University of Illinois at Chicago
Characterization of genome-wide.pdf (1.24 MB)

Characterization of genome-wide H3K27ac profiles reveals a distinct PM2.5-associated histone modification signature.

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journal contribution
posted on 2016-01-28, 00:00 authored by C. Liu, J. Xu, Y. Chen, X. Guo, Y. Zheng, Q. Wang, Y. Ni, Y. Zhu
BACKGROUND: Current studies of environmental health suggest a link between air pollution components, such as particulate matter (PM), and various diseases. However, the specific genes and regulatory mechanisms implicated in PM-induced diseases remain largely unknown. Epigenetic systems such as covalent modification of histones in chromatin may mediate environmental factors in gene regulation. Investigating the relationships between PM exposure and histone modification status may help understand the mechanisms underlying environment-associated health conditions. METHODS: In this study, we obtained genome-wide profiles of H3K27ac (histone 3 lysine 27 acetylation), known to be an active gene regulatory histone modification marker, in blood samples collected from four Chinese individuals exposed to high or low PM2.5 (particles with diameters up to 2.5 μm). RESULTS: The genome-wide chromatin immunoprecipitation sequencing (ChIP-Seq) data indicated a comprehensive differential H3K27ac landscape across the individual genomes, which was associated with high PM2.5. Moreover, a substantial number of these PM2.5-associated differential H3K27ac markers were in genes involved in immune cell activation, potentially linking these epigenetic changes with air pollution-induced immune and inflammatory responses. CONCLUSIONS: Our study provides the first genome-wide characterization of H3K27ac profiles in individuals subjected to different exposure levels of PM2.5. Future systematic investigations of the relationships between air pollutants and histone modifications in large population samples are warranted to elucidate the contributions of histone modifications to environment-associated diseases.


This work was supported, in part, by grants from the National Institutes of Health: ES00002 and R21ES020010 (to LH, AB), R21HG006367 (to WZ), and The Robert H. Lurie Comprehensive Cancer Center-Developmental Funds P30CA060553 (to WZ).


Publisher Statement

This is the copy of an article published in Environmental Health © 2015 BioMed Central Publications. © 2015 Liu et al.


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