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Molecular adaptations in the rat brain in depressive-like phenotype induced by prenatal dexamethasone administration

ABSTRACT: The study aimed to systematically investigate the molecular basis of alterations underlying depressive-like changes in the rats’ brain, in the animal model of depression induced by prenatal dexamethasone

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

DISEASE(S): Depression

SUBMITTER: Maciej Suski

LAB HEAD: Maciej Suski

PROVIDER: PXD051185 | Pride | 2024-11-15

REPOSITORIES: Pride

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Treadmill training and venlafaxine treatment on brain changes induced by prenatal dexamethasone.

Project description:Prenatal exposure to dexamethasone (DEX) is known to induce long-term behavioral and molecular impairments. This research investigated whether moderate physical exercise (treadmill running) and venlafaxine administration, or their combination, applied in early adulthood, could modulate the behavioral and brain molecular alterations induced by prenatal DEX exposure. It was demonstrated that both exercise and venlafaxine treatment ameliorated deficits in memory, depressive-like behavior, and anxiety-like behavior. Subsequent proteomic analysis of the frontal cortex revealed significant modulation in the proteome following each intervention.

2026-03-13 | PXD063194 | Pride

Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

Project description:Prenatal dexamethasone exposure (PDE) has long-term consequences in bone development. we investigated how PDE exerts persistent effect on bone metabolism in mouse offspring. Our results showed that PDE offspring exhibited reduced bone mass, fewer osteoblasts and diminished osteoprogenitors proliferation.And PDE increased MKP-1 expression, while decreasing H3 lysine 9 dimethylation (H3K9me2) at Mkp-1 gene locus. Mechanistically, dexamethasone suppressed osteoprogenitors proliferation by upregulating MKP-1 expression, notably through the inhibition of H3K9me2 modifications, which promoted demethylation and transcriptional activation of the Mkp-1 gene. Importantly, restoring histone methylation balance with PFI-90 treatment blocked the inhibitory effects of PDE on MAPK signaling in osteoprogenitors, and mitigated the detrimental impact of PDE on osteoprogenitor proliferation and bone development in the offspring. Therefore,we performed ChIP-seq for H3K9me2 to identify its role in related epigenetic changes.

2024-11-06 | GSE276769 | GEO

Prenatal Stress-induced Depressive-like Behavior is Associated with Brain Metabotranscriptome Remodeling and is Reversed by Acetyl-carnitine

Project description:Intergenerational stress increases lifetime susceptibility to depression and other psychiatric disorders. Whether intergenerational stress transmission is a consequence of in-utero neurodevelopmental disruptions or early-life mother-infant interaction is largely unknown, due to the complexity, superposition, and inseparability between the prenatal and postnatal mechanisms. Here we show that prenatal stress, through exposing pregnant mice to predator scent, induces depressive-like behavior and social deficits. Cross-fostering experiments indicate divergent and convergent mechanisms of both in utero and early-life parenting environments and support a two-hit model of stress transmission. According to this model, prenatal stress (first-hit) primes brain metabolome and transcriptome (metabotranscriptome), and increases vulnerability to the second-hit in early life, triggered by poor caregiving by the traumatized mothers. Metabolomics, transcriptomic and bioinformatics analyses reveal mechanisms that involve stress- and hypoxia- response metabolic pathways in the brains of the newborn mice, likely through the production of the epigenetic modifiers 2-Hydroxyglutaric acid and succinic acid. These responses produce long-lasting alterations in mitochondrial-energy metabolism, and epigenetic processes pertaining to DNA and chromatin modifications. We demonstrate that an early pharmacological intervention – correction of the mitochondria metabolism, and epigenetic modifications with acetyl-L-carnitine (ALCAR) supplementation - produces long-lasting protection against the behavioral deficits associated with intergenerational transmission of traumatic stress.

2021-04-01 | GSE171275 | GEO

ApoE-knockout mice liver on high fat diet treated with trehalose or agmatine.

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Urinary proteome differences in very low gestational age infants with and without preterm brain injury

Project description:Study utilizes advancements in proteomics technology to analyze urinary protein concentrations, aiming to better understand preterm brain injury and identify potential therapeutic targets.

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Urinary proteome differences in Hypoxic-Ischemic Encephalopathy newborns

Project description:Study utilizes advancements in proteomics technology to analyze urinary protein concentrations, aiming to better understand Hypoxic-Ischemic Encephalopathy brain injury and identify potential therapeutic targets.

