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Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

ABSTRACT: Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

PROVIDER: PRJNA786893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17182362_1.fastq.gz	Fastqsanger.gz
	SRR17182362_2.fastq.gz	Fastqsanger.gz
	SRR17182363_1.fastq.gz	Fastqsanger.gz
	SRR17182363_2.fastq.gz	Fastqsanger.gz
	SRR17182364_1.fastq.gz	Fastqsanger.gz

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Vitamin C deficiency causes cell type-specific epigenetic reprogramming and acute tubular necrosis

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

Maternal Vitamin D deficiency induces transcriptomic changes in newborn rat lungs

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

Vitamin C Deficiency Causes Cell Type-Specific Epigenetic Reprogramming and Acute Tubular Necrosis in a Mouse Model.

Project description:BackgroundVitamin C deficiency is found in patients with variable kidney diseases. However, the role of vitamin C as an epigenetic regulator in renal homeostasis and pathogenesis remains largely unknown.MethodsWe showed that vitamin C deficiency leads to acute tubular necrosis (ATN) using a vitamin C-deficient mouse model (Gulo knock-out). DNA/RNA epigenetic modifications and injured S3 proximal tubule cells were identified in the vitamin C-deficient kidneys using whole-genome bisulfite sequencing, methylated RNA immunoprecipitation sequencing, and single-cell RNA sequencing.ResultsIntegrated evidence suggested that epigenetic modifications affected the proximal tubule cells and fenestrated endothelial cells, leading to tubule injury and hypoxia through transcriptional regulation. Strikingly, loss of DNA hydroxymethylation and DNA hypermethylation in vitamin C-deficient kidneys preceded the histologic sign of tubule necrosis, indicating the causality of vitamin C-induced epigenetic modification in ATN. Consistently, prophylactic supplementation of an oxidation-resistant vitamin C derivative, ascorbyl phosphate magnesium, promoted DNA demethylation and prevented the progression of cisplatin-induced ATN.ConclusionsVitamin C played a critical role in renal homeostasis and pathogenesis in a mouse model, suggesting vitamin supplementation may be an approach to lower the risk of kidney injury.

| S-EPMC8975062 | biostudies-literature

Fam170a deficiency causes male infertility

Project description:Fam170a deficiency causes male infertility

| PRJNA1180445 | ENA

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 [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

Vitamin A deficiency affects gene expression in the Drosophila melanogaster head

Project description:We report genes and molecular pathways that respond to vitamin A deficiency.

2021-07-26 | GSE178712 | GEO

Tubular insulin-induced gene 1 deficiency promotes NAD+ consumption and exacerbates kidney fibrosis

Project description:<p>Profibrotic proximal tubular (PT) were identified as a unique phenotype of PTCs in renal fibrosis by single-cell RNA sequencing (scRNA-seq). Controlling the process of renal fibrosis requires understanding how to manage the S1 subset's branch to the S3 subset rather than to the profibrotic PT subset. Insulin-induced gene 1 (Insig1) is one of the branch-dependent genes involved in controlling this process, although its role in renal fibrosis is unknown. Here, we discovered that tubular Insig1 deficiency, rather than fibroblast Insig1 deficiency, play a detrimental role in the pathogenesis of renal fibrosis in vivo and in vitro. Overexpression of Insig1 profoundly inhibited renal fibrosis. Mechanistically, Insig1 deletion in PTCs boosted SREBP1 nuclear localization, increasing Aldh1a1 transcriptional activity, causing excessive NAD+ consumption and ER enlargement, as well as accelerating renal fibrosis. We also identified nicardipine as a selective inhibitor of Aldh1a1, which could restore NAD+ and maintain ER homeostasis, as well as improve renal fibrosis. Together, our findings support tubular Insig1 as a new therapeutic target for chronic kidney disease (CKD).</p>

1970-01-01 | MTBLS9985 | MetaboLights

Adoptive transfer of type 2 diabetes by hematopoietic stem cells reprogrammed in utero by vitamin D deficiency

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

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