The exposure of prenatal enriched environment promotes fetal neuronal development via activating AHR-Src pathway
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE233650 | GEO | 2026/05/20
REPOSITORIES: GEO
Similar Datasets
Project description:Interventions: Healthy control group:none;CRC group:Conventional drug therapy;Autonomous Sports Group:Home-based voluntary exercise training as part of regular treatment;EE group:Home based voluntary exercise training combined with environmental enrichment EE training on top of conventional treatment
Primary outcome(s): Physical Effort Scale (PA); depression (SDS) scale;anxiety (SAS) scale;perceived stress scale;Pittsburgh Sleep Quality Index Scale (PSQI); Piper Fatigue Modified Scale (RPFS);Piper Fatigue Modified Scale (RPFS);Colorectal Cancer Quality of Life Specific Scale (EORTC QLQ-CR38)
Study Design: Parallel
| 87692 | ecrin-mdr-crc
Project description:Previous studies reported that mice living in an enriched environment (EE) showed reduced growth of melanoma, colon and breast tumors. Our study extended the potential anti-tumor effect of EE exposure to pancreatic cancer, and firstly provided evidence demonstrating that EE exposure significantly inhibits tumor growth in a syngeneic murine model of pancreatic cancer. To further investigate the mechanisms underlying the EE-induced pancreatic tumor inhibition, we analyzed the gene expression changes in pancreatic tumor xenograft using an integrative transcriptomic and proteomic approach. Our results found that EE largely decreased the expression of genes associated with mitochondrial function at transcriptional level in pancreatic tumor, suggesting mitochondrial dysfunction in tumor cells may play a critical role in EE-induced anti-tumor phenotype. Three-week-old C57BL/6 mice were randomized to live in either enriched environment or standard environment conditions. Mice from both groups were given subcutaneous injection of Panc02 murine pancreatic cancer cells (6 M-CM-^W 105 cells per mouse) and lived in their respective homes for 5 additional weeks. Pooled RNA samples extracted from Panc02 tumors (6 mice for each group) were then subjected to Agilent-014868 Whole Mouse Genome 4M-bM-^XM-^S44k Microarray analyses.
2014-08-31 | E-GEOD-58306 | biostudies-arrayexpress
Project description:Purpose: A) compare the gene expression in whole DRG and in large diameter DRG neurons of mice exposed to EE compared to SH Results: we found that EE induces transcriptional changes promoting axon regeneration
2019-01-29 | GSE125793 | GEO
Project description:Wildtype Swiss webster mice were exposed to four weeks of either standard housing (SH) or environmental enrichment (EE) starting at one month of age. EE chambers were large mouse cages containing two nesting/burrowing materials, a running wheel, and toys that were changed every 3-4 days for novelty and exploration. By contrast, SH control mice were housed with an equal number of littermates in smaller, standard cages containing only one nesting material and no toys or running wheel. We used an antibody for Rbfox3 (NeuN) to sort neuronal nuclei from the dissociated frontal cortices of male mice reared in EE and SH conditions. Isolated neuronal nuclei were then subjected to ATAC-seq or nuclear RNA isolation (random hexamer priming) as per published protocols.
2021-11-17 | GSE176435 | GEO
Project description:Methylmercury (MeHg) is a global pollutant that readily crosses the blood–brain barrier and placenta, posing significant risks to fetal neurodevelopment. While the cerebellum is a recognized target of MeHg toxicity in adults, the mechanisms underlying fetal exposure remain poorly defined. In this study, we investigated the neurotoxic effects of low-dose MeHg exposure (0.2 ppm via drinking water) on the cerebellums of prenatal C57BL/6 mice using integrated transcriptomic and proteomic analyses. Cerebellar tissues collected from postnatal day 90–120 (P90–120) mice (n = 3/group) were processed for RNA sequencing and proteomics analysis. Differentially expressed genes (DEGs) and proteins (DEPs) revealed significant changes in multiple pathways associated with neurodegeneration, including Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Overlapping transcriptomic and proteomic findings identified potential underlying mechanisms such as chemical carcinogenesis driven by reactive oxygen species and retrograde endocannabinoid signaling, underscoring the central role of oxidative stress in MeHg-induced neurotoxicity. Collectively, these results indicate that prenatal MeHg exposure induces persistent molecular alterations consistent with neurodegenerative processes and synaptic dysfunction, despite the absence of overt behavioral changes at the time of sacrifice. The long-term consequences for delayed symptom onset and the potential contribution of these changes to the etiology of neurodevelopmental disorders warrant further investigation.
2026-02-06 | PXD068503 | Pride
Project description:Prenatal stress induced by maternal activation of the hypothalamic-pituitary-adrenal (HPA) axis and subsequent release of glucocorticoids can profoundly affect fetal brain development. This study investigates the molecular mechanisms underlying prenatal stress in Gallus gallus domesticus by analyzing the brain proteome of embryos exposed to corticosterone. Using one of the most comprehensive proteomic analyses of the developing chicken brain to date, in which over 6,500 proteins were quantified, we identified significant myelination deficits as a key pathological feature. These results are consistent with previous research in mammalian models, highlighting the utility of Gallus gallus as a non-mammalian model for studying the effects of prenatal stress on neurodevelopment.
