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scRNA-seq and scATAC-seq analyses highlight the role of TNF signaling pathway in chronic obstructive pulmonary disease model mice

  • 0Joint Laboratory for Translational Medicine Research, Liaocheng People's Hospital, Liaocheng, Shandong, China.
Plos One +

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May 9, 2025

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May 9, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Chronic obstructive pulmonary disease (COPD) involves persistent lung damage. This study reveals the tumor necrosis factor (TNF) signaling pathway is significantly altered in COPD model mice, suggesting its potential role in disease progression.

Area Of Science

  • Pulmonary Medicine
  • Immunology
  • Genomics

Background

  • Chronic obstructive pulmonary disease (COPD) is a progressive respiratory illness characterized by persistent lung damage from environmental exposures.
  • COPD affects alveoli and airways, leading to significant patient morbidity.

Purpose Of The Study

  • To investigate the molecular mechanisms underlying COPD pathogenesis using advanced sequencing techniques.
  • To identify key cellular and molecular pathways implicated in COPD development.

Main Methods

  • Established a COPD mouse model using cigarette smoke and lipopolysaccharide exposure.
  • Performed single-cell Assay for Transposase Accessible Chromatin (scATAC) sequencing and single-cell RNA sequencing (scRNA-seq) on lung tissues.
  • Analyzed and integrated scATAC-seq and scRNA-seq data to identify cell types, gene expression, and chromatin accessibility changes.

Main Results

  • scATAC-seq and scRNA-seq data showed consistent results in cell type identification and pathway analysis.
  • The tumor necrosis factor (TNF) signaling pathway was significantly enriched in COPD model mice across multiple cell types, including monocytes/macrophages, dendritic cells, and B cells.
  • Upregulation of tumor necrosis factor receptor 1 (TNFR1) and increased accessibility of genes like Il1b, Csf1, and Bcl3 were observed in COPD model cells.

Conclusions

  • The tumor necrosis factor (TNF) signaling pathway is strongly associated with the pathogenesis of COPD.
  • Findings highlight TNFR1 and specific gene accessibility as potential therapeutic targets for COPD.