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Sex-Dependent Changes of miRNA Levels in the Hippocampus of Adrenalectomized Rats Following Acute Corticosterone Administration

ABSTRACT: Sex-Dependent Changes of miRNA Levels in the Hippocampus of Adrenalectomized Rats Following Acute Corticosterone Administration

PROVIDER: PRJNA751373 | ENA |

REPOSITORIES: ENA

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Sex-Dependent Changes of miRNA Levels in the Hippocampus of Adrenalectomized Rats Following Acute Corticosterone Administration

Project description:We explored sex-biased effects of the primary stress glucocorticoid hormone corticosterone on the miRNA expression profile in the rat hippocampus. Adult adrenalectomized (ADX) female and male rats received a single corticosterone (10 mg/kg) or vehicle injection and after 6 h, hippocampi were collected for miRNA, mRNA and Western blot analyses. miRNA profiling microarrays showed a basal sex-biased miRNA profile in ADX rat hippocampi. Additionally, acute corticosterone administration triggered a sex-biased differential expression of miRNAs derived from genes located in several chromosomes and clusters on the X and 6 chromosomes. Putative promoter analysis unveiled that most corticosterone-responsive miRNA genes contained motifs for either direct or indirect glucocorticoid actions in both sexes. The evaluation of transcription factors indicated that almost 50 % of miRNA genes sensitive to corticosterone in both sexes was under glucocorticoid receptor regulation. Transcription factor-miRNA regulatory network analyses identified several transcription factors that regulate, activate or repress miRNA expression. Validated target mRNA analysis of corticosterone-responsive miRNAs showed a more complex miRNA-mRNA interaction network in males compared to females. Enrichment analysis revealed that several hippocampal-relevant pathways were affected in both sexes, such as neurogenesis and neurotrophin signaling. The evaluation of selected miRNA targets from these pathways displayed a strong sex difference in the hippocampus of ADX-vehicle rats. Corticosterone treatment did not change the levels of the miRNA targets and their corresponding tested proteins. Our data indicate that corticosterone exerts a sex-biased effect on hippocampal miRNA expression, which may engage in sculpting the basal sex differences observed at higher levels of hippocampal functioning.

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Corticosterone induces discrete epigenetic signatures in the dorsal and ventral hippocampus that depend upon sex and genotype: focus on methylated Nr3c1 gene

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Ventral hippocampal transcriptome analysis after acute corticosterone exposure.

Project description:Aim: We investigated the effect of acute corticosterone exposure 3 hours after subcutaneous injection on the ventral hippocampus transcriptome. Methods: Adult male mice were used in the experiment. Mice were sacrificed 3 hours after corticosterone (3mg/kg) of vehicle injection and the ventral hippocampus was dissected and snap-frozen. Subsequently, total RNA was isolated and send for 100bp paired-end sequencing by BGI.

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Genome-wide identification of glucocorticoid receptor binding sites in the whole hippocampus of adrenalectomised male rats given corticosterone infusion and stressed or non-stressed.

Project description:We have applied next-generation sequencing technology to obtain high through-put profiling of glucocorticoid receptor (GR) DNA binding in whole hippocampus from male rat brain. By obtaining sequence from immunoprecipitated, sonicated chromatin, we have generated genome-wide binding maps for GR in two contexts, testing whether chromatin is primed for GR binding according to the animal's acute experience. In one context (stressed) adrenalectomised rats are infused with corticosterone while undergoing restraint stress. In the second context (non-stressed control) rats are infused with the same corticosterone profile but restraint stress is omitted. We find that GR binding was highly similar suggesting factors other than GR binding may account for any context-dependent alterations in GR function associated with acute stress. We show that GR is positioned near to genes associated with structural and functional organisation of the hippocampus at largely intergenic and intronic sites. Glucocorticoid response element sequences support a majority of GR binding in this tissue but may be reinforced by NF-1 and/or basic-helix loop helix transcription factors binding their nearby recognition motifs. We found little evidence for tethering of GR to other factors, or for the usage of negative glucocorticoid response elements.

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Gene expression changes in mouse hippocampus after overnight exposure to corticosterone

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Inflammatory Signatures of Microglia in the Mouse Model of Corticosterone-Induced Depression

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Transcription profiling of mouse hippocampus treated with intracerebroventricular administration of LPS in a vehicle controlled experiment

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Reduced adult neurogenesis and neuronal abnormalities in the hippocampus underlie cognitive deficiency following prenatal administration of the anti-epileptic drug valproic acid

Project description:Prenatal exposure to valproic acid, an established anti-epileptic drug, has been reported to impair postnatal cognitive function of children from epileptic mothers. Nevertheless, its pathology and proper treatment to minimize the effects remain unknown. In mice, we found that the postnatal cognitive function impairment was mainly caused by a reduction of adult neurogenesis and abnormal neuronal features in the hippocampus, which could be ameliorated by voluntary running. Pregnant mice received an oral administration of methylcellulose (MC), valproic acid (VPA) or valpromide (VPM) once a day on three consecutive embryonic days (E) 12.5, E13.5, and E14.5 and were sampled 3hr after the last administration (E14.5), at E18.5, and at 12 weeks of age.

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RNA-sequencing in rat hippocampus following chronic ethanol and withdrawal

Project description:The objective of The Center for Alcohol Research in Epigenetics (CARE) is to identify gene regulatory pathways in hippocampus that are altered in response to chronic ethanol administration and withdrawal.

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The hippocampal response to acute corticosterone elevation is altered in a mouse model for Angelman syndrome

Project description:Angelman Syndrome (AS) is a severe neurodevelopmental disorder, caused by the neuronal absence of the ubiquitin protein ligase E3A (UBE3A). UBE3A promotes ubiquitin-mediated protein degradation and functions as a transcriptional coregulator of nuclear hormone receptors, including the glucocorticoid receptor (GR). Previous studies showed anxiety-like behavior and hippocampal-dependent memory disturbances in AS mouse models. Hippocampal GR is an important regulator of the stress response and memory formation, and we therefore investigated whether the absence of UBE3A in AS mice disrupted GR signaling in the hippocampus. We first established a strong cortisol-dependent interaction between the GR ligand binding domain and a UBE3A nuclear receptor box in a high-throughput interaction screen. In vivo, we found that UBE3A-deficient AS mice displayed significantly more variation in circulating corticosterone levels throughout the day compared to wildtypes (WT), with low to undetectable levels of corticosterone at the trough of the circadian cycle. Additionally, we observed an enhanced transcriptomic response in the AS hippocampus following acute corticosterone treatment. Surprisingly, chronic corticosterone treatment showed less contrast between AS and WT mice in the hippocampus and liver transcriptomic responses. This suggests that UBE3A limits the acute stimulation of GR signaling, likely as a member of the GR transcriptional complex. Altogether, these data indicate that AS mice are more sensitive to acute glucocorticoid exposure in the brain compared to WT mice. This suggests that stress responsiveness is altered in AS which could lead to anxiety symptoms.

2022-12-23 | GSE221378 | GEO

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