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Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

ABSTRACT: Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

PROVIDER: PRJNA490449 | ENA |

REPOSITORIES: ENA

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Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

Project description:Prenatal stress exposure is associated with the risk for psychiatric disorders later in life. This may be mediated via enhanced exposure to glucocorticoids (GCs), known to impact neurogenesis. We aimed to identify molecular mediators of these effects, focusing on long-lasting epigenetic changes. In a human hippocampal progenitor cell (HPC) line, we assessed the short- and long-term effects of GC exposure during neurogenesis on mRNA expression and DNA methylation (DNAm) profiles. GC exposure induced changes in DNAm at 27,812 CpG sites and in the expression of 3,857 transcripts at FDR ≤ 0.1 and an absolsute change in expression of 1.15. HPC gene expression and GC-affected DNAm profiles were enriched for changes observed during human fetal brain development. Differentially methylated sites (DMSs) with GC exposure clustered into four trajectories over HPC-differentiation, with transient as well as long-lasting DNAm changes. Lasting DMSs mapped to distinct functional pathways and were selectively enriched for poised and bivalent enhancer marks. Lasting DMSs had little correlation with lasting gene expression changes, but were associated with a significantly enhanced transcriptional response to a second acute GC challenge. A significant subset of lasting DMSs was also responsive to an acute GC-challenge in peripheral blood. These tissue-overlapping DMSs were used to compute a poly-epigenetic score that predicted exposure to conditions of excessive prenatal GC in newborn cord blood. Overall, our data suggest that early exposure to GCs can change the set point of future transcriptional responses to stress by inducing lasting DNAm changes. Such altered set points may relate to differential vulnerability to stress exposure later in life.

2019-03-01 | GSE119846 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

2019-03-01 | GSE119843 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

2019-03-01 | GSE119842 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

| PRJNA490442 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

| PRJNA490451 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

| PRJNA490444 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-01 | GSE119847 | GEO

Glucocorticoid exposure during hippocampal neurogenesis primes future stress response by inducing changes in DNA methylation.

Project description:Prenatal stress exposure is associated with risk for psychiatric disorders later in life. This may be mediated in part via enhanced exposure to glucocorticoids (GCs), which are known to impact neurogenesis. We aimed to identify molecular mediators of these effects, focusing on long-lasting epigenetic changes. In a human hippocampal progenitor cell (HPC) line, we assessed the short- and long-term effects of GC exposure during neurogenesis on messenger RNA (mRNA) expression and DNA methylation (DNAm) profiles. GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts (false discovery rate [FDR] ? 0.1 and absolute fold change [FC] expression ? 1.15). HPC expression and GC-affected DNAm profiles were enriched for changes observed during human fetal brain development. Differentially methylated sites (DMSs) with GC exposure clustered into 4 trajectories over HPC differentiation, with transient as well as long-lasting DNAm changes. Lasting DMSs mapped to distinct functional pathways and were selectively enriched for poised and bivalent enhancer marks. Lasting DMSs had little correlation with lasting expression changes but were associated with a significantly enhanced transcriptional response to a second acute GC challenge. A significant subset of lasting DMSs was also responsive to an acute GC challenge in peripheral blood. These tissue-overlapping DMSs were used to compute a polyepigenetic score that predicted exposure to conditions associated with altered prenatal GCs in newborn's cord blood DNA. Overall, our data suggest that early exposure to GCs can change the set point of future transcriptional responses to stress by inducing lasting DNAm changes. Such altered set points may relate to differential vulnerability to stress exposure later in life.

| S-EPMC7519233 | biostudies-literature

Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

Project description:Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

| PRJNA791634 | ENA

Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

Project description:A remarkable diversity in regenerative competency of extant species suggests an evolutionary influence, but few studies have identified potential selective pressures shaping this variation. Uncovering these selective pressures is critical to understanding the key molecular similarities, and differences, between regeneratorsand non-regenerators. Here we report that, in the highly-regenerative axolotl, an evolutionarily conserved body-wide stem cell activation response primes other limbs for faster regeneration, offering a selective advantage for this phenomenon. We further demonstrate the body-wide response requires peripheral nervous system input at these distant sites and is predicated on mTOR signaling. We definedgene expression changes within the signaling neural processes and nearby tissues, harboring responsive stem cells, leading to candidate genetic pathways central to this process. Functional experimentation confirmed a requirement for adrenergic signaling in amputation-induced activation of distant stem cells. Our study provides a direct link between body-wide cellular activation responses and regeneration, unifying previous reports from distant species of various natural regenerative abilities, such as planarians and mice, in a conceptual framework that centers the ability to convert the body-wide response to local tissue outgrowth as the key difference between regenerators and non-regenerators.

2022-01-01 | GSE192477 | GEO

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