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Smoke-related DNA methylation changes in the etiology of human disease
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Genomik. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).ORCID-id: 0000-0002-2915-4498
2014 (Engelska)Ingår i: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 23, nr 9, s. 2290-2297Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Exposure to environmental and lifestyle factors, such as cigarette smoking, affect the epigenome and might mediate risk for diseases and cancers. We have performed a genome-wide DNA methylation study to determine the effect of smoke and snuff (smokeless tobacco) on DNA methylation. A total of 95 sites were differentially methylated [false discovery rate (FDR) q-values < 0.05] in smokers and a subset of the differentially methylated loci were also differentially expressed in smokers. We found no sites, neither any biological functions nor molecular processes enriched for smoke-less tobacco-related differential DNA methylation. This suggests that methylation changes are not caused by the basic components of the tobacco but from its burnt products. Instead, we see a clear enrichment (FDR q-value < 0.05) for genes, including CPOX, CDKN1A and PTK2, involved in response to arsenic-containing substance, which agrees with smoke containing small amounts of arsenic. A large number of biological functions and molecular processes with links to disease conditions are also enriched (FDR q-value < 0.05) for smoke-related DNA methylation changes. These include 'insulin receptor binding', and 'negative regulation of glucose import' which are associated with diabetes, 'positive regulation of interleukin-6-mediated signaling pathway', 'regulation of T-helper 2 cell differentiation', 'positive regulation of interleukin-13 production' which are associated with the immune system and 'sertoli cell fate commitment' which is important for male fertility. Since type 2 diabetes, repressed immune system and infertility have previously been associated with smoking, our results suggest that this might be mediated by DNA methylation changes.

Ort, förlag, år, upplaga, sidor
2014. Vol. 23, nr 9, s. 2290-2297
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:uu:diva-217320DOI: 10.1093/hmg/ddt621ISI: 000334359100005PubMedID: 24334605OAI: oai:DiVA.org:uu-217320DiVA, id: diva2:692832
Tillgänglig från: 2014-02-02 Skapad: 2014-02-02 Senast uppdaterad: 2018-07-06Bibliografiskt granskad

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