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High cortisol in 5-year-old children causes loss of DNA methylation in SINE retrotransposons: a possible role for ZNF263 in stress-related diseases
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0003-4224-1032
Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Paediatrics in Linköping.
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2015 (English)In: Clinical Epigenetics, E-ISSN 1868-7083, ISSN 1868-7083, Vol. 7, no 1, 91Article in journal (Refereed) Published
Abstract [en]

Background: Childhood stress leads to increased risk of many adult diseases, such as major depression and cardiovascular disease. Studies show that adults with experienced childhood stress have specific epigenetic changes, but to understand the pathways that lead to disease, we also need to study the epigenetic link prospectively in children. Results: Here, we studied a homogenous group of 48 5-year-old children. By combining hair cortisol measurements (a well-documented biomarker for chronic stress), with whole-genome DNA-methylation sequencing, we show that high cortisol associates with a genome-wide decrease in DNA methylation and targets short interspersed nuclear elements (SINEs; a type of retrotransposon) and genes important for calcium transport: phenomena commonly affected in stress-related diseases and in biological aging. More importantly, we identify a zinc-finger transcription factor, ZNF263, whose binding sites where highly overrepresented in regions experiencing methylation loss. This type of zinc-finger protein has previously shown to be involved in the defense against retrotransposons. Conclusions: Our results show that stress in preschool children leads to changes in DNA methylation similar to those seen in biological aging. We suggest that this may affect future disease susceptibility by alterations in the epigenetic mechanisms that keep retrotransposons dormant. Future treatments for stress-and age-related diseases may therefore seek to target zinc-finger proteins that epigenetically control retrotransposon reactivation, such as ZNF263.

Place, publisher, year, edition, pages
BioMed Central, 2015. Vol. 7, no 1, 91
Keyword [en]
Stress; DNA methylation; ZNF263; Children; Retrotransposon; Cortisol; Transcription factor; EGR1; Blood; Hair
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-122055DOI: 10.1186/s13148-015-0123-zISI: 000360619500001PubMedID: 26339299OAI: oai:DiVA.org:liu-122055DiVA: diva2:885416
Note

Funding Agencies|Centre for Systems Neurobiology at Linkoping University; Swedish Research Council [K2005-72X-11242-11A, K2008-69X-20826-01-4]; Swedish Child Diabetes Foundation; JDRF Wallenberg Foundation [K 98-99D-12813-01A]; Medical Research Council of Southeast Sweden (FORSS); Swedish Council for Working Life and Social Research [FAS2004-1775]

Available from: 2015-12-18 Created: 2015-10-19 Last updated: 2017-12-01

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Nätt, DanielJohansson, IngelaFaresjö, TomasLudvigsson, JohnnyThorsell, Annika

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Nätt, DanielJohansson, IngelaFaresjö, TomasLudvigsson, JohnnyThorsell, Annika
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Division of Cell BiologyFaculty of Medicine and Health SciencesDivision of Clinical SciencesDivision of Community MedicineDepartment of Paediatrics in LinköpingDivision of Neuro and Inflammation Science
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