding the miRNA population of BALF or the lung tissue derived exosomes in COPD and IPF. Here, we determined and compared the miRNA profiles of BALF and lung tissue-derived exosomes from healthy non-smokers, healthy smokers, and patients with COPD and IPF in independent cohorts.ResultsExosome characterization using NanoSight particle tracking and TEM demonstrated that the BALF-derived exosomes were approximately 89.85 nm in size and ∼2.95 × 1010 particles/mL. Lung-derived exosomes were ∼146.04 nm in size and ∼2.38 × 1011 particles/mL. NGS results identified three differentially expressed miRNAs in the BALF, while one in the lung-derived exosomes from COPD patients as compared to healthy non-smokers. Of these, three- and five-fold downregulation of miR-122-5p amongst the lung tissue-derived exosomes from COPD patients as compared to healthy non-smokers and smokers, respectively. Interestingly, there were key 55 differentially expressed miRNAs in the lung tissue-derived exosomes of IPF patients compared to non-smoking controls.ConclusionsOverall, we identified specific miRNAs to develop as biomarkers or targets for pathogenesis of these chronic lung diseases.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 94%

Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

Kaur

Maremanda

Campos

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Our results are in accordance with previous literature (50)(51)(52). For instance, Zhu et al (2020) demonstrated the downregulation of miR-122-5p in the sputum and plasma of COPD patients and proved that it functions as a negative regulator of IL-17A production (50). It is pertinent to mention here that though we did not find any commonly altered miRNAs in the exosomes from BALF or lung tissues of COPD patients, we found links that associate miRNA-mediated modulation of IL17-signalling amongst the diseased individual.…”

Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

Distinct Exosomal miRNA Profiles from BALF and Lung Tissue from COPD and IPF Patients

Kaur

Maremanda

Campos

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Chronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) are chronic, progressive lung ailments which are characterized by distinct pathologies. Early detection biomarkers and disease mechanisms for these debilitating diseases are lacking. Exosomes are small extracellular vesicles attributed to carry proteins, mRNA, miRNA and sncRNA to facilitate cell-to-cell communication under normal and diseased conditions. Exosomal miRNAs have been studied in relation to many diseases. However, there is little to no knowledge regarding the miRNA population of BALF or the lung tissue derived exosomes in COPD and IPF. Here, we determined and compared the miRNA profiles of BALF and lung tissue-derived exosomes from healthy non-smokers, healthy smokers, and patients with COPD and IPF in independent cohorts. Results: Exosome characterization using NanoSight particle tracking and TEM demonstrated that the BALF-derived exosomes were approximately 89.85 nm in size and ~2.95 X 1010 particles/mL. Lung-derived exosomes were ~146.04 nm in size and ~2.38 X 1011 particles/mL. NGS results identified three differentially expressed miRNAs in the BALF, while one in the lung-derived exosomes from COPD patients as compared to healthy non-smokers. Of these, three- and five-fold downregulation of miR-122-5p amongst the lung tissue-derived exosomes from COPD patients as compared to healthy non-smokers and smokers, respectively. Interestingly, there were key 55 differentially expressed miRNAs in the lung tissue-derived exosomes of IPF patients compared to non-smoking controls. Conclusions: Overall, we identified specific miRNAs to develop as biomarkers or targets for pathogenesis of these chronic lung diseases.

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“…In the next step, hPASMCs and rPASMCs were co-transfected with the wild-type or mutant-type MALAT1 promoter in conjunction with miR-146a mimics or a negative control miRNA. At 24 h after the transfection was started, the luciferase activity in transfected cells was evaluated by using a dual luciferase reporter gene assay kit (Promega) on a TD-20/20 luminometer (Turner Biosystems, Sunnyvale, CA, United States) based on the general protocols provided by the manufacturers of both the reporter gene assay kit and the luminometer ( Zhou et al, 2020 ; Zhu et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

Effect of Methylation Status of lncRNA-MALAT1 and MicroRNA-146a on Pulmonary Function and Expression Level of COX2 in Patients With Chronic Obstructive Pulmonary Disease

Lee

Xu²,

et al. 2021

Front. Cell Dev. Biol.

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This study aimed to investigate the role of methylation of MALAT1 and miR-146a in the pathogenesis of chronic obstructive pulmonary disease (COPD). COPD patients were grouped according to their methylation status of MALAT1 and miR-146a promoters, and we found that forced vital capacity, volume that has been exhaled at the end of the first second of forced expiration, and diffusion capacity for carbon monoxide were the highest in the MALAT1 HYPO + miR-146a HYPER group and lowest in the MALAT1 HYPER + miR-146a HYPO group, and COPD patients with hypermethylated MALAT1 showed lower expression of MALAT1 than that in the COPD patients with hypomethylated MALAT1. Meanwhile, miR-146a was the most significantly upregulated in the MALAT1 HYPER + miR-146a HYPO group and the most significantly downregulated in the MALAT1 HYPO + miR-146a HYPER group. Both prostaglandin E1 and cyclooxygenase 2 (COX2) expression were the highest in the MALAT1 HYPO + miR-146a HYPER group and the lowest in the MALAT1 HYPER + miR-146a HYPO group. In conclusion, our results established a MALAT1/miR-146a/COX2 signaling axis. The overexpression of MALAT1 could increase the expression of COX2 by inhibiting the expression of miR-146a, thus affecting the pulmonary function of COPD patients.

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Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Cited by 21 publications

References 42 publications

Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

Distinct exosomal miRNA profiles from BALF and lung tissue from COPD and IPF patients

Distinct Exosomal miRNA Profiles from BALF and Lung Tissue from COPD and IPF Patients

Effect of Methylation Status of lncRNA-MALAT1 and MicroRNA-146a on Pulmonary Function and Expression Level of COX2 in Patients With Chronic Obstructive Pulmonary Disease

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