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Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age.

ABSTRACT: Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age.

PROVIDER: PRJNA1011255 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25836655_1.fastq.gz	Fastqsanger.gz
	SRR25836655_2.fastq.gz	Fastqsanger.gz
	SRR25836656_1.fastq.gz	Fastqsanger.gz
	SRR25836656_2.fastq.gz	Fastqsanger.gz
	SRR25837657_1.fastq.gz	Fastqsanger.gz

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Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [scRNA-seq]

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

Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [RNA-seq]

2024-09-30 | GSE242041 | GEO

Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [RNA-seq]

Project description:Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [RNA-seq]

| PRJNA1011260 | ENA

Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [scRNA-seq]

Project description:Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age [scRNA-seq]

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Vitamin D deficiency during development permanently alters liver cell composition and function.

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.

2022-05-10 | GSE194417 | GEO

Prenatal vitamin D deficiency alters immune cell proportions of offspring in young adult age.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-09-30 | GSE242043 | GEO

Prenatal vitamin D deficiency alters immune cell proportions of young adult offspring through alteration of long-term stem cell fates.

Project description:Vitamin D deficiency is a common deficiency worldwide, particularly among women of reproductive age. During pregnancy, it increases the risk of immune-related diseases in offspring later in life. However, exactly how the body remembers exposure to an adverse environment during development is poorly understood. Herein, we explore the effects of prenatal vitamin D deficiency on immune cell proportions in offspring using vitamin D deficient mice established by dietary manipulation. We show that prenatal vitamin D deficiency alters immune cell proportions in offspring by changing the transcriptional properties of genes downstream of vitamin D receptor signaling in hematopoietic stem and progenitor cells of both the fetus and adults. Further investigations of the associations between maternal vitamin D levels and cord blood immune cell profiles from 75 healthy pregnant women and their term babies also confirm that maternal vitamin D levels significantly affect immune cell proportions in the babies. Thus, lack of prenatal vitamin D, particularly at the time of hematopoietic stem cell migration from the liver to the bone marrow, has long-lasting effects on immune cell proportions. This highlights the importance of providing vitamin D supplementation at specific stages of pregnancy.

| S-EPMC10515841 | biostudies-literature

Prenatal maternal vitamin D deficiency sex-dependently programs adipose tissue metabolism and energy homeostasis in offspring

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

Poor maternal nutrition during gestation alters prenatal muscle growth and development in offspring

Project description:We hypothesized that poor maternal nutrition during gestation would reduce the growth and development of offspring muscle prenatally, reduce the number of myogenic progenitor cells, and result in changes in the global expression of genes involved in prenatal muscle development and function. Ewes were fed a control (100% NRC)-, restricted (60% NRC),- or over-fed (140% NRC) diet beginning at day 30 of gestation until day 45, 90, and 135 of gestation or until parturition. In offspring, we report altered secondary: primary muscle fiber ratios and percent PAX7 positive cells during fetal development. In addition, changes in muscle mRNA expression were observed between maternal dietary treatments and over timepoints during gestation. In conclusion, poor maternal nutrition during gestation contributes to altered offspring muscle growth during early fetal development which persists throughout the fetal stage.

2019-12-01 | GSE124327 | GEO

Phosphoproteomic profiling of hippocampus from offspring rats exposed to prenatal stress

Project description:Prenatal stress (PS) could cause depression of offprsing. Here, relative quantitative phosphoproteomics of hippocampus of PS-S and CON offspring rats were performed using LC-MS/MS to confirm known pathways and identify new areas of depression. A total of 6,790 phosphopeptides, 9,817 phosphorylation sites and 2978 phosphoproteins were detected. Among the 2978 phosphoproteins, 1760 (59.09%) with more than two phosphorylated sites, ENSRNOP00000023460 protein has more than 117 phosphorylated sites, and the average distribution of modification sites per 100 amino acids was 2.97. There were 197 different phophpeptides, including 140 increased phosphopeptides and 57 decreased phosphopeptides in PS-S offspring rats when compared to the CON offspring rats. These differential phosphopeptides corresponded to 100 upregulated and 44 downregulated phosphoproteins respectively. GO enrichment analysis these different phosphoproteins in the first five enrichments of CC category, MF category and BP category were involved in a total of 35 different phosphoproteins and these phosphoproteins were mainly related to myelin, microtubule and synapse associated proteins. The first five enrichment of KEGG pathways were found to be involved in many essential biological pathways, and the first five pathways included amphetamine addiction, insulin secretion, cushing syndrome and circadian entrainment signaling pathway. And these first five pathways were related to nine proteins including Adcy9, Apc, Cacna1c, Camk2a, Camk2b, Camk2g, Ctnnd2, Grin2a, Stx1a. Further research is needed to understand the precise role of these pathways in the depressive-like behavior of offspring rats caused by PS.

2021-12-30 | PXD019117 | Pride

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