Salmon peptides limit obesity‐associated metabolic disorders by modulating a gut‐liver axis in vitamin D‐deficient mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB27659 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2684850_1.fastq.gz | Fastqsanger.gz | |||
| ERR2684850_2.fastq.gz | Fastqsanger.gz | |||
| ERR2684860_1.fastq.gz | Fastqsanger.gz | |||
| ERR2684860_2.fastq.gz | Fastqsanger.gz | |||
| ERR2684870_1.fastq.gz | Fastqsanger.gz |
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Project description:In humans, vitamin D3 is a secosteroid, a prohormonal precursor of biologically active hydroxyforms. Vitamin D3 is related to periodontitis. The third American Health and Nutrition Survey found that plasma 25(OH)D3 levels are negatively correlated with attachment loss in people aged >50 years. The relationship between vitamin D3 and periodontitis remains to be investigated. We sent human gingival fibroblasts treated by vitamin D3 for transcriptome sequencing.
2022-09-09 | GSE212728 | GEO
Project description:Background: In addition to its canonical functions, vitamin D has been proposed to be an important mediator of the immune system. Despite ample sunshine, vitamin D deficiency is prevalent (> 80%) in the Middle East, resulting in a high rate of supplementation. However, the underlying molecular mechanisms of the specific regimen and potential factors affecting an individual’s response to vitamin D are not well characterized. Objective: To characterize changes in blood transcriptomic and the potential mechanisms associated with vitamin D3 supplementation and response. Design: In this intervention study, one hundred vitamin D-deficient women were given a weekly oral dose (50,000 IU) of vitamin D3 for three months. A high-throughput targeted PCR, composed of 264 genes representing important blood transcriptomic fingerprints in health and disease states, was performed on pre- and post-supplementation blood samples to profile the molecular response to vitamin D3. Multivariate, network, gene ontology, and literature mining analyses were used for the interpretation of the transcriptomic profiling results. Results: We identified 54 differentially expressed genes that were strongly modulated by vitamin D3 supplementation. Network analyses showed significant changes in the immune-related pathways such as TLR4/CD14 and IFN receptors, and catabolic processes related to NFkB, which were subsequently confirmed by gene ontology enrichment analyses. We proposed a model for vitamin D3 response, using the reduced expression of the molecules involved and the receptor-mediated intra-cellular signaling leading to reduce cytokine production. Conclusions: Blood-transcriptomic profiles of vitamin D3 response were generated using a targeted blood gene panel. Vitamin D has a strong effect on the immune system, G-coupled protein receptor signaling, and the ubiquitin system. We highlighted the major molecular changes and biological processes induced by vitamin D3, which will help to further investigate the effectiveness of vitamin D supplementation among individuals in the Middle East.
2021-05-19 | GSE157939 | GEO
Project description:The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), induces stable tolerogenesis in dendritic cells (DC). This process involves the Vitamin D receptor (VDR) which translocates to the nucleus, binds its cognate genomic sites and promotes epigenetic and transcriptional remodeling. In this study, we investigated the interplay between the vitamin D receptor (VDR) and transcription factors to induce DNA methylation changes, which might provide phenotypic stability to the tolerogenic phenotype of DCs.
2022-02-23 | GSE145584 | GEO
Project description:Complex autoimmune diseases have proven difficult to dissect down to their causative genetic mechanisms. As a result, epidemiological data from different human association studies are often merged to arrive at a working hypothesis. In one of such examples, lack of sun exposure and consequent lower serum vitamin D3 levels has been proposed to increase risk of autoimmunity, attributing vitamin D3 an immune regulatory role. However, conclusive evidence demonstrating its efficacy in treating autoimmune diseases is missing. In this study, we have used a forward genetics approach to positionally identify polymorphic nucleotides controlling T cell-dependent inflammatory diseases using congenic mouse strains. Here, we identify the vitamin D3 receptor (Vdr) as a driver of inflammation. Congenic mice carrying a polymorphic Vdr allele overexpressed the receptor selectively in activated T cells, thereby escaping systemic calcaemic side effects that often constitute a confounding factor in the study of immunomodulation by vitamin D3. Mice overexpressing Vdr in T cells developed more severe collagen-induced arthritis (CIA) and exhibited an enhanced antigen-specific CD4+ T cell response. Deficiency of vitamin D3 completely protected mice from CIA by limiting the activation of antigen-specific T cell responses, and arthritis susceptibility was restored by re-administration of vitamin D3. We demonstrate that vitamin D3 signalling specifically through Vdr predominantly acts to enhance T cell proliferation, thereby contributing to inflammation. In conclusion, our results demonstrate that genetically determined expression of VDR codetermines the pro-inflammatory behaviour of activated T cells. Furthermore, our data suggest that the anti-inflammatory properties of vitamin D3 might be limited by high expression of VDR at the site of inflammation.
