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RNA-Seq expression analysis of chronic asthmatic mice with Bu-Shen-Yi-Qi formula treatment and prediction of regulated gene targets of anti-airway remodeling

ABSTRACT: Airway remodeling is one of the typical pathological characteristics of asthma. While, the structural changes of the airways in asthma are complex, which impedes the development of novel asthma targeted therapy. Our previous study have shown that Bu-Shen-Yi-Qi formula (BSYQF) could ameliorate airway remodeling in chronic asthmatic mice by modulating airway inflammation and oxidative stress in the lung. To further explore the molecular mechanism of BSYQF, in this study we analyzed the lung transcriptome of control, asthma mice with/without BSYQF treatment. Using RNA-sequencing analysis, we found that BSYQF treatment completely or partial reversed a group of genes that induced expression changes in asthma. Additionally, based on previous result we identified 21 differential expression genes (DEGs). Then through inputting 21 DEGs into Ingenuity Pathway Analysis (IPA) database to construct gene network, we inferred Adipoq, SPP1 and TNC which are located at critical nodes in the network, may be key regulators of BSYQF's anti-remodeling effect. Our results provide a preliminary clue to the molecular mechanism of anti-remodeling of BSYQF in asthma.

ORGANISM(S): Mus musculus

PROVIDER: GSE155071 | GEO | 2021/01/01

REPOSITORIES: GEO

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Project description:Monkey disease models, which are comparable to humans in terms of genetic, anatomical, and physiological characteristics, are important for understanding disease mechanisms and evaluating the efficiency of biological treatments. Here, we established an A.suum-induced model of asthma in cynomolgus monkeys to profile airway inflammation and remodeling in the lungs by single-cell transcriptomic sequencing (scRNA-seq). The asthma model results in airway hyperresponsiveness and remodeling, demonstrated by pulmonary function test and histological characterization. scRNA-seq reveals that the model elevates the numbers of stromal, epithelial and mesenchymal cells (MCs). Particularly, the model increases the numbers of endothelial cells (ECs), fibroblasts (Fibs) and smooth muscle cells (SMCs) in the lungs, with upregulated gene expression associated with cell functions enriched in cell migration and angiogenesis in ECs and Fibs, and VEGF-driven cell proliferation, apoptotic process and complement activation in SMCs. Interestingly, we discover a novel Fib subtype that mediates type I inflammation in the asthmatic lungs. Moreover, MCs cells in the asthmatic lungs are found to regulate airway remodeling and immunological responses, with elevated gene expression enriched in cell migration, proliferation, angiogenesis and innate immunological responses. Despite the fact that the numbers of epithelial cells in the asthma lungs do not change at the time of lung tissue collection, their gene expressions are significantly altered, with an enrichment in the biological processes of IL-17 signaling pathway and apoptosis in the majority of subtypes of epithelial cells. Moreover, the ubiquitin process and DNA repair are more prevalent in ciliated epithelial cells. Last, cell-to-cell interaction analysis reveals a complex network among stromal cells, MCs and macrophages that contribute to the development of asthma and airway remodeling. Our findings provide a critical resource for understanding the principle underlying airway remodeling and inflammation in a monkey model of asthma, as well as valuable hints for the future treatment of asthma, especially the airway remodeling-characterized refractory asthma.

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RNA-Seq expression analysis of chronic asthmatic mice with Bu-Shen-Yi-Qi formula treatment and prediction of regulated gene targets of anti-airway remodeling

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