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Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

ABSTRACT: Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

PROVIDER: PRJNA318502 | ENA |

REPOSITORIES: ENA

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Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

Project description:Chronic early life stress increases adult susceptibility to numerous health problems linked to chronic inflammation. One way that this may occur is via glucocorticoid-induced developmental programming. To gain insight into such programming, we treated zebrafish embryos with cortisol and examined the effects on adults. In adulthood, the treated fish maintained elevated basal cortisol levels in the absence of exogenous cortisol, and constitutively mis-expressed genes involved in defense response and its regulation. Adults derived from cortisol-treated embryos displayed defective tailfin regeneration, heightened basal expression of pro-inflammatory genes, and failure to appropriately regulate those genes following injury or immunological challenge. These results support the hypothesis that chronically elevated glucocorticoid signaling early in life directs development of a pro-inflammatory adult phenotype, at the expense of immunoregulation and somatic regenerative capacity. 30 samples total were analyzed. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to DMSO control as embryos. 9 caudal fins samples (0, 2 and 4dpa), 3 blood samples and 3 muscle samples from adults exposed to cortisol (1 micromolar) as embryos.

2016-06-01 | E-GEOD-80260 | biostudies-arrayexpress

Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

2016-06-01 | GSE80260 | GEO

Danio rerio

Project description:Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation [adults]

| PRJNA318414 | ENA

Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-01 | E-GEOD-80286 | biostudies-arrayexpress

Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation

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

2016-06-01 | GSE80286 | GEO

Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation.

Project description: Not available

| S-EPMC5004618 | biostudies-literature

Chronic glucocorticoid exposure in early development leads to neuroendocrine, metabolic, and immune dysregulation in adult zebrafish

Project description:Chronic early life stress can affect development of the neuroendocrine stress system, leading to its persistent dysregulation and consequently increased disease risk in adulthood. One contributing factor is thought to be epigenetic programming in response to chronic glucocorticoid exposure during early development. We have previously shown that zebrafish embryos treated chronically with cortisol develop into adults with constitutively elevated whole body cortisol and aberrant immune gene expression. The objective of the experiments reported here was to further characterize the phenotype of those adults. We find that adult zebrafish derived from cortisol-treated embryos have aberrant cortisol tissue distribution and dynamics, which correlate with differential transcriptional activity of key glucocorticoid-responsive regulatory genes klf9 and fkbp5 in blood and brain.

2019-10-28 | GSE137987 | GEO

RNAseq measurement of cortisol induced gene expression change under knockout of glucocorticoid receptor (nr3c1)

Project description:We found that GR mediates most of the effects of the treatment, and paradoxically, that the transcriptome of cortisol-treated larvae is more like that of larvae lacking a GR than that of larvae with a GR, suggesting that the cortisol-treated larvae develop GR resistance.

2020-07-15 | GSE144884 | GEO

Transcriptomic Evidence that Cortisol Alters Perinatal Epicardial Adipose Tissue Maturation

Project description:Cortisol administration during late gestation in ewes, modeling maternal stress, resulted in transcriptomic changes suggesting altered maturation and metabolic changes to the offspring heart. This study investigates the effects of cortisol on epicardial adipose tissue (EAT), a visceral fat pad associated with adverse cardiovascular conditions in adults. Pregnant ewes were treated with either 1 or 0.5 mg/kg/day cortisol from 115 days gestation to term and EAT collected from term fetuses (control: n=8, maternal cortisol 1 mg/kg/day: n=6) or two-week-old lambs (control: n=7, maternal cortisol 0.5mg/kg/day: n=9). Transcriptomic modeling was used to identify pathways altered by maternal cortisol over-exposure. Transcriptomic modeling confirmed the brown fat phenotype of EAT at term and a transition towards white fat at two weeks of age in EAT of control fetuses/lambs, and highlighted a role of immune responses, including complement-coagulation, and serotonin in this transition. Maternal cortisol (1mg/kg/day) increased the lipid peroxidation product 4-hydroxynonenal in EAT of term fetuses, but did not affect the number of activated macrophages or size of the lipid droplets in the depot; transcriptomics suggested an earlier metabolic maturation of EAT via, in part, increased immune responses. Conversely the transcriptomics in EAT of two-week-old lambs of ewes treated with a lower dose of cortisol (0.5mg/kg/day) suggested decreased metabolism of several substrates through both mitochondrial and cytosolic actions, and delayed maturation of EAT associated with a longer period of adipogenesis and angiogenesis.

2019-07-10 | GSE119254 | GEO

RNAseq measurement of cortisol induced gene expression change under knockout of Klf9

Project description:We found that a frameshift deletion introduced into exon 1 of zebrafish klf9 eliminates the DNA binding domain and significantly reduces expression of the mature transcript. RNA-seq shows that klf9 is required for the pro-inflammatory transcriptomic effects of chronic cortisol treatment. klf9 is one of a core set of genes consistently found to be upregulated by chronic cortisol exposure.

2020-07-15 | GSE144885 | GEO

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