Reduced DNA methylation and psychopathology following endogenous hypercortisolism – a genome-wide study

Patients with Cushing’s Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes in DNA methylation that are associated with persisting neuropsychological consequences. Genome-wide DNA methylation was assessed in 48 women w...

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Published inScientific reports Vol. 7; no. 1; p. 44445
Main Authors Glad, Camilla A. M., Andersson-Assarsson, Johanna C., Berglund, Peter, Bergthorsdottir, Ragnhildur, Ragnarsson, Oskar, Johannsson, Gudmundur
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 16.03.2017
Nature Publishing Group
Subjects
45/22
631/208/177
631/337/176/1988
Adrenocorticotropic hormone
Anxiety
cognitive impairments
Cortisol
Cushing syndrome
cushings-syndrome
Deoxyribonucleic acid
DNA
DNA methylation
DNA probes
Endocrinology and Diabetes
Endokrinologi och diabetes
Fatigue
Gene mapping
Genes
Genomes
glucocorticoid-receptor
homeostatic synaptic plasticity
hpa-axis
Humanities and Social Sciences
major depressive disorder
Mental depression
multidisciplinary
Nervous system diseases
Pituitary
pituitary-adrenal axis
posttraumatic-stress-disorder
Probes
Psychopathology
receptor gene nr3c1
Remission
Science
Science & Technology - Other Topics
Smoking
trans-retinoic acid
Online AccessGet full text
ISSN2045-2322
2045-2322
DOI10.1038/srep44445

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Abstract Patients with Cushing’s Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes in DNA methylation that are associated with persisting neuropsychological consequences. Genome-wide DNA methylation was assessed in 48 women with CS in long-term remission (cases) and 16 controls matched for age, gender and education. The Fatigue impact scale and the comprehensive psychopathological rating scale were used to evaluate fatigue, depression and anxiety. Cases had lower average global DNA methylation than controls (81.2% vs 82.7%; p  = 0.002). Four hundred and sixty-one differentially methylated regions, containing 3,246 probes mapping to 337 genes were identified. After adjustment for age and smoking, 731 probes in 236 genes were associated with psychopathology (fatigue, depression and/or anxiety). Twenty-four gene ontology terms were associated with psychopathology; terms related to retinoic acid receptor signalling were the most common (adjusted p  = 0.0007). One gene in particular, COL11A2 , was associated with fatigue following a false discovery rate correction. Our findings indicate that hypomethylation of FKBP5 and retinoic acid receptor related genes serve a potential mechanistic explanation for long-lasting GC-induced psychopathology.
AbstractList Patients with Cushing’s Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes in DNA methylation that are associated with persisting neuropsychological consequences. Genome-wide DNA methylation was assessed in 48 women with CS in long-term remission (cases) and 16 controls matched for age, gender and education. The Fatigue impact scale and the comprehensive psychopathological rating scale were used to evaluate fatigue, depression and anxiety. Cases had lower average global DNA methylation than controls (81.2% vs 82.7%; p  = 0.002). Four hundred and sixty-one differentially methylated regions, containing 3,246 probes mapping to 337 genes were identified. After adjustment for age and smoking, 731 probes in 236 genes were associated with psychopathology (fatigue, depression and/or anxiety). Twenty-four gene ontology terms were associated with psychopathology; terms related to retinoic acid receptor signalling were the most common (adjusted p  = 0.0007). One gene in particular, COL11A2 , was associated with fatigue following a false discovery rate correction. Our findings indicate that hypomethylation of FKBP5 and retinoic acid receptor related genes serve a potential mechanistic explanation for long-lasting GC-induced psychopathology.
Patients with Cushing’s Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes in DNA methylation that are associated with persisting neuropsychological consequences. Genome-wide DNA methylation was assessed in 48 women with CS in long-term remission (cases) and 16 controls matched for age, gender and education. The Fatigue impact scale and the comprehensive psychopathological rating scale were used to evaluate fatigue, depression and anxiety. Cases had lower average global DNA methylation than controls (81.2% vs 82.7%; p = 0.002). Four hundred and sixty-one differentially methylated regions, containing 3,246 probes mapping to 337 genes were identified. After adjustment for age and smoking, 731 probes in 236 genes were associated with psychopathology (fatigue, depression and/or anxiety). Twenty-four gene ontology terms were associated with psychopathology; terms related to retinoic acid receptor signalling were the most common (adjusted p = 0.0007). One gene in particular, COL11A2, was associated with fatigue following a false discovery rate correction. Our findings indicate that hypomethylation of FKBP5 and retinoic acid receptor related genes serve a potential mechanistic explanation for long-lasting GC-induced psychopathology.
ArticleNumber 44445
Author Berglund, Peter
Johannsson, Gudmundur
Ragnarsson, Oskar
Glad, Camilla A. M.
Andersson-Assarsson, Johanna C.
Bergthorsdottir, Ragnhildur
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  givenname: Johanna C.
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  fullname: Andersson-Assarsson, Johanna C.
  organization: Department of Molecular and Clinical Medicine, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg
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  givenname: Peter
  surname: Berglund
  fullname: Berglund, Peter
  organization: Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg
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  givenname: Ragnhildur
  surname: Bergthorsdottir
  fullname: Bergthorsdottir, Ragnhildur
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  surname: Ragnarsson
  fullname: Ragnarsson, Oskar
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  givenname: Gudmundur
  surname: Johannsson
  fullname: Johannsson, Gudmundur
  organization: Department of Internal Medicine and Clinical Nutrition, University of Gothenburg and Department of Endocrinology, Institute of Medicine at Sahlgrenska Academy, Sahlgrenska University Hospital
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28300138$$D View this record in MEDLINE/PubMed
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Snippet Patients with Cushing’s Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes...
Patients with Cushing's Syndrome (CS) in remission were used as a model to test the hypothesis that long-standing excessive cortisol exposure induces changes...
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StartPage 44445
SubjectTerms 45/22
631/208/177
631/337/176/1988
Adrenocorticotropic hormone
Anxiety
cognitive impairments
Cortisol
Cushing syndrome
cushings-syndrome
Deoxyribonucleic acid
DNA
DNA methylation
DNA probes
Endocrinology and Diabetes
Endokrinologi och diabetes
Fatigue
Gene mapping
Genes
Genomes
glucocorticoid-receptor
homeostatic synaptic plasticity
hpa-axis
Humanities and Social Sciences
major depressive disorder
Mental depression
multidisciplinary
Nervous system diseases
Pituitary
pituitary-adrenal axis
posttraumatic-stress-disorder
Probes
Psychopathology
receptor gene nr3c1
Remission
Science
Science & Technology - Other Topics
Smoking
trans-retinoic acid
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Title Reduced DNA methylation and psychopathology following endogenous hypercortisolism – a genome-wide study
URI https://link.springer.com/article/10.1038/srep44445
https://www.ncbi.nlm.nih.gov/pubmed/28300138
https://www.proquest.com/docview/1903378932
https://pubmed.ncbi.nlm.nih.gov/PMC5353706
https://gup.ub.gu.se/publication/252965
https://www.nature.com/articles/srep44445.pdf
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