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

Liu C, Xu J, Chen Y, Guo X, Zheng Y, Wang Q, Chen Y, Ni Y, Zhu Y, Joyce BT, Baccarelli A, Deng F, Zhang W, Hou L - Environ Health (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, USA. cliu55@uic.edu.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Overview of the study design and analysis workflow. Nuclei were extracted from blood samples of four individuals under low or high exposure of outdoor PM2.5. Standard protocol was used for ChIP-Seq experiments. Bioinformatics software (in brackets) and in-house scripts were used to analyze the sequencing data. The functions of differential H3K27ac loci were evaluated using public databases. ChIP: chromatin immunoprecipitation; IP: immunoprecipitation; GO: gene ontology
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Fig1: Overview of the study design and analysis workflow. Nuclei were extracted from blood samples of four individuals under low or high exposure of outdoor PM2.5. Standard protocol was used for ChIP-Seq experiments. Bioinformatics software (in brackets) and in-house scripts were used to analyze the sequencing data. The functions of differential H3K27ac loci were evaluated using public databases. ChIP: chromatin immunoprecipitation; IP: immunoprecipitation; GO: gene ontology

Mentions: Figure 1 shows the general workflow of this study. Briefly, four individuals subjected to different PM2.5 exposure levels were profiled for genome-wide H3K27ac profiles using ChIP-Seq. A standard ChIP-Seq data analysis pipeline was performed to identify differential histone modification loci between the two exposure groups.Fig. 1


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

Liu C, Xu J, Chen Y, Guo X, Zheng Y, Wang Q, Chen Y, Ni Y, Zhu Y, Joyce BT, Baccarelli A, Deng F, Zhang W, Hou L - Environ Health (2015)

Overview of the study design and analysis workflow. Nuclei were extracted from blood samples of four individuals under low or high exposure of outdoor PM2.5. Standard protocol was used for ChIP-Seq experiments. Bioinformatics software (in brackets) and in-house scripts were used to analyze the sequencing data. The functions of differential H3K27ac loci were evaluated using public databases. ChIP: chromatin immunoprecipitation; IP: immunoprecipitation; GO: gene ontology
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4537530&req=5

Fig1: Overview of the study design and analysis workflow. Nuclei were extracted from blood samples of four individuals under low or high exposure of outdoor PM2.5. Standard protocol was used for ChIP-Seq experiments. Bioinformatics software (in brackets) and in-house scripts were used to analyze the sequencing data. The functions of differential H3K27ac loci were evaluated using public databases. ChIP: chromatin immunoprecipitation; IP: immunoprecipitation; GO: gene ontology
Mentions: Figure 1 shows the general workflow of this study. Briefly, four individuals subjected to different PM2.5 exposure levels were profiled for genome-wide H3K27ac profiles using ChIP-Seq. A standard ChIP-Seq data analysis pipeline was performed to identify differential histone modification loci between the two exposure groups.Fig. 1

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, USA. cliu55@uic.edu.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus