Ontology highlight
ABSTRACT:
PROVIDER: PRJNA682368 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13190534_1.fastq.gz | Fastqsanger.gz | |||
| SRR13190534_2.fastq.gz | Fastqsanger.gz | |||
| SRR13190535_1.fastq.gz | Fastqsanger.gz | |||
| SRR13190535_2.fastq.gz | Fastqsanger.gz |
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Project description:Maternal vitamin D deficiency impairs heart formation in mouse offspring through a change in 3D-chromatin structure
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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:Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life. Experiment Overall Design: Crossing of hypercholesterolemic female with normocholesterolemic male and vice versa, determination of susceptabilioty to atherosclerosis in offspring
2008-06-14 | E-GEOD-6134 | biostudies-arrayexpress
Project description:Vitamin D, a fat-soluble vitamin, plays a critical role in calcium homeostasis, the immune system, and normal development. Many epidemiological cohort studies globally have found high prevalence rates of vitamin D deficiency and insufficiency, recognized as an important health issue that needs to be solved. In particular, reproductive age and pregnant women low in vitamin D status may confer risks of diseases like obesity on their offspring. While observational studies have suggested associations between prenatal vitamin D deficiency and metabolic phenotypes in offspring, not yet determined is whether prenatal vitamin D deficiency permanently alters the development of the liver, a major metabolic organ. We tested the histopathology and the transcriptomic profiles of livers from male C57BL/6J mice exposed to prenatal vitamin D deficiency through a maternal dietary intervention model. We found that prenatal vitamin D deficiency increases the prevalence of histopathological changes in the liver, and alters its gene expression profile. Cell subtype proportion analysis showed that the liver of prenatal vitamin D deficiency alters non-parenchymal cells of the liver, specifically macrophages, a subset of endothelial cells, and dendritic cells. Our results indicate the long-term memory of prenatal vitamin D deficiency exposure in the adult liver, a potential contributor to offspring health risks.
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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.
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Project description:Maternal exposure to balanced nutrition is critical for supporting embryonic development. Exposure to imbalanced nutrition during pregnancy, such as a high-fat diet (HFD), has been reported to negatively impact offspring, leading to conditions such as congenital heart disease. One possible mechanism is that metabolic stress from imbalanced food intake alters the function of epigenetic regulators, leading to abnormal transcriptional output in embryos. In this study, we observed that maternal exposure to a high-fat diet led to noncompaction cardiomyopathy (NCC) in embryos at E15.5. At the molecular level, maternal HFD exposure resulted in significantly reduced 5hmC production and chromatin remodeling in embryonic heart tissue collected from E15.5 embryos. Interestingly, maternal vitamin C treatment countered the negative impact of HFD exposure and restored the metabolic changes observed in pregnant mice, as well as the NCC phenotype observed in E15.5 embryos. This restoration is possibly due to the replenishment of iron, a co-factor of the Tet enzyme, in its reduced form. We further used a cardiac-specific Tet-triple knockout mouse model to confirm that the cardioprotective outcomes of maternal vitamin C treatment in HFD conditions are attributable to the enhanced activity of TET enzymes. Collectively, our results suggest a crosstalk between maternal nutrition exposure, such as HFD or vitamin C, and epigenetic rewriting during embryonic heart development。
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Project description:Maternal Vitamin C is required in vivo for proper DNA demethylation and development of fetal germ cells in a mouse model of Vitamin C deficiency. Withdrawal of Vitamin C from the maternal diet does not affect overall embryonic development but leads to defects in the fetal germline, which persist well after Vitamin C re-supply during late gestation. The transcriptome of germ cells from Vitamin C-deficient embryos is remarkably similar to that of embryos carrying a mutation in Tet1, which is responsible for DNA demethylation and activation of regulators of meiosis. In agreement with these results, Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in Vitamin C during gestation recapitulates a mutation in Tet1 and disrupts germline reprogramming and development. Our work further indicate that the embryonic germline is sensitive to perturbations of the maternal diet, providing a potential intergenerational mechanism for adjusting fecundity to environmental quality.
2019-07-01 | GSE125496 | GEO
Project description:Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life. Keywords: Atheroslcersosis development
2007-08-08 | GSE6134 | GEO
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.
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