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DNA methylome signatures of prenatal exposure to synthetic glucocorticoids in hippocampus and peripheral whole blood of female guinea pigs in early life

ABSTRACT: DNA methylome signatures of prenatal exposure to synthetic glucocorticoids in hippocampus and peripheral whole blood of female guinea pigs in early life

PROVIDER: PRJNA686115 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13268700.fastq.gz	Fastqsanger.gz
	SRR13268701.fastq.gz	Fastqsanger.gz
	SRR13268702_1.fastq.gz	Fastqsanger.gz
	SRR13268702_2.fastq.gz	Fastqsanger.gz
	SRR13268703.fastq.gz	Fastqsanger.gz

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DNA methylome signatures of prenatal exposure to synthetic glucocorticoids in hippocampus and peripheral whole blood of female guinea pigs in early life

Project description:We examined the hypothesis that prenatal synthetic glucocorticoids (sGC) administration alters DNA methylation signatures in Guinea pig offspring hippocampus and whole blood. Guinea pigs were treated with sGC or saline in late gestation. Genome-wide modifications of DNA methylation were analyzed using reduced representation bisulfite sequencing in juvenile female offspring.

2020-12-18 | GSE163447 | GEO

DNA methylome signatures of prenatal exposure to synthetic glucocorticoids in hippocampus and peripheral whole blood of female guinea pigs in early life.

Project description:Synthetic glucocorticoids (sGC) are administered to women at risk of preterm delivery, approximately 10% of all pregnancies. In animal models, offspring exposed to elevated glucocorticoids, either by administration of sGC or endogenous glucocorticoids as a result of maternal stress, show increased risk of developing behavioral, endocrine, and metabolic dysregulation. DNA methylation may play a critical role in long-lasting programming of gene regulation underlying these phenotypes. However, peripheral tissues such as blood are often the only accessible source of DNA for epigenetic analyses in humans. Here, we examined the hypothesis that prenatal sGC administration alters DNA methylation signatures in guinea pig offspring hippocampus and whole blood. We compared these signatures across the two tissue types to assess epigenetic biomarkers of common molecular pathways affected by sGC exposure. Guinea pigs were treated with sGC or saline in late gestation. Genome-wide modifications of DNA methylation were analyzed at single nucleotide resolution using reduced representation bisulfite sequencing in juvenile female offspring. Results indicate that there are tissue-specific as well as common methylation signatures of prenatal sGC exposure. Over 90% of the common methylation signatures associated with sGC exposure showed the same directionality of change in methylation. Among differentially methylated genes, 134 were modified in both hippocampus and blood, of which 61 showed methylation changes at identical CpG sites. Gene pathway analyses indicated that prenatal sGC exposure alters the methylation status of gene clusters involved in brain development. These data indicate concordance across tissues of epigenetic programming in response to alterations in glucocorticoid signaling.

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miRNA levels in F1-F3 male germ cells and female F2 PFC following prenatal exposure to sGC in guinea pigs

Project description:Stress and glucocorticoid exposure during pregnancy alters neurodevelopment and behavior in offspring, and these effects extend multiple generations through a paternal lineage. The epigenetic mechanisms that govern this transgenerational transmission are unclear. We hypothesized that maternal exposure to multiple courses of sGC in late pregnancy would result in altered miRNA levels in germs cells of male guinea pigs across three generations. Further, our behavioral data indicate that F2 females exhibit altered behaviors following sGC exposure. Thus, we evaluated the miRNA profile of F2 female prefrontal cortex to determine the mechanisms responsible for these behavioral changes and to compare these data to our germ cell miRNA analysis. We used miRNA microarray to evaluate the miRNA levels in F1-F3 germ cells and F2 female PFC in guinea pigs that were exposed to control and F0 prenatal sGC exposure. We identified no significant changes to miRNA levels in both F1-F3 germ cells and F2 PFC from guinea pigs in the sGC group.

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The Transgenerational Effects of Prenatal Synthetic Glucocorticoids on the Hippocampus Cortex

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miRNA levels in caput and cauda sperm in adult male guinea pigs following synthetic glucocorticoid exposure

Project description:It has been demonstrated that males exposed to adversity prior to conception sire offspring exhibiting abnormal behaviour and neuroendocrine function. Epigenetic factors such as microRNA (miRNA) within sperm may be responsible for driving these effects. Synthetic glucocorticoids (sGC) are a class of drug that are commonly prescribed and may have implications for intergenerational transmission. Therefore, we hypothesized that caput and cauda sperm miRNA profiles will be altered following sGC exposure in guinea pigs. We used miRNA microarray to evaluate the miRNA levels of caput and cauda sperm isolated from guinea pigs exposed to control and water treated with sGC. We identified a subset of miRNAs with low levels in cauda sperm of guinea pigs exposed to sGC.

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The Transgenerational Effects of Prenatal Synthetic Glucocorticoids on the Hippocampus Cortex

Project description:First generation animals (F1) were exposed to multiple courses of synthetic glucocorticoids in utero. Animals were then bred to produce second (F2) and third (F3) generation offspring. These animals underwent behavioural assessmenets before sacrifice. In this experiment the prefrontal cortex for F1, F2, and F3 female animals, as well as F1 males (Control and sGC) have been extracted via micro-punch and RNA has been extracted.

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Project description:The Transgenerational Effects of Prenatal Synthetic Glucocorticoids on the Prefrontal Cortex

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