Epitranscriptomic 5-Methylcytosine Profile in PM2.5-induced Mouse Pulmonary Fibrosis
- Author:
Han XIAO
1
;
Liu HANCHEN
;
Zhang ZEZHONG
;
Yang WENLAN
;
Wu CHUNYAN
;
Liu XUEYING
;
Zhang FANG
;
Sun BAOFA
;
Zhao YONGLIANG
;
Jiang GUIBIN
;
Yang YUN-GUI
;
Ding WENJUN
Author Information
1. College of Life Sciences
- Keywords:
PM2.5 exposure;
mRNA m5C;
Pulmonary fibrosis;
Inflammation;
Immune response
- From:
Genomics, Proteomics & Bioinformatics
2020;18(1):41-51
- CountryChina
- Language:Chinese
-
Abstract:
Exposure of airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 lm (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 epitranscrip-tomic 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.
