Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA103359 | ENA |
REPOSITORIES: ENA
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Project description:Placental abnormalities are associated with specific windows of embryo culture in a mouse model
| PRJNA795897 | ENA
Project description:Assisted Reproductive Technologies (ART) employ gamete/embryo handling and culture in vitro to produce offspring. ART pregnancies have increased risk of low birth weight, abnormal placentation, pregnancy complications, and imprinting disorders. We and others have previously shown that embryo culture induces low birth weight, abnormal placental morphology, and lower levels of DNA methylation in placentas in a mouse model of ART. We hypothesized that these adverse effects are linked to a subtle disruption of specific biological processes during preimplantation development. To test this hypothesis, we performed embryo culture for several discrete periods of preimplantation development and assessed fetal and placental outcomes at term. We observed a reduction in fetal:placental ratio in two distinct windows of preimplantation embryo development, while placental morphological abnormalities and reduced imprinting control region methylation were associated with culture prior to the morula stage. We also provide evidence that extended culture to the blastocyst stage induces additional placental DNA methylation changes compared to embryos transferred at the morula stage, and that female concepti exhibited a higher loss of DNA methylation than males. Altogether, this study identifies specific developmental windows of susceptibility and potential targets for embryo culture optimization.
2022-04-11 | GSE193271 | GEO
Project description:Purpose: Fetal alcohol spectrum disorders (FASD) result from ethanol exposure to the developing fetus. FASD occur in up to 1-5% of live births in the United States and there currently is no cure. Ethanol exposure to the developing central nervous system (CNS) has profound effects on learning and memory, impulse control, and motor function, resulting from neuropathology. The purpose of the current study was to perform transcriptome analysis to evaluate the effects of early postnatal ethanol exposure in the hippocampus and cerebellum. Methods: Postnatal C57BL/6 mice were treated with 4g/kg of ethanol from P4-P9, brains were harvested 24h after the final treatment at P10, hippocampi and cerebella were microdissected, RNA was isolated, and RNASeq analysis was performed. We compared differences in gene expression, sex-dependent expression, and global biological pathways associated with disruptions in hippocampal and cerebellar genes between the ethanol and vehicle treated neonates. Results: Ethanol caused both an up and down regulation of genes associated with the hippocampus and cerebellum, which may result in the disruption of normal circuitry and maturation and growth in these brain regions. Ethanol increased the expression of genes associated with the S phase of the cell cycle in both the hippocampus and cerebellum. In the cerebellum, ethanol increased effector gene expression, and in the hippocampus, genes associated with different interneuron lineages were altered. Postnatal ethanol exposure also resulted in altered expression of genes associated with oligodendrocyte lineages and myelination, along with alterations in microglia associated genes. Conclusion: Collectively, these data indicate that ethanol has profound effects on the hippocampus and cerebellum, resulting in alterations of gene expression and biological pathways regulating neurodevelopment. These studies may have important implications concerning alcohol-induced neuropathology and the neurological effects seen across the life span in FASD.
2021-08-04 | GSE166196 | GEO
Project description:Moderate alcohol exposure during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse model of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear. We used a microarray experiment and focused on the genes identified by both to evaluate the genome-wide alterations to the adult brain transcriptome caused by prenatal ethanol exposure. To generate samples, female C57BL/6J mice were given ethanol injections (2.5g/kg of ethanol in saline) twice on gestational days 8 and 11 to produce acute ethanol exposure effects. Control females were injected with the same volume of saline. Females were mated. Whole brain RNA from adult (postnatal day 70) male ethanol-exposed offspring was extracted. RNA samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice).
2011-12-16 | E-GEOD-34469 | biostudies-arrayexpress
Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.
2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress
Project description:Moderate alcohol exposure during pregnancy can result in brain gene expression changes in resulting offspring. We have developed a mouse model of FASD that involves moderate ethanol exposure in mid-gestation (trimester 2 equivalent) achieved by injections of ethanol. We have previously shown that this model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that there will be gene expression changes immediately following acute ethanol exposure in the fetal brain. We used a microarray experiment and focused on the genes identified to evaluate the genome-wide alterations to the fetal brain transcriptome caused by prenatal ethanol exposure. To generate samples, female C57BL/6J mice were given ethanol injections (2.5g/kg of ethanol in saline) twice on gestational days 14 and 16 to produce acute ethanol exposure effects. Control females were injected with the same volume of saline. Dams were sacrified on gestational day 16, following ethanol exposure, and whole brains from fetuses were then extracted. RNA was isolated from brain tissue and samples from three mice were pooled to reduce litter effects and the pooled samples were hybridized on Affymetrix arrays (2 control and 2 ethanol chips, total n=12 mice).
