Maternal vitamin D deficiency impairs heart formation in mouse offspring through a change in 3D-chromatin structure
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PROVIDER: PRJNA683656 | ENA |
REPOSITORIES: ENA
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Project description:The origins of congenital heart diseases, the most common congenital diseases are still largely unknown. Environmental factors are now emerging as major causes of these diseases. Vitamin D deficiency has become a public health burden, notably for childbearing age, pregnant and breastfeeding women. Since maternal 25-hydroxyvitamin D (25(OH)D) determined fetal and neonatal 25(OH)D status, foetuses exposed to insufficient levels of vitamin D, may feature developmental defects.Herein, we investigated the effects of maternal vitamin D deficiency on cardiovascular defects in early and later life of offsprings as well as the molecular mechanisms underlying vitamin D effect.Eight weeks before and during pregnancy, C57BL/6JRj female mice received a sufficient or vitamin D deficient diet ((1.0 IU/g in control vs 0.0 IU/g in Vitamin D Deficient (VDD) group). E16.5 Embryos of maternal VDD diet featured hypertrophic heart revealed by a thicker left ventricular (LV) wall and septum. RNAseq analysis of LV revealed 1555 transcripts differentially expressed in the VDD group and among them cardiac transcription factors and constitutive cardiac genes (tbx5, gata4, myl2). Anti-Vitamin D receptor (VDR) Chip-seq from chromatin of E16.5 LV uncovered different targeting of tbx5 and tbx3 loci by VDR in the VDD vs control embryos. Anti-CTCF ChIP-loop experiments focusing on the Tbx3 and Tbx5 loci uncovered a change in the Topology Associated Domains associated with these loci. Herein, we investigated the effects of maternal vitamin D deficiency on cardiovascular defects in early and later life of offsprings as well as the molecular mechanisms underlying vitamin D effect.Eight weeks before and during pregnancy, C57BL/6JRj female mice received a sufficient or vitamin D deficient diet ((1.0 IU/g in control vs 0.0 IU/g in Vitamin D Deficient (VDD) group). E16.5 Embryos of maternal VDD diet featured hypertrophic heart revealed by a thicker left ventricular (LV) wall and septum. RNAseq analysis of LV revealed 1555 transcripts differentially expressed in the VDD group and among them cardiac transcription factors and constitutive cardiac genes (tbx5, gata4, myl2). Anti-Vitamin D receptor (VDR) Chip-seq from chromatin of E16.5 LV uncovered different targeting of tbx5 and tbx3 loci by VDR in the VDD vs control embryos. Anti-CTCF ChIP-loop experiments focusing on the Tbx3 and Tbx5 loci uncovered a change in the Topology Associated Domains associated with these loci.
2023-12-31 | GSE162895 | GEO
Project description:In utero environment is crucial to ensure normal development of the fetus and to program metabolic health throughout the life. Beside macronutrients, the role of micronutrients, including vitamin D, begins to be explore. The aim of this study was to decipher the impact of maternal vitamin D deficiency (VDD), in normal and high-fat (HF) diet context, on adipose tissue metabolism and energy homeostasis in offspring, considering sex-specific responses. Body weight, energy expenditure, and spontaneous activity was differential impacted in juvenile male and female offspring born from VDD mice. In adulthood, a HF diet combined with maternal VDD disrupted glucose homeostasis and adiposity in male offspring but not in females. Such phenotypes were associated to different transcriptomic profiles in adipose tissue, which could be related to differential modulation of plasma 17b-estradiol concentrations. Thus, maternal VDD sex-dependently modulated metabolic fate of the offspring, especially when associated with HF diet in adulthood.