2020-09-28 | PXD019876 | Pride
Project description:Dietary supplementation of vitamin D is commonly recommended to patients with multiple sclerosis (MS). We investigated the effect of 1,25-dihydroxyvitamin-D3 (1,25-(OH)2D3) on the brain proteome in the cuprizone model during remyelination. Mice were demyelinated with dietary cuprizone for 7 weeks. The mice received intra-peritoneal injections of 1,25-(OH)2D3 or placebo twice a week, from week 6 and throughout week 10. Brain samples were taken after 7 weeks (demyelinated), after 8 weeks (1 week remyelination) and after 10 weeks (3 weeks of remyelination). The six experimental groups were labeled with TMT, mixed mode HPLC fractionation, and applied to LC-MS which enabled quantification of 5062 proteins with high confidence.
2017-08-16 | PXD002347 | Pride
Project description:In this study, we investigated the effect of vitamin D supplementation on tumorigenesis in a thioacetamide (TAA)-induced rat intrahepatic cholangiocarcinoma model as vitamin D is known to have a spectrum of anticancer activities. Using PET, we found that tumor formation and progression were suppressed in rats fed a diet supplemented with 6 IU/g vitamin D3(+6D) as compared to the group fed a 2 IU/g vitamin D3 diet (+2D) or controls. Microarray analysis of the tumors that arose revealed that vitamin D supplementation caused significant up- and down regulation in 21 and 16 genes, respectively.
2015-08-01 | GSE48961 | GEO
Project description:The general objective of the study was to determine modulation of gene expression by environmental factors, with a special emphasis on bone formation. For this reason, the specific period of treatment was chosen between 5-6 days post-fertilization (dpf), when bone formation and calcification are taking place. We show that treatment with Vitamin D3 (VitD3) causes a clear increase of bone formation, as illustrated by cranial skeleton staining of the bone matrix by Alizarin Red, by morphometric analysis of the resulting images and by gene expression studies of selected genes. Thus, a whole genome micro-array experiment was conducted to identify genes that may be involved in the observed effect on bone formation.
2015-02-27 | E-MTAB-3286 | biostudies-arrayexpress
Project description:We wanted to examine the effect of vitamin D3 and endogenous mutant p53 expressed in SKBR3 cells on gene expression paterns. Expression microarray analysis was performed on SKBR3 cells without or with endogenous mutp53 knockdown, with or without 1a25-vitamin D3 treatment.
2009-12-29 | GSE19670 | GEO
Project description:Previous reports have shown low vitamin D serum levels and polymorphisms in the vitamin D receptor (VDR) to be associated with increased risk for TB. Given that 1α,25-dihydroxyvitamin D3 has a role in lipid metabolism control, we tested whether the link between 1α,25-dihydroxyvitamin D3 and tuberculosis involves macrophage lipid metabolism. Since formation of lipid droplets (LD) is a hallmark of lipid dysregulation in M. tuberculosis-infected macrophages, we measured LD content as a readout of altered lipid metabolism in infected THP-1 cells. Induction of LD, which peaked by 24 hours post-infection was prevented by addition of 1α,25-dihydroxyvitamin D3 at the time of infection. To investigate the mechanism of 1α,25-dihydroxyvitamin D3 modulation of LD formation, we analyzed the transcriptome of M. tuberculosis-infected THP-1 cells with and without 1α,25-dihydroxyvitamin D3 treatment.
2014-07-01 | GSE57028 | GEO
Project description:Vitamin D’s ability to prevent colorectal cancer (CRC) has been suspected for nearly 30 years, but has never been directly studied in humans. The biologically active version of vitamin D, 1,25(OH)2D3, cannot be readily used in humans because of its tendency to cause serum calcium levels to rise. In contrast, 25(OH)D3 (ie calcifediol) does not have this side effect. The investigators previous research suggests that the enzyme necessary to convert 25(OH)D3 (calcifediol) into active 1,25(OH)D3 is present in cells lining the large intestine (colon).
Aberrant crypt foci (ACF) are very small (ie microscopic) collections of abnormally shaped cells that are a commonly used marker of CRC risk. Screening colonoscopy at UIC routinely uses methods that allow ACF counting to be done as a part of standard practice. ACF’s are not fixed, like polyps or cancers, but can disappear as a person’s risk for developing CRC decreases.
The investigators propose giving patient’s with 10 or more ACF’s 25(OH)D3 (calcifediol) or placebo, and determining if there is a drug-dependant decrease in ACF number. The primary objective is to determine whether 25(OH)D3 (calcifediol) supplementation, compared to placebo, causes significant reduction of ACF number from baseline levels. The primary endpoint will be change in ACF number.
| 2123484 | ecrin-mdr-crc