2013-01-08 | E-GEOD-43324 | biostudies-arrayexpress
Project description:In this study, we describe the use of high-throughput sequencing to investigate the developmental basis of preimplantation embryos sired by alcohol-exposed males through in vitro fertilization (IVF). We exposed C57BL/6J male mice to one of three treatment groups. Sexually mature males were randomly selected to voluntarily consume 0% ethanol (control), 6% ethanol, or 10% ethanol for ten weeks. After treatment, the males were sacrificed for sperm collection and cryopreservation for IVF procedures. C57BL/6J donor females remained naïve to alcohol and were synchronized and superovulated before being sacrificed for oocyte collection. Oocytes underwent IVF with the cryopreserved semen and incubated until they reached the morula stage. The morulae sired by ethanol-exposed sperm exhibited altered transcriptional signatures compared to the control-sired morulae. Quick Biology Inc. sequencing core isolated total RNA from three pools (10-15 cells) of unsexed morulae from each control and ethanol preconception treatment. After obtaining the sequencing data, we conducted deep-sequencing analyses of the morulae transcriptomes. This experiment revealed sire alcohol consumption modifies preimplantation embryo genetic pathways controlling mitochondrial dysfunction and oxidative phosphorylation. This experiment furthers our understanding of growth and development changes induced by preconception paternal exposures.
2022-10-07 | GSE214726 | GEO
Project description:The role astrocytes play in brain development and function has come under increased focus as the diversity of roles they are involved in has become apparent. We have previously shown ethanol exposed astrocytes alter neuronal neurite outgrowth in an in vitro co-culture system and that ethanol alters the astrocyte produced extracellular matrix (ECM) in vitro, with similar alterations in vivo. Here we utilize the translating ribosome affinity purification (TRAP) procedure in Aldh1l1-EGFP/Rpl10a transgenic mouse primary cortical astrocyte cultures to transcriptionally and translationally profile the astrocyte response to ethanol. We found large differences in the total RNA pool in comparison to the translating RNA pool while the ethanol response within each pool showed a large degree of overlap. Comparisons to published datasets indicate the in vitro model used here are most similar to PD1-PD7 in vivo cortical astrocytes and the ethanol regulated genes showed significant overlap with models of chronic ethanol exposure in astrocytes and a model of third-trimester ethanol exposure in the hippocampus and cerebellum. These findings will further our understanding of the effects of ethanol on astrocyte gene expression and protein translation and how these changes alter brain development.
2023-06-21 | GSE227891 | GEO
Project description:Endotoxin-induced uveitis (EIU) in rodents is a good animal model to study uveitis and associated acute retinal inflammation. To understand the pathogenic mechanism of uveitis and screen the potential targets for treatment, we analyzed the retinal proteomic profiles of EIU and normal C57BL/6J mice using a data-independent acquisition-based mass spectrometry (SWATH-MS).
2022-08-12 | PXD033532 | Pride
Project description:Ethanol is a well-known teratogen. While this teratogenic potential is well-characterized clinically, the mechanisms through which ethanol exposure results in developmental defects remain unclear. Here we use the zebrafish model to elucidate eye-specific mechanisms that may underlie ethanol-mediated microphthalmia (reduced eye size), using time-series microarray analysis of gene expression of eye tissues of embryos exposed to 1.5% ethanol vs. untreated embryos. We identified 62 genes differentially expressed in ethanol-treated as compared to control zebrafish eyes from all sampling times over the period of retinal neurogenesis (24-48 hours post-fertilization). Application of the EDGE (extraction of differential gene expression) algorithm identified over 3000 genes differentially expressed over developmental time in ethanol-treated embryo eyes as compared to untreated embryo eyes. These lists included several genes indicating a mis-regulated cellular stress response (heat shock response) due to ethanol exposure. Combined treatment with sub-threshold levels of ethanol and a morpholino (MO) targeting heat shock factor 1 (hsf-1) mRNA resulted in a microphthalmic phenotype, suggesting convergent molecular pathways. Manipulation of the heat shock response by thermal preconditioning partially prevented ethanol-mediated microphthalmia while maintaining Hsf-1 expression. Together these data are consistent with roles for reduced Hsf-1 in mediating microphthalmic effects of embryonic ethanol exposure in zebrafish.
2014-01-01 | GSE51427 | GEO