Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases

Soni, Dharmendra Kumar; Biswas, Roopa

doi:10.3389/fgene.2021.767348

Cited by 19 publications

(11 citation statements)

References 196 publications

(186 reference statements)

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“…miRNAs are small non-coding RNA sequences of ±22 nucleotides that regulate gene expression at post-transcriptional level by repressing translation of specific mRNA targets through complementary pairing with their 3' untranslated regions. Growing evidence points to their potential role in chronic inflammatory diseases impacting lung tissues, such as in CF (15)(16)(17)(18)(19)(20)(21). Indeed, studies have shown that CF patients have a dysregulation in the expression of number of miRNAs, including those targeting the mutated CFTR transporter or its derivatives, such as miR-145 or miR-494 (18,22), or those involved in inflammatory pathology, such as the miR-126, miR-17 or miR-155 (23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation

et al. 2023

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Previous studies have reported sex disparity in cystic fibrosis (CF) disease, with females experiencing more pulmonary exacerbations and frequent microbial infections resulting in shorter survival expectancy. This concerns both pubertal and prepubertal females, which is in support to the prominent role of gene dosage rather than the hormonal status. The underlying mechanisms are still poorly understood. The X chromosome codes for a large number of micro-RNAs (miRNAs) that play a crucial role in the post-transcriptional regulation of several genes involved in various biological processes, including inflammation. However, their level of expression in CF males and females has not been sufficiently explored. In this study, we compared in male and female CF patients the expression of selected X-linked miRNAs involved in inflammatory processes. Cytokine and chemokine profiles were also evaluated at both protein and transcript levels and cross-analyzed with the miRNA expression levels. We observed increased expression of miR-223-3p, miR-106a-5p, miR-221-3p and miR-502-5p in CF patients compared to healthy controls. Interestingly, the overexpression of miR-221-3p was found to be significantly higher in CF girls than in CF boys and this correlates positively with IL-1β. Moreover, we found a trend toward lower expression in CF girls than in CF boys of suppressor of cytokine signaling 1 (SOCS1) and the ubiquitin-editing enzyme PDLIM2, two mRNA targets of miR-221-3p that are known to inhibit the NF-κB pathway. Collectively, this clinical study highlights a sex-bias in X-linked miR-221-3p expression in blood cells and its potential contribution to sustaining a higher inflammatory response in CF girls.

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Section: Introductionmentioning

confidence: 99%

Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation

et al. 2023

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“…Long non-coding ribonucleic acids (lncRNAs) are greater than 200 nucleotides, have no protein coding functions, and are widely involved in biological processes (13,14). Most lncRNAs have been implicated in the occurrence and development of COPD (15,16). LncRNA nuclear enriched abundant transcript 1 (NEAT1) is thought to be involved in a variety of cancers and inflammatory diseases (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Involvement of NEAT1/PINK1-mediated mitophagy in chronic obstructive pulmonary disease induced by cigarette smoke or PM2.5

