Role of airway epithelial cell miRNAs in asthma

Boateng, Eistine; Kovačević, Draginja; Oldenburg, Vladimira; Rådinger, Madeleine; Krauss‐Etschmann, Susanne

doi:10.3389/falgy.2022.962693

Cited by 5 publications

(3 citation statements)

References 121 publications

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“…The membrane of each cilium surrounds an axoneme which has a repeating ‘9 + 2’ structure: nine microtubule doublets which surround two central microtubules. These microtubules move relative to one another through force generated by dynein arms to move cilia in a coordinated manner ( 23 ). Ciliated epithelial cell differentiation occurs in the absence of Notch signalling.…”

Section: Epithelial Structure and Cell Typesmentioning

confidence: 99%

Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD

et al. 2023

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The airway epithelium comprises of different cell types and acts as a physical barrier preventing pathogens, including inhaled particles and microbes, from entering the lungs. Goblet cells and submucosal glands produce mucus that traps pathogens, which are expelled from the respiratory tract by ciliated cells. Basal cells act as progenitor cells, differentiating into different epithelial cell types, to maintain homeostasis following injury. Adherens and tight junctions between cells maintain the epithelial barrier function and regulate the movement of molecules across it. In this review we discuss how abnormal epithelial structure and function, caused by chronic injury and abnormal repair, drives airway disease and specifically asthma and chronic obstructive pulmonary disease (COPD). In both diseases, inhaled allergens, pollutants and microbes disrupt junctional complexes and promote cell death, impairing the barrier function and leading to increased penetration of pathogens and a constant airway immune response. In asthma, the inflammatory response precipitates the epithelial injury and drives abnormal basal cell differentiation. This leads to reduced ciliated cells, goblet cell hyperplasia and increased epithelial mesenchymal transition, which contribute to impaired mucociliary clearance and airway remodelling. In COPD, chronic oxidative stress and inflammation trigger premature epithelial cell senescence, which contributes to loss of epithelial integrity and airway inflammation and remodelling. Increased numbers of basal cells showing deregulated differentiation, contributes to ciliary dysfunction and mucous hyperproduction in COPD airways. Defective antioxidant, antiviral and damage repair mechanisms, possibly due to genetic or epigenetic factors, may confer susceptibility to airway epithelial dysfunction in these diseases. The current evidence suggests that a constant cycle of injury and abnormal repair of the epithelium drives chronic airway inflammation and remodelling in asthma and COPD. Mechanistic understanding of injury susceptibility and damage response may lead to improved therapies for these diseases.

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Section: Epithelial Structure and Cell Typesmentioning

confidence: 99%

Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD

et al. 2023

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“…Mir-21, mir-223, and Let-7a were selected for their role in the development and pathogenesis of different forms of asthma. Recent asthma-specific findings show their role as significant contributor to the asthma process [20][21][22]. Further studies on more miRNAs will be required.…”

Section: Limitations Of the Studymentioning

confidence: 99%

“…Despite extensive investigations into the role of miRNAs in the development of asthma [21][22][23], to date, studies on the functioning of exosomal miRNAs in this disease are lacking [24]. Based on the above, we therefore believe that alterations of intracellular miRNAs and circulating miRNAs can probably be implicated in the etiopathogenesis of asthma and of severe asthma.…”

Section: Introductionmentioning

confidence: 99%

MiRNA and Exosomal miRNA as New Biomarkers Useful to Phenotyping Severe Asthma

Soccio,

Moriondo,

Lacedonia

et al. 2023

Biomolecules

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Severe asthma (SA) is a chronic inflammatory disease of the airways. Due to the extreme heterogeneity of symptoms, new biomarkers are currently needed. MiRNAs are non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. In biological fluids, miRNAs are contained within exosomes, vesicles capable of giving miRNAs considerable stability and resistance to degradation by RNAses. The main function attributed to the exosomes is intercellular communication. The goal of our study was to analyze intracellular and exosomal miRNAs in order to demonstrate their potential use as non-invasive biomarkers of asthma by showing, in particular, their role in SA. We detected miRNAs by qRT-PCR in both serum and serum-derived-exosomes of asthmatic patients and healthy controls. The levels of almost all analyzed intracellular miRNAs (miR-21, miR-223, and let-7a) were greater in asthmatic patients vs. healthy control, except for miR-223. In detail, miR-21 was greater in SA, while let-7a increased in mild-to-moderate asthma. On the other hand, in exosomes, all analyzed miRNAs were higher in SA. This study identified a series of miRNAs involved in SA, highlighting their potential role in asthma development and progression. These results need validation on a larger cohort.

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