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Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Epitranscriptomic 5-Methylcytosine Profile in PM2.5-induced Mouse Pulmonary Fibrosis
Xiao Han1, Hanchen Liu2, Zezhong Zhang3
1College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China; CAS Key Laboratory of Genomic and Precision Medicine, Collaborative Innovation Center of Genetics and Development, College of Future Technology, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; Sino-Danish College, University of Chinese Academy of Sciences, Beijing 101408, China.
Abstract:
Exposure of airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM2.5) is epidemiologically associated with lung dysfunction and respiratory symptoms, including pulmonary fibrosis. However, whether epigenetic mechanisms are involved in PM2.5-induced pulmonary fibrosis is currently poorly understood. Herein, using a PM2.5-induced pulmonary fibrosis mouse model, we found that PM2.5 exposure leads to aberrant mRNA 5-methylcytosine (m5C) gain and loss in fibrotic lung tissues. Moreover, we showed the m5C-mediated regulatory map of gene functions in pulmonary fibrosis after PM2.5 exposure. Several genes act as m5C gain-upregulated factors, probably critical for the development of PM2.5-induced fibrosis in mouse lungs. These genes, including Lcn2, Mmp9, Chi3l1, Adipoq, Atp5j2, Atp5l, Atpif1, Ndufb6, Fgr, Slc11a1, and Tyrobp, are highly related to oxidative stress response, inflammatory responses, and immune system processes. Our study illustrates the first epitranscriptomic RNA m5C profile in PM2.5-induced pulmonary fibrosis and will be valuable in identifying biomarkers for PM2.5 exposure-related lung pathogenesis with translational potential.
Insights
Airborne fine particulate matter (PM2.5) exposure alters RNA methylation in mouse lungs, contributing to pulmonary fibrosis. This study reveals key genes involved in PM2.5-induced lung disease.
Area of Science:
- Environmental Health
- Molecular Biology
- Epigenetics
Background:
- Particulate matter (PM2.5) exposure is linked to lung diseases like pulmonary fibrosis.
- The role of epigenetic mechanisms, specifically RNA modifications, in PM2.5-induced lung fibrosis is not well understood.
Purpose of the Study:
- To investigate the involvement of mRNA 5-methylcytosine (m5C) modifications in the pathogenesis of PM2.5-induced pulmonary fibrosis.
- To map the m5C-mediated gene regulatory network in response to PM2.5 exposure in lung tissue.
Main Methods:
- Utilized a mouse model of PM2.5-induced pulmonary fibrosis.
- Analyzed aberrant mRNA m5C gain and loss in fibrotic lung tissues.
- Identified m5C-regulated genes associated with PM2.5 exposure.
Main Results:
- PM2.5 exposure induced significant changes in mRNA m5C levels in mouse lungs.
- Several m5C gain-upregulated genes (e.g., Lcn2, Mmp9, Chi3l1) were identified as critical factors in fibrosis development.
- These genes are implicated in oxidative stress, inflammation, and immune responses.
Conclusions:
- This study presents the first epitranscriptomic RNA m5C profile in PM2.5-induced pulmonary fibrosis.
- The findings highlight the role of m5C modifications in PM2.5-related lung pathogenesis.
- Identified genes may serve as potential biomarkers for PM2.5 exposure and lung disease.
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