Lin¹,

Zhang²,

Guo³

et al. 2022

Ann Transl Med

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Background: This study sought to explore the underlying mechanism of long non-coding ribonucleic acid nuclear enriched abundant transcript 1 (NEAT1) and PTEN-induced kinase 1 (PINK1)-mediated mitophagy in chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) or fine particular matter (PM 2.5 ). Methods:In total, 30 male Wistar Rats were divided into the following 3 groups: (I) the COPD group exposed to CS (CSM); (II) the COPD group exposed to PM 2.5 (PMM); and (III) the control (Ctrl) group.Pulmonary function, the enzyme-linked immunoassay analysis results, the histopathology results, and the ultrastructures of the lung tissues were examined in the 3 groups, and NEAT1 expression levels and the mitophagy-related protein PINK1, Parkin, LC3B, and p62 levels were assessed by quantitative reverse transcription PCR (RT-qPCR) and Western blotting. The A549 cells were transfected with small interfering ribonucleic acid (siRNA) targeting NEAT1, and subsequently stimulated with CS extract (CSE) and PM 2.5 suspension (PMS). Mitochondrial dysfunction and enhanced mitophagy were observed, and the expression of the NEAT1/PINK1 pathway was assessed by RT-qPCR and Western blotting. Results: Both the CSM and PMM groups had a lower tidal volume (V T ), minute ventilation (MV), and a higher respiratory rate (f) than the Ctrl group. The interleukin (IL)-6, IL-8, and tumor necrosis factoralpha levels in the serum and bronchoalveolar lavage fluid of the CSM and PMM groups were significantly increased. The histological examination results revealed airway remodeling, the formation of pulmonary bullae, and emphysema in the CSM and PMM groups. Subsequently, the ultrastructures of the lung tissues in the CSM and PMM groups showed mitochondrial swelling and autophagosomes. Additionally, NEAT1 expression, the level of the mitophagy-related protein PINK1, Parkin, and the ratio of LC3-II/I increased synchronously. Further, NEAT1 siRNA blocked PINK1 expression, inhibited mitochondrial dysfunctions, and mitophagy activation in the A549 cells exposed to CSE or PMS. Conclusions: Our results suggest that CS and PM 2.5 exposure induce mitochondrial dysfunction, and the NEAT1/PINK1 pathway plays a critical role in the occurrence and development of COPD by regulating mitophagy.

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“…Accumulating evidence has suggested that noncoding RNAs (ncRNAs) play important roles in a variety of inflammatory diseases, particularly allergic asthma. 12 Importantly, ncRNAs, including long noncoding RNAs (lncRNAs) with sizes larger than 200 nucleotides, microRNAs (miRNAs), and circular RNAs (circRNAs), among others, are being recognized as important molecules regulating coding genes at the transcriptional or posttranscriptional level in individuals with allergic asthma. 13 Multiple studies have emphasized that the effects of miRNAs on the initiation and maintenance of asthma are mainly achieved by regulating the expression of mRNAs at the posttranscriptional level.…”

Section: Discussionmentioning

confidence: 99%

The Specific microRNA Profile and Functional Networks for Children with Allergic Asthma

Zhang¹,

Zhang²,

Feng³

et al. 2022

JAA

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Background: Allergic asthma is the most common type of asthma and often occurs in early life with increasing comorbidities, including atopic dermatitis and allergic rhinitis. MicroRNAs (miRNAs) are involved in the pathogenesis of numerous immune and inflammatory disorders, particularly allergic inflammation. The specific miRNA profiles of children with allergic asthma have not been fully delineated and still require in-depth study.Objective: This study aimed to identify the expression profile of miRNAs and constructed a network of the interactions between differentially expressed miRNAs and target mRNAs to provide novel insights into understanding the pathogenesis of allergic asthma. Materials and Methods: In this study, we performed high-throughput sequencing of peripheral blood mononuclear cells (PBMCs) from children in the acute phase of asthma. Bioinformatics approaches, including miRanda, Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, were employed to predict novel therapeutic and diagnostic targets for allergic asthma. Real-time quantitative PCR was conducted to detect the expression of aberrantly expressed miRNAs. Results: One hundred and sixty-one differentially expressed miRNAs were identified in children with allergic asthma, including 140 conserved miRNAs and 21 novel miRNAs. A total of 8929 targeted mRNAs (44,186 transcripts) associated with differentially expressed miRNAs were predicted and significantly enriched in the cGMP-PKG signalling pathway, cholinergic synapse, and salivary secretion. We also found that miRNA-370-3p targeted PKG and MLCP molecules in the cGMP-PKG signalling pathway and was involved in the pathogenesis of allergic asthma. Conclusion:We identified the miRNA profile of PBMCs in children with allergic asthma and also found that miRNA-370-3p targeted PKG and MLCP molecules in the cGMP-PKG signalling pathway, which provides a novel insight into understanding the pathogenesis of allergic asthma and investigating new targets for the treatment of allergic asthma in children.

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Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases

Cited by 19 publications

References 196 publications

Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation

Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation

Involvement of NEAT1/PINK1-mediated mitophagy in chronic obstructive pulmonary disease induced by cigarette smoke or PM2.5

The Specific microRNA Profile and Functional Networks for Children with Allergic Asthma

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