NGS-Muscle of swine supplemented with cholecalciferol and 25(OH)D
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA832094 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18920013.fastq.gz | Fastqsanger.gz | |||
| SRR18920014.fastq.gz | Fastqsanger.gz | |||
| SRR18920015.fastq.gz | Fastqsanger.gz | |||
| SRR18920016.fastq.gz | Fastqsanger.gz | |||
| SRR18920017.fastq.gz | Fastqsanger.gz |
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Project description:According to RNA-seq results, application of vitamin D in the form of 25(OH)D in swine diet can be beneficial for myogenesis, energy production and muscle fibre formation by influencing TOR signalling pathway. However, the use of vitamin D in the form of 25(OH)D may reduce muscle respiratory capacity.
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Project description:This pilot clinical trial studies cholecalciferol in treating patients with colorectal cancer. The use of cholecalciferol may slow disease progression in patients with colorectal cancer.
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Project description:Fibroblast growth factor 23 (FGF23) is produced and secreted by osteocytes and is essential for maintaining phosphate homeostasis. One of the main regulators of FGF23, 1,25-dihydroxyvitamin D (1,25(OH)2D3), is primarily synthesized in the kidney from 25-hydroxyvitamin D (25(OH)D) by 1α-hydroxylase (encoded by CYP27B1). Hitherto, it is unclear whether osteocytes can convert 25(OH)D and thereby allow for 1,25(OH)2D3 to induce FGF23 production and secretion locally. Here, we differentiated MC3T3-E1 cells towards osteocyte-like cells expressing and secreting FGF23. Treatment with 10-6 M 25(OH)D resulted in conversion of 25(OH)D to 150 pmol/L 1,25(OH)2D3 and increased FGF23 expression and secretion but the converted amount of 1,25(OH)2D3 was insufficient to trigger an FGF23 response, so the effect on FGF23 was most likely directly caused by 25(OH)D. Interestingly, combining phosphate with 25(OH)D resulted in a synergistic increase in FGF23 expression and secretion, likely due to activation of additional signaling pathways by phosphate. Blockage of the vitamin D receptor (VDR) only partially abolished the effects of 25(OH)D or 25(OH)D combined with phosphate on Fgf23, while completely inhibiting the upregulation of cytochrome P450 family 24 subfamily A member 1 (Cyp24a1), encoding for 24-hydroxylase. RNA sequencing and in silico analyses showed that this could potentially be mediated by the nuclear receptors Retinoic Acid Receptor b (RARB) and Estrogen Receptor 2 (ESR2). Taken together, we demonstrate that osteocytes are able to convert 25(OH)D to 1,25(OH)2D3, but this is insufficient for FGF23 activation, implicating a direct effect of 25(OH)D in the regulation of FGF23, which occurs at least partially independent from its cognate vitamin D receptor Moreover, phosphate and 25(OH)D synergistically increase expression and secretion of FGF23, which warrants investigating consequences in patients receiving a combination of vitamin D analogues and phosphate supplements. These observations help us to further understand the complex relations between, phosphate, vitamin D and FGF23.
2024-08-01 | GSE239761 | GEO
Project description:Background & Aims: Active vitamin D, 1α,25(OH)2D3, is a nuclear hormone with roles in colonic homeostasis and carcinogenesis, yet mechanisms underlying these effects are incompletely understood. Human organoids are an ideal system to study genomic and epigenomic host-environment interactions. Here, we utilize human colonic organoids to measure 1α,25(OH)2D3 responses on genome-wide gene expression and chromatin accessibilityover time. Methods: Human colonic organoids were cultured and treated in triplicate with either 100nM 1α,25(OH)2D3 or vehicle control for 4 and 18 hours (h) for chromatin accessibility, and 6 and 24hfor gene expression. DNA and RNA were extracted for ATAC- and RNA-sequencing, respectively. Differentially accessible peaks were analyzed using DiffBind and EdgeR; differentially expressed genes were analyzed using DESeq2. Motif enrichment was determined using HOMER. Results: At 6h and 24h, 2870 and 2721 differentially expressed genes, respectively (FDR<5%) were identified with overall stronger responses with 1α,25(OH)2D3. Similarly, 1α,25(OH)2D3 treatment led to stronger chromatin accessibility especially at 4h. The vitamin D receptor (VDR) motif was strongly enriched among open chromatin peaks with 1α,25(OH)2D3 treatment accounting for 30.5% and 11% of target sequences at 4h and 18h, respectively (FDR<1%). A number of genes such as CYP24A1, FGF19, MYC, FOS and TGFBR2 showed significant transcriptional and chromatin accessibility responses to 1α,25(OH)2D3 treatment with open chromatin located distant from promoters for some gene regions. Conclusions: Assessment of chromatin accessibility and transcriptional responses to 1α,25(OH)2D3 yielded new observations about vitamin D genome-wide effects in the colon facilitated by application of human colonic organoids. This framework can be applied to study host-environment interactions between individuals and populations in future.
