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.
Jie CuiZexi LvFangzhou TengLa YiWeifeng TangWenQian WangWuniqiemu TulakeJingjing QinXueyi ZhuYing WeiJing-Cheng DongPublished in: Evidence-based complementary and alternative medicine : eCAM (2021)
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 had 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. In this study, we analysed the lung transcriptome of control mice and asthmatic mouse model with/without BSYQF treatment. Using RNA-sequencing (RNA-seq) analysis, we found that 264/1746 (15.1%) of transcripts showing abnormal expression in asthmatic mice were reverted back to completely or partially normal levels by BSYQF treatment. Additionally, based on previous results, we identified 21 differential expression genes (DEGs) with fold changes (FC) > (±) 2.0 related to inflammatory, oxidative stress, mitochondria, PI3K/AKT, and MAPK signal pathways which may play important roles in the mechanism of the anti-remodeling effect of BSYQF treatment. Through inputting 21 DEGs into the IPA database to construct a gene network, we inferred Adipoq, SPP1, and TNC which were located at critical nodes in the network may be key regulators of BSYQF's anti-remodeling effect. In addition, the quantitative real-time polymerase chain reaction (qRT-PCR) result for the selected four DEGs matched those of the RNA-seq analysis. Our results provide a preliminary clue to the molecular mechanism of the anti-remodeling effect of BSYQF in asthma.
Keyphrases
- rna seq
- single cell
- lung function
- oxidative stress
- chronic obstructive pulmonary disease
- pi k akt
- signaling pathway
- mouse model
- genome wide
- gene expression
- high fat diet induced
- cystic fibrosis
- cell proliferation
- dna damage
- poor prognosis
- air pollution
- emergency department
- early stage
- ischemia reperfusion injury
- genome wide identification
- allergic rhinitis
- squamous cell carcinoma
- metabolic syndrome
- lymph node
- copy number
- transcription factor
- induced apoptosis
- insulin resistance
- reactive oxygen species
- neoadjuvant chemotherapy
- binding protein
- heat shock protein
- heat shock
- rectal cancer