ArticleEpigenetics2017
Genome-wide Methyl-Seq analysis of blood-brain targets of glucocorticoid exposure.
Article in Epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Steroid hormone-mediated epigenetic programming during puberty: uncovering links to depression.Epigenomics · 2025Review
- Exploring the relationship between methylation of the cortisol receptor genes and brain and cognitive outcomes in individuals with elevated amyloid-β.Research square · 2025Article
- Targeted DNA Methylation Using Modified DNA Probes: A Potential Therapeutic Tool for Depression and Stress-Related Disorders.International journal of molecular sciences · 2025Article
- Cell-Derived Epigenomic Markers of Chronic Stress Distinguish Breast Cancer Phenotypes.The Yale journal of biology and medicine · 2025Article
- Epigenetic Mechanisms Modulated by Glucocorticoids With a Focus on Cushing Syndrome.The Journal of clinical endocrinology and metabolism · 2024Review
- Glucocorticoid effects on the brain: from adaptive developmental plasticity to allostatic overload.The Journal of experimental biology · 2024Review
- Blood DNA methylation ofFrontiers in epigenetics and epigenomics · 2024Article
- An epigenetic synopsis of parental substance use.Epigenomics · 2023Review
- DNA Methylation Alterations in Fractionally Irradiated Rats and Breast Cancer Patients Receiving Radiotherapy.International journal of molecular sciences · 2022Article
- Article
- Corticosterone induces discrete epigenetic signatures in the dorsal and ventral hippocampus that depend upon sex and genotype: focus on methylated Nr3c1 gene.Translational psychiatry · 2022Article
- Identification of glucocorticoid-related molecular signature by whole blood methylome analysis.European journal of endocrinology · 2022Article
- Characterization of glucocorticoid-induced loss of DNA methylation of the stress-response geneEpigenetics · 2021Article
- Cross-species Association Between Telomere Length and Glucocorticoid Exposure.The Journal of clinical endocrinology and metabolism · 2021Article
- Naturalistic Stress Hormone Levels Drive Cumulative Epigenomic Changes along the Cellular Lifespan.International journal of molecular sciences · 2021Article
- The Developmental Chronnecto-Genomics (Dev-CoG) study: A multimodal study on the developing brain.NeuroImage · 2021Article
- Glucocorticoid exposure during hippocampal neurogenesis primes future stress response by inducing changes in DNA methylation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Influence of prenatal transportation stress-induced differential DNA methylation on the physiological control of behavior and stress response in suckling Brahman bull calves.Journal of animal science · 2020Article
- Genome-wide DNA methylation investigation of glucocorticoid exposure within buccal samples.Psychiatry and clinical neurosciences · 2019Article
- Identification of dynamic glucocorticoid-induced methylation changes at the FKBP5 locus.Clinical epigenetics · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic exposure to glucocorticoids (GCs) can lead to psychiatric complications through epigenetic mechanisms such as DNA methylation (DNAm). We sought to determine whether epigenetic changes in a peripheral tissue can serve as a surrogate for those in a relatively inaccessible tissue such as the brain. DNA extracted from the hippocampus and blood of mice treated with GCs or vehicle solution was assayed using a genome-wide DNAm platform (Methyl-Seq) to identify differentially methylated regions (DMRs) induced by GC treatment. We observed that ∼70% of the DMRs in both tissues lost methylation following GC treatment. Of the 3,095 DMRs that mapped to the same genes in both tissues, 1,853 DMRs underwent DNAm changes in the same direction. Interestingly, only 209 DMRs (<7%) overlapped in genomic coordinates between the 2 tissues, suggesting tissue-specific differences in GC-targeted loci. Pathway analysis showed that the DMR-associated genes were members of pathways involved in metabolism, immune function, and neurodevelopment. Also, changes in cell type composition of blood and brain were examined by fluorescence-activated cell sorting. Separation of the cortex into neuronal and non-neuronal fractions and the leukocytes into T-cells, B-cells, and neutrophils showed that GC-induced methylation changes primarily occurred in neurons and T-cells, with the blood tissue also undergoing a shift in the proportion of constituent cell types while the proportion of neurons and glia in the brain remained stable. From the current pilot study, we found that despite tissue-specific epigenetic changes and cellular heterogeneity, blood can serve as a surrogate for GC-induced changes in the brain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.