2020-12-09 | GSE162856 | GEO
Project description:Vitamin D as a pro-hormone is known to generate anticancer effects by various mechanisms. Vitamin D can be converted to 25-hydroxyvitamin D(25(OH)D) by the enzyme vitamin D-25-hydroxylase in the liver.25(OH)D is the precursor of 1,25‑dihydroxyvitamin D(1,25(OH)2D, also called calcitriol) and can be transformed by the enzyme CYP27B1. The distribution of CYP27B1 is mainly in the kidney, but also in other tissues like breast and colon. So far, research about the anticancer effects of Vitamin D mainly chooses 1,25‑dihydroxyvitamin D as the study object in vitro. However, there is increasing evidence showing that 25(OH)D also can generate anticancer effects by transforming into 1,25(OH)2D in the manner of autocrine and paracrine. Our study aims to explore the influence of 25(OH)D on breast cancer and provides the variation on the expression of RNA in the breast cancer cells cultured with 100nM 25(OH)D.
2024-05-15 | GSE247667 | GEO
Project description:Vitamin D is a pro-hormone that possesses various anticancer effects through diverse mechanisms. The enzyme vitamin D-25-hydroxylase can convert vitamin D into 25-hydroxyvitamin D (25(OH)D) in the liver. 25(OH)D serves as the precursor of 1,25-dihydroxyvitamin D (1,25(OH)2D or calcitriol), which can be transformed into 1,25(OH)2D by the enzyme CYP27B1. CYP27B1 is primarily distributed in the kidneys but can also be found in other tissues, such as the breast and colon. Although 1,25-dihydroxyvitamin D has been the primary object of in vitro studies, emerging evidence suggests that 25(OH)D can also generate anticancer effects by transforming into 1,25(OH)2D in the manner of autocrine and paracrine. Our study aims to investigate the impact of 25(OH)D on breast cancer and its effect on the expression of small RNA in breast cancer cells cultured with 100nM 25(OH)D.
2024-05-15 | GSE250048 | GEO
Project description:Patients with chronic kidney disease (CKD) demonstrate complex mineral metabolism derangements and a high prevalence of vitamin D deficiency. However, the optimal method of 25-hydroxyvitamin D (25(OH)D) repletion is unknown, and trials analysing the comparative efficacy of cholecalciferol and ergocalciferol in this population are lacking. We conducted a randomised clinical trial of cholecalciferol 1250?g (50 000 IU) weekly v. ergocalciferol 1250?g (50 000 IU) weekly for 12 weeks in forty-four non-dialysis-dependent patients with stage 3-5 CKD. The primary outcome was change in total 25(OH)D from baseline to week 12 (immediately after therapy). Secondary analyses included the change in 1,25-dihydroxyvitamin D (1,25(OH)2D), parathyroid hormone (PTH), D2 and D3 sub-fractions of 25(OH)D and 1,25(OH)2D and total 25(OH)D from baseline to week 18 (6 weeks after therapy). Cholecalciferol therapy yielded a greater change in total 25(OH)D (45·0 (sd 16·5) ng/ml) v. ergocalciferol (30·7 (sd 15·3) ng/ml) from baseline to week 12 (P<0·01); this observation partially resulted from a substantial reduction in the 25(OH)D3 sub-fraction with ergocalciferol. However, following cessation of therapy, no statistical difference was observed for total 25(OH)D change from baseline to week 18 between cholecalciferol and ergocalciferol groups (22·4 (sd 12·7) v. 17·6 (sd 8·9) ng/ml, respectively; P=0·17). We observed no significant difference between these therapies with regard to changes in serum PTH or 1,25(OH)2D. Therapy with cholecalciferol, compared with ergocalciferol, is more effective at raising serum 25(OH)D in non-dialysis-dependent CKD patients while active therapy is ongoing. However, levels of 25(OH)D declined substantially in both arms following cessation of therapy, suggesting the need for maintenance therapy to sustain levels.
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Project description:Recently, it has been reported that 25(OH)D3 (25D3) has physiological bioactivity in certain tissues derived from the Cyp27b1 knockout mice. To investigate 25D3 function in the kidney as an informational crossroad of various calciotropic substances, we employed CRISPR-Cas9 system to knock out the Cyp27b1 gene in the mouse renal tubular cell line, mDCT cells. Unlike the previously reported mice targeted to the Cyp27b1 gene systemically, Cyp27b1 knockout mDCT cells did not produce any measurable 1a,25(OH)2D3 (1,25D3) after 25D3 administration. As was seen in the treatment with 10-8 M and higher dose of 1,25D3, we found that 10-7 M of 25D3 could translocate VDR into the nucleus and promoted expression of the representative 1,25D3-responsive Cyp24a1 gene in the Cyp27b1 knockout mDCT cells. The exhaustive target gene profiles of 25D3 showed results closely mimicking those of 1,25D3. Subsequently, we confirmed that 25D3 induced the expression of a calcium reabsorption-related gene, Calbindin-D9K gene, in a similar way to 1,25D3. As another example among others, we found that both 1,25D3 and 25D3 induced the expression of Megalin gene. Our ChIP assay identified that two VDRE sites at the upstream region of the Megalin gene contributed to such gene activation. Together, we surmise that the ability to stimulate VDR target genes may provide a novel perspective with 25D3 contribution in certain tissues.
2019-08-30 | GSE136594 | GEO