摘要
Exposure of airborne particulate matter(PM)with an aerodynamic diameter less than 2.5μm(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 mRNA5-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,Slc11 a1,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.
基金
supported by the State Key Program of the National Natural Science Foundation of China(Grant No.91643206)
the Strategic Priority Research Program of the Chinese Academy of Sciences(Grant No.XDB14030300)
the Chinese Academy of Sciences/State Administration of Foreign Experts Affairs(CAS/SAFEA)International Partnership Program for Creative Research Teams of China
作者简介
Xiao Han,Equal contribution;Hanchen Liu,Equal contribution;Zezhong Zhang,Equal contribution;corresponding author:Wenjun DingE-mail:dingwj@ucas.ac.cn;corresponding author:Yun-Gui Yang,E-mail:ygyang@big.ac.cn
