Vitamin D deficiency during development permanently alters liver cell composition and function.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA800454 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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:We report genes and molecular pathways that respond to vitamin A deficiency.
2021-07-26 | GSE178712 | GEO
Project description:This study demonstrates that transplantation of fetal liver hematopoietic stem cells (FL-HSCs) from fetuses subjected to vitamin D (VD) deficiency in utero induced persistent insulin resistance to VD sufficient recipient mice. Transcriptional changes associated with intrauterine vitamin D deficiency where identified through microarray analysis of mouse BMMs from vitamin D deficient and sufficient conditions.
2023-05-18 | GSE158763 | GEO
Project description:The recently described roles of vitamin C as an epigenetic regulator playsa crucial role in normal physiological development and pathological conditions.However, the epigenetic regulatory role of vitamin C in renal homeostasis andpathogenesis remains largely unknown. We aim to reveal that vitamin C deficiency promoted acute tubular necrosis,and provide a potential mechanism for epigenetic therapy in preventing the progression of chronic kidney disease.
2021-12-09 | GSE190371 | GEO
Project description:Vitamin D deficiency exacerbates UV/endorphin and opioid addiction
| PRJNA720566 | ENA
Project description:Analysis of livers from 74-day old male rats fed vitamin A sufficient or vitamin A deficient diet for 53 days. Either 10ug or 2ug of total RNA used in standard Affymetrix protocol Keywords = rat Keywords = liver Keywords = vitamin A deficiency Keywords: other
2005-06-30 | GSE1600 | 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.
2023-12-31 | GSE162895 | GEO
Project description:Gut-draining mesenteric and celiac lymph nodes (mLNs and celLNs) critically contribute to peripheral tolerance towards food and microbial antigens by efficiently supporting the de novo induction of regulatory T cells (Tregs). These tolerogenic properties of mLNs and celLNs are stably imprinted within stromal cells (SCs) by microbial signals and vitamin A (VA), respectively. In the present study, we demonstrated that a transient neonatal gastrointestinal infection long-lastingly affects the functionality of celLN by permanently abrogating the efficient Treg-inducing capacity of celLN SCs. The neonatal infections durably shifted the heterogeneity of celLN SCs with permanently altered expression of genes involved in chemotaxis and inflammatory responses, resulting in a lastingly skewed dendritic cell (DC) composition. Mechanistically, transiently reduced VA levels caused the long-lastingly impaired celLN function, which could be rescued by an early-life VA supplementation. Together, our data highlight the therapeutic potential of VA treatment post gastrointestinal infections in infants.
2023-12-31 | GSE183390 | GEO
Project description: Not available
| S-EPMC4690049 | biostudies-literature