miRNA‐34b/c regulates mucus secretion in RSV‐infected airway epithelial cells by targeting FGFR1

Li, Wenkai; Du, Xiao; Yang, Yu; Lin, Yuan; Yang, Ming; Qin, Ling; Wang, Leyuan; Zhou, Kai; Xiang, Yang; Qu, Xiangping; Liu, Huijun; Qin, Xiaoqun; Xiao, Gelei; Liu, Chi

doi:10.1111/jcmm.16988

Cited by 7 publications

(5 citation statements)

References 38 publications

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“…In humans, mucin expression during infection is regulated by a panoply of miRNAs, namely miR-34b/c (Li et al. 2021 ), miR-146a (Zhong et al. 2011 ), miR-378 (Skrzypek et al.…”

Section: Discussionmentioning

confidence: 99%

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The forecasting power of the mucin-microbiome interplay in livestock respiratory diseases

Mach

2024

Veterinary Quarterly

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Complex respiratory diseases are a significant challenge for the livestock industry worldwide. These diseases considerably impact animal health and welfare and cause severe economic losses. One of the first lines of pathogen defense combines the respiratory tract mucus, a highly viscous material primarily composed of mucins, and a thriving multi-kingdom microbial ecosystem. The microbiome-mucin interplay protects from unwanted substances and organisms, but its dysfunction may enable pathogenic infections and the onset of respiratory disease. Emerging evidence also shows that noncoding regulatory RNAs might modulate the structure and function of the microbiome-mucin relationship. This opinion paper unearths the current understanding of the triangular relationship between mucins, the microbiome, and noncoding RNAs in the context of respiratory infections in animals of veterinary interest. There is a need to look at these molecular underpinnings that dictate distinct health and disease outcomes to implement effective prevention, surveillance, and timely intervention strategies tailored to the different epidemiological contexts.

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“…In humans, mucin expression during infection is regulated by a panoply of miRNAs, namely miR-34b/c (Li et al. 2021 ), miR-146a (Zhong et al. 2011 ), miR-378 (Skrzypek et al.…”

Section: Discussionmentioning

confidence: 99%

“…Several miRNAs have been shown to regulate the glycan biosynthetic enzymes and regulate the expression of mucin genes in the respiratory tract of humans, including miR-34b/c (Li et al. 2021 ), miR-146a (Zhong et al. 2011 ), miR-378 (Skrzypek et al.…”

Section: Introductionmentioning

confidence: 99%

The forecasting power of the mucin-microbiome interplay in livestock respiratory diseases

Mach

2024

Veterinary Quarterly

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“…NAC was previously found to restore the sensitivity of gefitinib-resistant lung cancer cells to gefitinib that is a major epithelial growth factor receptor tyrosine kinase inhibitor, suggesting the inhibitory effects of NAC on EGFR activation in epithelial cells [24]. With regard to NAC inhibition on mucin hypersecretion caused by RSV infection [25], a previous study, similar as our study, reported that NAC reduce airway inflammation and responsiveness, goblet cell hyperplasia, and lung fibrosis by increasing levels of ROS, nuclear factor erythroid 2-related factor 2, and MUC5AC protein [26]. The present study analyzed the HSPA6 expression in RSV-infected BEAS-2B cells treated with and without NAC.…”

Section: Discussionmentioning

confidence: 99%

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

Chi¹,

Shan²,

Cui³

2022

Analytical Cellular Pathology

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Objective. Respiratory syncytial virus (RSV) infection is an important cause of hospitalization of children worldwide, leading to significant morbidity and mortality. RSV infection leads to increasing inflammatory and apoptosis events in the airway epithelium through mechanisms involving ROS generation. The antioxidant N-acetyl-L-cysteine (NAC) has been shown to inhibit influenza virus replication and to reduce the secretion of inflammatory and apoptotic mediators during virus infection. The study aims to investigate the effects of NAC on human bronchial epithelial cells BEAS-2B and HSPA6 expression during RSV infection. Methods. CCK-8 assays were performed to evaluate cell survival. The production of proinflammatory factors, TNF-α, IL-6, IL-1β, IL-18, and MUC5AC was examined by quantitative real-time PCR and ELISA. Oxidative stress was determined by reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH)/glutathione disulfide (GSSG) ratio. Immunoblotting analysis of epidermal growth factor receptor (EGFR) and its phosphorylation was performed. The antiviral effect of NAC was assessed by determining viral titers using plaque assay. Results. RSV infection reduced cell survival, promoted the release of proinflammatory factors, increased the ROS production and MDA concentration, and diminished the SOD activity and GSH/GSSG ratio, all which were attenuated by NAC treatment. Accordingly, NAC treatment inhibited the activation of EGFR and MUC5AC in BEAS-2B cells with RSV infection. Furthermore, NAC administration resulted in a marked decrease in RSV-induced HSPA6 expression in BEAS-2B cells. Concomitantly, EPB treatment led to an evident inhibition of RSV fusion gene and viral replication in RSV-infected BEAS-2B cells. Conclusion. This work supports the use of NAC to exert antimucin synthesis, anti-inflammatory, antioxidant, and antiviral effects on airway epithelium during RSV infection.