2026-03-16 | PXD071111 | Pride

Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

Project description:Prenatal dexamethasone exposure modificates H3K9me2 at the Mkp-1 locus in bone marrow osteoprogenitors

| PRJNA1158832 | ENA

Aberrant DNA methylation of hypothalamic angiotensin receptor in prenatal-programmed hypertension

Project description:Malnutrition during pregnancy, which causes prenatal exposure to excessive glucocorticoid, induces adverse metabolic programming leading to hypertension in offspring. Pregnant rats receiving a low-protein diet exhibited moderate downregulation of 11-beta-dehydrogenase isozyme 2, which inactivates corticosterone, in the placenta, resulting in prenatal exposure to excessive corticosterone. In offspring of pregnant rats receiving a low-protein diet or dexamethasone, mRNA expression of angiotensin receptor type 1a (Agtr1a) in the paraventricular nucleus (PVN) of the hypothalamus was upregulated, concurrent with reduced expression of DNA methyltransferase 3a (Dnmt3a), reduced binding of DNMT3a to the Agtr1a promoter, and DNA demethylation, suggesting hypothalamic Agtr1a expression is epigenetically modulated by excess glucocorticoid. Dexamethasone treatment of PVN cells downregulated DNMT3a while upregulating Agtr1a, and decreased DNMT3a binding and DNA demethylation at the Agtr1a promoter. Consistent with Agtr1a upregulation in the hypothalamus, salt loading increased BP in both types of offspring. Even without dexamethasone treatment, hypothalamic neuron-specific DNMT3a-deficient mice, in which Agtr1a was upregulated, exhibited salt-induced BP elevation. By contrast, dexamethasone-treated Agtr1a-deficient mice failed to show salt-induced BP elevation, despite reduced expression of DNMT3a. Thus, epigenetic modulation of hypothalamic angiotensin signaling contributes to salt-sensitive hypertension induced by prenatal glucocorticoid excess in offspring of mothers that are malnourished during pregnancy.

2018-11-30 | GSE119235 | GEO

Adverse Childhood Experiences, DNA Methylation, and Depressive Symptoms in Black Pregnant Women

Project description:Background: Prenatal depression, affecting up to a quarter of all pregnancies in the United States, contributes to morbidity and mortality and is associated with increased risk of adverse birth and long-term mental health outcomes. Adverse childhood experiences (ACEs, or experiences of abuse, neglect, or family dysfunction experienced prior to age 18) are a strong predictor of adult depression and adverse health outcomes. The present study investigated whether epigenetic modification in the form of DNA methylation (DNAm) of four stress-related, glucocorticoid pathway genes (CRH, CRHR1, FKBP5, NR3C1) me-diates associations between ACEs and depressive symptoms among Black pregnant women. Methods: Using a cross-sectional design, we examined the mediating role of DNAm on the relationship between depressive symptoms (Center for Epidemiologic Studies Depression Scale (CES-D)) and ACEs (Centers for Disease Control and Prevention 10-item questionnaire), in a subsample (n = 61) of Black pregnant women who were participants of the Biosocial Impacts of Black Births (BIBB) study. Results: A significant association was found between ACEs and depressive symptoms scores (TE α_X = 2.29 with p_TE = 6.60 × 105). DNAm on five CpG sites within two genes significantly mediated the relationship between ACEs and depressive symptoms (cg03238273 on CRHR1, and cg08845721, cg16594263, cg19820298, and cg23430507 on NR3C1). Conclusions: This study provides evidence that DNAm partially mediated the association of ACEs and depressive symptoms during pregnancy among Black pregnant women. Understanding the mo-lecular pathways underlying the mediating effect of ACEs on depressive symptoms among Black pregnant women can illuminate biological markers that help identify and treat pregnant women who are at an increased risk for depression following childhood trauma.

2025-12-31 | GSE311619 | GEO

Hypermethylation in the ZBTB20 gene is associated with major depressive disorder

Project description:Genome-wide MeDIP-Sequencing was carried out on a total of 50 monozygotic twin pairs from the UK and Australia that are discordant for depression. We show that major depressive disorder is associated with significant hypermethylation within the coding region of ZBTB20, and is replicated in an independent cohort of 356 unrelated case-control individuals. The twins with major depressive disorder also show increased global variation in methylation in comparison with their unaffected co-twins. ZBTB20 plays an essential role in the specification of the Cornu Ammonis-1 field identity in the developing hippocampus, a region previously implicated in the development of major depressive disorder. Epigenetic study of MZ twins discordant for Major Depressive Disorder

2014-01-21 | E-GEOD-54222 | biostudies-arrayexpress

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