2022-06-22 | GSE206372 | GEO
Project description:Initiation of a vitamin A deficient diet in mid-gestation, maintained in the post-weaning diet is sufficient to cause liver and serum retinoid depletion. Wild type C57Bl/6J timed mated pregnant dams were administered either a defined vitamin A sufficient low fat (12 percent kcal from fat) diet or matched vitamin A deficient diet from embryonic day 10.5. Vitamin A sufficient offspring were weaned onto either a high fat diet (60 percent kcal from fat) or maintained on the low fat 12 percent kcal from fat diet for 11 weeks (14 weeks of age). Gestational vitamin A deficient offspring were maintained on the same vitamin A deficient diet until 14 weeks of age. The impact of the maternal diet on a post-weaning high fat diet was compared to a standard maternal breeder diet followed by the post-weaning high fat diet.
2016-10-12 | GSE87845 | GEO
Project description:Vitamin D deficiency is a common micronutrient deficiency worldwide, especially among reproductive-age women, and vitamin D deficiency during pregnancy increases the risks of offspring’s immune-related diseases later in life. The mechanisms of how our body remembers the exposure status of an adverse environment during development have not been fully elucidated yet. Here we show that prenatal vitamin D deficiency exposure alters the immune cell proportion of the offspring at the prenatal and adult stage, which is attributed to transcriptional alterations of vitamin D receptor downstream genes. Further, we assessed the association between maternal vitamin D status and cord blood immune cell profiles from 75 healthy mother and their term baby pairs and found that maternal vitamin D deficiency significantly alters immune cell proportion in cord blood. Our findings demonstrate that prenatal vitamin D deficiency alters the immune cell compositions of offspring by changing the transcriptional properties of stem cells and altering long-term stem cell fate decisions.
2024-09-30 | GSE242042 | GEO
Project description:Vitamin D deficiency is a common micronutrient deficiency worldwide, especially among reproductive-age women, and vitamin D deficiency during pregnancy increases the risks of offspring’s immune-related diseases later in life. The mechanisms of how our body remembers the exposure status of an adverse environment during development have not been fully elucidated yet. Here we show that prenatal vitamin D deficiency exposure alters the immune cell proportion of the offspring at the prenatal and adult stage, which is attributed to transcriptional alterations of vitamin D receptor downstream genes. Further, we assessed the association between maternal vitamin D status and cord blood immune cell profiles from 75 healthy mother and their term baby pairs and found that maternal vitamin D deficiency significantly alters immune cell proportion in cord blood. Our findings demonstrate that prenatal vitamin D deficiency alters the immune cell compositions of offspring by changing the transcriptional properties of stem cells and altering long-term stem cell fate decisions.
2024-09-30 | GSE242041 | GEO
Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest (this study) and after acute stress.
2014-07-01 | E-GEOD-47846 | biostudies-arrayexpress
Project description:Transcriptomic analysis of lungs from newborn rats born to vitamin D adequate and vitamin D deficient mothers Vitamin D deficiency during pregnancy is common and is related to several maternal and fetal morbidities. Past studies suggest that vitamin D plays a role in normal lung development and we have shown that vitamin D regulates lung alveolar and vascular growth and preserves lung structure in experimental bronchopulmonary dysplasia (BPD) through improved pro-angiogeneic signaling. In addition, maternal vitamin D deficiency causes abnormal airway, alveolar, and vascular growth, as well as impaired lung function and airway hyper-reactivity in newborn rats. However, the mechanisms responsible for these physiologic effects are unknown. To gain insight into the role that maternal vitamin D status has on fetal lung development we used an unbiased transcriptomic approach to identify pathways altered in the lungs of offspring from vitamin D deficient dams.
2020-09-01 | GSE136736 | GEO
Project description:Maternal benzophenone exposure impairs hippocampus development and cognitive function in mouse offspring
| PRJNA701110 | ENA
Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).
2014-07-01 | E-GEOD-47847 | biostudies-arrayexpress
Project description:Cecal microbiome of C-, WD- and REV-dams at weaning and in their offspring (C-offspring, WD-offspring, and REV-offspring, respectively) at 4 months.
| PRJEB64354 | ENA