MicroRNA Dysregulation in Pulmonary Arteries from Chronic Obstructive Pulmonary Disease. Relationships with Vascular Remodeling

Musri, Melina M.; Coll-Bonfill, Núria; Maron, Bradley A.; Peinado, Víctor I.; Wang, Rui-Sheng; Altirriba, Jordi; Blanco, Isabel; Oldham, William M.; Tura-Ceide, Olga; García-Lucio, Jéssica; Cruz-Thea, Benjamin de la; Meister, Gunter; Loscalzo, Joseph; Barberà, Joan Albert

doi:10.1165/rcmb.2017-0040oc

Cited by 37 publications

(33 citation statements)

References 52 publications

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“…Thereby, gastrodin has been considered as a potential therapeutic agent for diverse diseases such as Tourette syndrome, 7 myocardial infarction, 8 alcoholic liver disease 6,9 and acute lung injury. [11][12][13] For instance, in vivo and in vitro data demonstrated that miR-3202 could protect smokers from COPD. microRNAs (miRNAs) are a sort of small non-coding RNAs that are latterly discovered.…”

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confidence: 99%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.

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mentioning

confidence: 99%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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“…E2F1, a key proliferative factor, 29 , 30 was found to be targeted by miR-197 and participate in the vascular remodeling of COPD. 12 In fact, despite of ZFP161 and SP4, the remaining transcription factors have been reported in COPD, 31 – 33 which in turn supports the importance of these candidate DEMs in the pathogenesis of COPD.…”

Section: Discussionmentioning

confidence: 85%

<p>Construction of Potential miRNA–mRNA Regulatory Network in COPD Plasma by Bioinformatics Analysis</p>

Zhu¹,

Ye²,

Wang³

et al. 2020

COPD

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Background Chronic obstructive pulmonary disease (COPD) has become a major cause of morbidity and mortality worldwide. Increasing evidence indicates that aberrantly expressed microRNAs (miRNAs) are involved in the pathogenesis of COPD. However, an integrative exploration of miRNA–mRNA regulatory network in COPD plasma remains lacking. Methods The microarray datasets GSE24709, GSE61741, and GSE31568 were downloaded from the GEO database and analyzed using GEO2R tool to identify differentially expressed miRNAs (DEMs) between COPD and normal plasma. The consistently changing miRNAs in the three datasets were screened out as candidate DEMs. Potential upstream transcription factors and downstream target genes of candidate DEMs were predicted by FunRich and miRNet, respectively. Next, GO annotation and KEGG pathway enrichment analysis for target genes were performed using DAVID. Then, PPI and DEM-hub gene network were constructed using the STRING database and Cytoscape software. Finally, GSE56768 was used to evaluate the hub gene expressions. Results A total of nine (six upregulated and three downregulated) DEMs were screened out in the above three datasets. SP1 was predicted to potentially regulate most of the downregulated DEMs, while YY1 and E2F1 could regulate both upregulated and downregulated DEMs. 1139 target genes were then predicted, including 596 upregulated DEM target genes and 543 downregulated DEM target genes. Target genes of DEMs were mainly enriched in PI3K/Akt signaling pathway, mTOR signaling pathway, and autophagy. Through the DEM-hub gene network construction, most of the hub genes were found to be potentially modulated by miR-497-5p, miR-130b-5p, and miR-126-5p. Among the top 12 hub genes, MYC and FOXO1 expressions were consistent with that in the GSE56768 dataset. Conclusion In the study, potential miRNA–mRNA regulatory network was firstly constructed in COPD plasma, which may provide a new insight into the pathogenesis and treatment of COPD.

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“…NGF has also been implicated in viral respiratory infections, either by enhancing viral entry into the cell or airway inflammation (50,51) .Since nicotine stimulated expression of NGF , we then focused on determining whether miR-98 regulated NGF expression (21). miR-98 upregulation has been associated with vascular remodeling in smokers and patients with COPD (52). Decreased miR-98 levels have been associated with the development of pulmonary fibrosis in a model of bleomycininduced lung injury (53).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling

Wongtrakool

Jang

et al. 2020

Journal of Biological Chemistry

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Evolving evidence suggests nicotine may contribute to impaired asthma control by stimulating expression of nerve growth factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness (AHR). We explored the hypothesis that nicotine increases NGF by reducing lung fibroblast (LF) microRNA-98 (miR-98) and PPARγ levels thus promoting airway remodeling. Levels of NGF, miR-98, PPARγ, fibronectin 1 (FN1), endothelin-1 (ET-1), and collagen (COL1A1, and COL3A1) were measured in human LFs isolated from smoking donors, in mouse primary lung fibroblasts (LFs) exposed to nicotine (50 µg/ml), and in whole lung homogenates from mice chronically exposed to nicotine (100 µg/ml) in the drinking water. In selected studies, these pathways were manipulated in LFs with miR-98 inhibitor (anti-miR-98), miR-98 overexpression (miR-98 mimic), or the PPARγ agonist, rosiglitazone. Compared to unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse LFs and mouse lung homogenates. In contrast, nicotine reduced miR-98 levels in LFs in vitro and in lung homogenates in vivo. Treatment with anti-miR-98 alone was sufficient to recapitulate increases in NGF, FN1, and ET-1, while treatment with a miR-98 mimic significantly suppressed luciferase expression in cells transfected with a luciferase reporter linked to the putative seed sequence in the NGF 3’UTR and also abrogated nicotine-induced increases in NGF, FN1, and ET-1 in LFs. Similarly, rosiglitazone increased miR-98 and reversed nicotine-induced increases in NGF, FN1, and ET-1. Taken together, these findings demonstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.

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MicroRNA Dysregulation in Pulmonary Arteries from Chronic Obstructive Pulmonary Disease. Relationships with Vascular Remodeling

Cited by 37 publications

References 52 publications

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

<p>Construction of Potential miRNA–mRNA Regulatory Network in COPD Plasma by Bioinformatics Analysis</p>

MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling

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