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Sci Rep. 2017 Mar 7;7:43345. doi: 10.1038/srep43345.

ELF-MF exposure affects the robustness of epigenetic programming during granulopoiesis.

Author information

1
Department of Biomedicine, University of Basel, Mattenstrasse 28, Basel, CH-4058, Switzerland.
2
Swiss Tropical and Public Health Institute, Socinstrasse 57, Basel, CH-4002, Switzerland.
3
University of Basel, Petersplatz 1, Basel, CH-4001, Switzerland.
4
SIB Swiss Institute of Bioinformatics, Basel, Switzerland.
5
IT'IS Foundation, Zeughausstrasse 43, Zürich, CH-8004, Switzerland.
6
Swiss Federal Institute of Technology (ETH), Zürich, CH-8006, Switzerland.

Abstract

Extremely-low-frequency magnetic fields (ELF-MF) have been classified as "possibly carcinogenic" to humans on the grounds of an epidemiological association of ELF-MF exposure with an increased risk of childhood leukaemia. Yet, underlying mechanisms have remained obscure. Genome instability seems an unlikely reason as the energy transmitted by ELF-MF is too low to damage DNA and induce cancer-promoting mutations. ELF-MF, however, may perturb the epigenetic code of genomes, which is well-known to be sensitive to environmental conditions and generally deranged in cancers, including leukaemia. We examined the potential of ELF-MF to influence key epigenetic modifications in leukaemic Jurkat cells and in human CD34+ haematopoietic stem cells undergoing in vitro differentiation into the neutrophilic lineage. During granulopoiesis, sensitive genome-wide profiling of multiple replicate experiments did not reveal any statistically significant, ELF-MF-dependent alterations in the patterns of active (H3K4me2) and repressive (H3K27me3) histone marks nor in DNA methylation. However, ELF-MF exposure showed consistent effects on the reproducibility of these histone and DNA modification profiles (replicate variability), which appear to be of a stochastic nature but show preferences for the genomic context. The data indicate that ELF-MF exposure stabilizes active chromatin, particularly during the transition from a repressive to an active state during cell differentiation.

PMID:
28266526
PMCID:
PMC5339735
DOI:
10.1038/srep43345
[Indexed for MEDLINE]
Free PMC Article

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