The Potential Role and Regulatory Mechanisms of MUC5AC in Chronic Obstructive Pulmonary Disease

Li, Jingyuan; Ye, Zuguang

doi:10.3390/molecules25194437

Cited by 30 publications

(23 citation statements)

References 107 publications

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“…Five hub genes, including MUC5AC, BCL6, TET2, NFE2L2, and VDR were detected from the PPIs network. MUC5AC, BCL6, NFE2L2, and VDR have been documented as having an association with the pathogenesis of lung diseases [ [39] , [40] , [41] , [42] ]. In module analysis, VDR and NFE2l2 were clustered together which was performed to suggest more effective drug compounds.…”

Section: Discussionmentioning

confidence: 99%

Common genetic aspects between COVID-19 and sarcoidosis: A network-based approach using gene expression data

Mogal

Sompa

Junayed

et al. 2022

Biochemistry and Biophysics Reports

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The pandemic situation of novel coronavirus disease 2019 (COVID-19) is a global threat on our current planet, with its rapid spread and high mortality rate. Sarcoidosis patients are at high risk to COVID-19 severity for having lung injuries as well as treating with immunosuppressive agents. So, physicians are in dilemma whether they should use immunosuppressive agents or not for the patients with sarcoidosis history and COVID-19 infection. Therefore, common factors should be identified to provide effective treatment. For determining the common genes between COVID-19 and sarcoidosis, GSE164805 and GSE18781 were retrieved from the Gene Expression Omnibus (GEO) database. Common upregulated genes were identified by using R language to investigate their involved pathways and gene ontologies (GO). With the aid of the STRING Cytoscape plugin tool, protein-protein interactions (PPIs) network was constructed. From the PPIs network, Hub genes and essential modules were detected by using Cytohubba, and MCODE respectively. For hub genes, TFs, TFs-miRNA, and drug, interaction networks were built through the NetworkAnalyst web platform. A total of 34 common upregulated genes were identified and among them, five hub genes, including TET2, MUC5AC, VDR, NFE2L2, and BCL6 were determined. In addition, a cluster having VDR and NFE2L2 was detected from the PPIs network. Moreover, 32 transcription factors and 9 miRNA were recognized for hub genes. Furthermore, vitamin D and some of its analogous compounds were obtained from the drug interaction network. In conclusion, hub genes identified in this study might have potential roles in modulating COVID-19 infection and sarcoidosis. However, further studies are required to corroborate this study.

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Section: Discussionmentioning

confidence: 99%

Common genetic aspects between COVID-19 and sarcoidosis: A network-based approach using gene expression data

Mogal

Sompa

Junayed

et al. 2022

Biochemistry and Biophysics Reports

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“…In patients with COPD, the overexpression and hypersecretion of mucins can increase the concentrations of the contents up to 15%, resulting in viscous and elastic mucus being cleared difficultly and adhering more readily to the airway [ 26 ]. Therefore, excess mucus aggravates airway obstruction, increases airway reactivity, and reduces pulmonary function [ 27 ]. Approximately 95% of the total mucins secreted in the airway epithelium was produced by goblet cells and can be detected with AB/PAS staining [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Guifu Dihuang Pills Ameliorated Mucus Hypersecretion by Suppressing Muc5ac Expression and Inactivating the ERK-SP1 Pathway in Lipopolysaccharide/Cigarette Smoke-Induced Mice

Zhang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Mucus hypersecretion is a hallmark of chronic obstructive pulmonary disease (COPD) and is associated with increasing sputum production and declining pulmonary function. Therefore, reducing mucus secretion can be a new therapeutic opportunity for preventing COPD. The Guifu Dihuang pill (GFDHP) is a classical Chinese medicine and has been used as an immunoregulator for treatment of kidney yang deficiency syndrome, including hypothyroidism, adrenocortical hypofunction, chronic bronchitis, and COPD, for more than 2000 years. However, the protective effects and mechanisms of GFDHP against mucus hypersecretion in COPD remain obscure. The aim of the present study was to explore the inhibitory effects of GFDHP on lipopolysaccharide/cigarette smoke- (LPS/CS-) induced Mucin5ac (Muc5ac) overproduction and airway goblet cell hyperplasia in mice. The mice were randomly assigned into 6 groups: control, model, GFDHP-L, GFDHP-M, GFDHP-H, and dexamethasone. The mice were given LPS twice through intranasal inhalation and then exposed to CS daily for 6 weeks. Three doses of GFDHP were orally administered daily during the last 3 weeks of the experiment. Pulmonary function was examined with an EMKA pulmonary system, and pulmonary hyperpermeability and lung damage were evaluated with an in vivo imaging system. Inflammatory cells and cytokines in bronchoalveolar lavage fluid (BALF) were detected with a cell count analyzer and though ELISA analysis, respectively. Lung pathological changes and airway goblet cell hyperplasia were analyzed with hematoxylin and eosin and Alcian blue periodic acid Schiff staining. The protein expression levels of Muc5ac and extracellular signal-regulated kinase (ERK)-specificity protein1 (SP1) signaling pathway were measured with Western blot and immunohistochemistry. The results demonstrated that GFDHP improved pulmonary function and suppressed mouse pulmonary hyperpermeability and edema. GFDHP suppressed inflammatory cell infiltration and cytokine release in BALF, thereby elevating pulmonary function. It ameliorated lung pathological changes and airway goblet cell hyperplasia, and suppressed expression levels of Muc5ac mRNA and protein and phospho-ERK and SP1 levels in the lung tissues of the COPD mice. In conclusion, GFDHP inhibited mucus hypersecretion induced by LPS/CS by suppressing the activation of the ERK-SP1 pathway.

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“…In COPD, these mechanisms may be impaired, accompanied by mucus hypersecretion. Mucus hypersecretion is associated with mucins, of which MUC5AC is considered the most important [31,32]. MUC5AC is produced predominantly by goblet cells of the bronchial epithelium [33].…”

Section: The Innate Immune Function Of Airway Epithelial Cellsmentioning

confidence: 99%

Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease

Kotlyarov

2022

IJMS

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Chronic obstructive pulmonary disease (COPD) is a common, socially significant disease characterized by progressive airflow limitation due to chronic inflammation in the bronchi. Although the causes of COPD are considered to be known, the pathogenesis of the disease continues to be a relevant topic of study. Mechanisms of the innate immune system are involved in various links in the pathogenesis of COPD, leading to persistence of chronic inflammation in the bronchi, their bacterial colonization and disruption of lung structure and function. Bronchial epithelial cells, neutrophils, macrophages and other cells are involved in the development and progression of the disease, demonstrating multiple compromised immune mechanisms.

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The Potential Role and Regulatory Mechanisms of MUC5AC in Chronic Obstructive Pulmonary Disease

Cited by 30 publications

References 107 publications

Common genetic aspects between COVID-19 and sarcoidosis: A network-based approach using gene expression data

Common genetic aspects between COVID-19 and sarcoidosis: A network-based approach using gene expression data

Guifu Dihuang Pills Ameliorated Mucus Hypersecretion by Suppressing Muc5ac Expression and Inactivating the ERK-SP1 Pathway in Lipopolysaccharide/Cigarette Smoke-Induced Mice

Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease

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