2025-10-27 | PXD055206 | Pride
Project description:Previous studies reported that mice living in an enriched environment (EE) showed reduced growth of melanoma, colon and breast tumors. Our study extended the potential anti-tumor effect of EE exposure to pancreatic cancer, and firstly provided evidence demonstrating that EE exposure significantly inhibits tumor growth in a syngeneic murine model of pancreatic cancer. To further investigate the mechanisms underlying the EE-induced pancreatic tumor inhibition, we analyzed the gene expression changes in pancreatic tumor xenograft using an integrative transcriptomic and proteomic approach. Our results found that EE largely decreased the expression of genes associated with mitochondrial function at transcriptional level in pancreatic tumor, suggesting mitochondrial dysfunction in tumor cells may play a critical role in EE-induced anti-tumor phenotype.
2014-08-31 | GSE58306 | GEO
Project description:Psychological loss is a common experience that erodes well-being and negatively impacts quality of life. The molecular underpinnings of loss are poorly understood, making it challenging to develop treatment strategies. Here, we investigate the mechanisms of loss using an enrichment removal (ER) paradigm in rats. RNA-seq was used to investigate the molecular landscape of the basolateral amygdala (BLA), a region previously implicated in loss, in adult male Sprague-Dawley rats following ER. Rats were subjected to standard housing (SH) for 6 weeks, environmental enrichment (EE) for 6 weeks, or enrichment removal (ER), consisting of 4 weeks of EE followed by 2 weeks of removal into impoverished conditions (n=10/pool/group). Rats were then perfused and micropunches were collected from the basolateral amygdala (BLA) for bulk RNA-seq.
2022-07-15 | GSE208028 | GEO
Project description:Psychological loss is a common experience that erodes well-being and negatively impacts quality of life. The molecular underpinnings of loss are poorly understood, making it challenging to develop treatment strategies. Here, we investigate the mechanisms of loss using an enrichment removal (ER) paradigm in rats. RNA-seq was used to investigate the molecular landscape of the basolateral amygdala (BLA), a region previously implicated in loss, in adult male Sprague-Dawley rats following ER. Rats were subjected to standard housing (SH) for 6 weeks, environmental enrichment (EE) for 6 weeks, or enrichment removal (ER), consisting of 4 weeks of EE followed by 2 weeks of removal into impoverished conditions (n=6/group). Rats were then perfused and micropunches were collected from the basolateral amygdala (BLA) for bulk RNA-seq.
2022-07-15 | GSE208026 | GEO
Project description:Huntington’s disease is a fatal autosomal dominant neurodegenerative disorder, characterized by neuronal cell loss, primarily in the striatum, cortex, and hippocampus, causing motor, cognitive, and psychiatric impairments. Unfortunately, no treatments are yet available to modify the progression of the disease. Recent evidence from Huntington’s disease mouse models suggests that protein phosphorylation (catalysed by kinases and hydrolysed by phosphatases) might be dysregulated, making this major posttranslational modification a potential area of interest to find novel therapeutic targets. Furthermore, environmental enrichment (EE), used to model an active lifestyle in preclinical models, has been shown to alleviate Huntington’s disease-related motor and cognitive symptoms. However, the molecular mechanisms leading to these therapeutic effects are still largely unknown. In this study, we applied a phosphoproteomics approach combined with proteomic analyses on brain samples from pre-motor symptomatic R6/1 Huntington’s disease male mice (HD mice) and their wild-type (WT) littermates, after being housed either in EE conditions, or in standard housing (SH) conditions from 4 to 8 weeks of age (n=6 per group). We hypothesised that protein phosphorylation dysregulations occur prior to motor onset in this mouse model, in two highly affected brain regions, the striatum and hippocampus. Furthermore, we hypothesised that these phosphoproteome alterations are rescued by EE. When comparing 8-week-old HD mice and WT mice in SH conditions, our analysis revealed 229 differentially phosphorylated peptides in the striatum, compared to only 15 differentially phosphorylated peptides in the hippocampus (statistical thresholds FDR0.05, FC1.5). At the same disease stage, minor differences were found in protein expression, with 24 and 22 proteins dysregulated in the striatum and hippocampus, respectively. Notably, we found no differences in striatal protein phosphorylation and protein expression when comparing HD mice and their WT littermates in EE conditions. In the hippocampus, only four peptides were differentially phosphorylated between the two genotypes under EE conditions, and 22 proteins were differentially expressed. Together, our data indicates that protein phosphorylation dysregulations occur in the striatum of HD mice, prior to motor symptoms, and that the kinases and phosphatases leading to these changes in protein phosphorylation might be viable drug targets to consider for this disorder. Furthermore, we show that an early environmental intervention was able to rescue the changes observed in protein expression and phosphorylation in the striatum of HD mice and might underlie the beneficial effects of EE, thus identifying novel therapeutic targets.
2023-03-11 | PXD032205 | Pride