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“…In particular, some miRNAs show prominent roles in regulating airway mucus homeostasis. For example, it was found that miRNA-34b/c regulated mucus secretion in RSV-infected airway epithelial cells and that miRNA-330 regulated IL-13-induced MUC5AC secretion in human bronchial epithelial cells [ 14 , 53 ]. In addition, tumour necrosis factor- α promoted airway mucus hypersecretion by inhibiting miR-146a-5p and miR-134-5p levels [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Effective Component Compatibility of Bufei Yishen Formula III Which Regulates the Mucus Hypersecretion of COPD Rats via the miR-146a-5p/EGFR/MEK/ERK Pathway

Liu

Wei

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. The effective-component compatibility of Bufei Yishen formula III (ECC-BYF III) with 5 ingredients (ginsenoside Rh1, astragaloside, icariin, nobiletin, and paeonol) has been shown to protect against chronic obstructive pulmonary disease (COPD). The present study aimed to observe the effects of ECC-BYF III in a COPD rat model and dissect its potential mechanisms in regulating mucus hypersecretion via the miR-146a-5p/epidermal growth factor receptor (EGFR)/MEK/ERK pathway. Methods. COPD model rats were treated with normal saline, ECC-BYF III, or N-acetylcysteine (NAC). Pulmonary function, lung tissue histology with H & E and AB-PAS staining, expression levels of interleukin (IL)-4, IL-6, IL-1β, MUC5AC, MUC5B, and FOXA2 in lung tissues and the mRNA and proteins involved in the miR-146a-5p/EGFR/MEK/ERK pathway were evaluated. Results. The COPD rats showed a significant decrease in the pulmonary function and serious pathological damage to the lung tissue. ECC-BYF III and NAC significantly improved the ventilation function and small airway pathological damage in the COPD rats. The goblet cells and the expression levels of IL-1β, IL-6, MUC5AC, and MUC5B were increased in the COPD rats and were significantly decreased after ECC-BYF III or NAC intervention. The expression levels of IL-4 and FOXA2 in the COPD rats were markedly decreased and were improved in the ECC-BYF III and NAC groups. ECC-BYF III appeared to have a potent effect in restoring the reduced expression of miR-146a-5p. The increased phosphorylation levels of EGFR, MEK, and ERK1/2 and the protein expression levels of SPDEF in the lungs of COPD rats could be significantly reduced by ECC-BYF III. Conclusions. ECC-BYF III has a significant effect in improving the airway mucus hypersecretion in COPD model rats, as well as a protective effect against limited pulmonary function and injured lung histopathology. The protective effect of ECC-BYF III in reducing airway mucus hypersecretion in COPD may involve the miR-146a-5p/EGFR/MEK/ERK pathway.

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miRNA‐34b/c regulates mucus secretion in RSV‐infected airway epithelial cells by targeting FGFR1

Cited by 7 publications

References 38 publications

The forecasting power of the mucin-microbiome interplay in livestock respiratory diseases

The forecasting power of the mucin-microbiome interplay in livestock respiratory diseases

N-Acetyl-L-Cysteine Protects Airway Epithelial Cells during Respiratory Syncytial Virus Infection against Mucin Synthesis, Oxidative Stress, and Inflammatory Response and Inhibits HSPA6 Expression

Effective Component Compatibility of Bufei Yishen Formula III Which Regulates the Mucus Hypersecretion of COPD Rats via the miR-146a-5p/EGFR/MEK/ERK Pathway

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