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  Genome-wide DNA methylation levels and altered cortisol stress reactivity following childhood trauma in humans

Houtepen, L. C., Vinkers, C. H., Carrillo-Roa, T., Hiemstra, M., van Lier, P. A., Meeus, W., et al. (2016). Genome-wide DNA methylation levels and altered cortisol stress reactivity following childhood trauma in humans. NATURE COMMUNICATIONS, 7: 10967. doi:10.1038/ncomms10967.

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Houtepen, Lotte C.1, Autor
Vinkers, Christiaan H.1, Autor
Carrillo-Roa, Tania2, Autor           
Hiemstra, Marieke1, Autor
van Lier, Pol A.1, Autor
Meeus, Wim1, Autor
Branje, Susan1, Autor
Heim, Christine M.1, Autor
Nemeroff, Charles B.1, Autor
Mill, Jonathan1, Autor
Schalkwyk, Leonard C.1, Autor
Creyghton, Menno P.1, Autor
Kahn, Rene S.1, Autor
Joels, Marian1, Autor
Binder, Elisabeth B.1, 2, Autor           
Boks, Marco P. M.1, Autor
Affiliations:
1external, ou_persistent22              
2Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society, ou_2035295              

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 Zusammenfassung: DNA methylation likely plays a role in the regulation of human stress reactivity. Here we show that in a genome- wide analysis of blood DNA methylation in 85 healthy individuals, a locus in the Kit ligand gene (KITLG; cg27512205) showed the strongest association with cortisol stress reactivity (P = 5.8 x 10 (-6)). Replication was obtained in two independent samples using either blood (N = 45, P = 0.001) or buccal cells (N = 255, P = 0.004). KITLG methylation strongly mediates the relationship between childhood trauma and cortisol stress reactivity in the discovery sample (32% mediation). Its genomic location, a CpG island shore within an H3K27ac enhancer mark, and the correlation between methylation in the blood and prefrontal cortex provide further evidence that KITLG methylation is functionally relevant for the programming of stress reactivity in the human brain. Our results extend preclinical evidence for epigenetic regulation of stress reactivity to humans and provide leads to enhance our understanding of the neurobiological pathways underlying stress vulnerability.

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Sprache(n): eng - English
 Datum: 2016-03
 Publikationsstatus: Online veröffentlicht
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 Identifikatoren: ISI: 000372497900001
DOI: 10.1038/ncomms10967
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Titel: NATURE COMMUNICATIONS
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: London, UK : Nature
Seiten: - Band / Heft: 7 Artikelnummer: 10967 Start- / Endseite: - Identifikator: ISSN: 2041-1723