MicroRNA Regulation of Airway Inflammation and Airway Smooth Muscle Function: Relevance to Asthma

Deshpande, Deepak A.; Dileepan, Mythili; Walseth, Timothy F.; Subramanian, Subbaya; Kannan, Mathur

doi:10.1002/ddr.21267

Cited by 33 publications

(28 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, in acute cerebral infarction patients, plasma miR‐338‐3p level was associated with the expression of C‐reactive protein, which was a crucial inflammatory factor in atherosclerosis . Additionally, miR‐338‐3p was abnormally expressed in the serum of patients with asthma and chronic obstructive pulmonary diseases . In the present research, for the first time, we validated that the upregulation of miR‐338‐3p alleviated LPS‐induced inflammatory injury in 16HBE cells.…”

Section: Discussionsupporting

confidence: 68%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

View full text Add to dashboard Cite

Background: Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods: Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL-6), IL-8 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR-338-3p were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The direct interaction between circ_0038467 and miR-338-3p was validated by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR-338-3p was downregulated in LPS-treated 16HBE cells. Circ_0038467 knockdown or miR-338-3p overexpression attenuated LPS-induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR-338-3p in 16HBE cells. MiR-338-3p mediated the alleviated effect of circ_0038467 knockdown on LPS-induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR-338-3p axis-mediated regulation in LPS-induced 16HBE cell inflammatory injury. Conclusions: The current work had led to the identification of circ_0038467 knockdown that alleviated LPS-induced inflammatory injury in 16HBE cells at least partly through sponging miR-338-3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

show abstract

Section: Discussionsupporting

confidence: 68%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

View full text Add to dashboard Cite

show abstract

“…3 In asthmatic patients, inflammatory cytokines like interleukin-4 (IL-4), IL-5, and IL-13 are altered along with asthma exacerbation. 4 Similarly, BD patients are found to have dysfunction of inflammation when the disease is aggravated or subsides.…”

Section: Introductionmentioning

confidence: 99%

Significantly Higher Prevalence Rate of Asthma and Bipolar Disorder Co-Morbidity

Wang

Chen

et al. 2016

Medicine

View full text Add to dashboard Cite

Asthma and bipolar disorder (BD) are 2 distinct diseases that share similar pathophysiology. This study aimed to determine their relationship thorough a meta-analysis of articles on their comorbidity rate.The aim of the study is to examine the overall prevalence rate of BD in asthmatic patients and of asthma in BD patients compared to healthy controls.Electronic research of PubMed and ClinicalTrials.gov was performed.Articles discussing the prevalence rate of BD in patients with/without asthma and the prevalence rate of asthma in those with/without BD, as well as clinical trials in humans and case-controlled trials or cohort studies, were all included. Case reports or series and nonclinical trials were excluded.Through a random-effects model, a meta-analysis of the results of 4 studies comparing the prevalence rate of BD in patients with/without asthma, and in 6 studies comparing the prevalence rate of asthma in subjects with/without BD were performed.There were significantly higher prevalence rates of BD in asthmatic patients than in healthy controls (P < .001) and of asthma in BD patients than in healthy controls (P < .001). Only the patient's mean age significantly modulated the odds ratio of the prevalence rate of asthma in BD patients (slope = 0.015, P < .001).Only 10 studies were included and most were cross-sectional studies. The possible confounding effect of medication on BD or asthma onset was not investigated. Any possible etiology of the comorbidity was also not determined.This meta-analysis highlights the importance of the significantly high comorbid rate of BD and asthma, and the positive association with age. Special attention must be given to the comorbidity of asthma and BD, especially in older patients.

show abstract

“…In addition to its normal functions, assembling evidences suggest that miRNA are also involved in various pathological conditions such as cardiomyopathies [8], atherosclerosis [9], obesity [10] and cancer [11]. Most importantly, emerging evidences suggest that miRNAs play crucial roles in inflammation responses [12], as well as in acute lung injury and ARDS [13]. …”

Section: Introductionmentioning

confidence: 99%

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Wang

Chen

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: The present study addressed the potential involvement of microRNAs in acute respiratory distress syndrome (ARDS)-related inflammation and elucidates the underlying molecular mechanism. Methods: ARDS rat model was established by lipopolysaccharide, with compromised gas exchange capacity and lung edema. The inflammatory cells from bronchoalveolar lavage fluid (BALF) were profiled with automatic blood cell analyzer. The relative fluorescence intensity of BALF-derived macrophages was analyzed by flow cytometry. The relative microRNA expression was determined using microarray and Taqman assay. The secretory interleukin (IL)-10 was measured by enzyme-linked immunosorbent assay. Luciferase reporter assay was performed to determine the regulatory effects of miR-211 and NF-κB on IL-10 and miR-211 expressions, respectively. Chromatin immunoprecipitation (ChIP) was conducted to detect the direct binding of NK-κB on miR-211 promoter. The protein level was determined by Western blot. Results: The provoked acute inflammation was characterized with increased total cells, macrophages, neutrophils and lymphocytes. The relative expression of miR-211 was aberrantly up-regulated in BALF-derived macrophages from ARDS rats, which was accompanied with reduction of secretory IL-10. We further demonstrated that miR-211 inhibited IL-10 expression by binding to its 3’-UTR. The expression of miR-211 was modulated by NF-κB. Conclusion: Here we elucidated a crucial role of NF-κB/miR-211/IL-10 signaling axis in ARDS-related inflammation.

show abstract

MicroRNA Regulation of Airway Inflammation and Airway Smooth Muscle Function: Relevance to Asthma

Cited by 33 publications

References 75 publications

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Significantly Higher Prevalence Rate of Asthma and Bipolar Disorder Co-Morbidity

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Contact Info

Product

Resources

About