Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169559 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR517903_1.fastq.gz | Fastqsanger.gz | |||
| SRR517903_2.fastq.gz | Fastqsanger.gz | |||
| SRR519717_1.fastq.gz | Fastqsanger.gz | |||
| SRR519717_2.fastq.gz | Fastqsanger.gz | |||
| SRR519718_1.fastq.gz | Fastqsanger.gz |
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Project description:Vitamin D receptors (VDR) are abundantly expressed in developing zebrafish as early as 48 hours post-fertilization, and prior to the development of a mineralized skeleton, and mature intestine and kidney. We probed the role of VDR in zebrafish biology by examining changes in expression of RNA by whole transcriptome shotgun sequencing (RNA-seq) in fish treated with picomolar concentrations of the VDR ligand and hormonal form of vitamin D3, 1a,25-dihydroxyvitamin D3 (1a,25(OH)2D3). We observed significant changes in RNAs encoding proteins of fatty acid, amino acid, and xenobiotic metabolism pathways, and RNAs of transcription factors, leptin, peptide hormones, receptor-activator of NFkB ligand (RANKL), and calcitonin-like ligand receptor pathways. Early small, and subsequent massive changes in >10% of expressed cellular RNAs were observed. At day 2 (24h 1a,25(OH)2D3-treatment), only 5 RNAs were differentially expressed (hormone vs. vehicle). On day 4 (72h-treatment), 78 RNAs; on day 6 (120h-treatment) 1040 RNAs; and on day 7 (144h-treatment), 1755 RNAs were differentially expressed in response to 1a,25(OH)2D3. Fewer RNAs (n = 482) were altered in day 7 embryos treated for 24h with 1a,25(OH)2D3 vs. those treated with hormone for 144h. At 7 days, in 1a,25(OH)2D3-treated embryos, pharyngeal cartilage was larger and mineralization was greater. Changes in expression of RNAs for transcription factors, peptide hormones, and RNAs encoding proteins integral to fatty acid, amino acid, leptin, calcitonin-like ligand receptor, RANKL and xenobiotic metabolism pathways, demonstrate heretofore unrecognized mechanisms by which 1a,25(OH)2D3 functions in vivo in developing eukaryotes.
2012-06-29 | GSE38575 | GEO
Project description:Vitamin D receptors (VDR) are abundantly expressed in developing zebrafish as early as 48 hours post-fertilization, and prior to the development of a mineralized skeleton, and mature intestine and kidney. We probed the role of VDR in zebrafish biology by examining changes in expression of RNA by whole transcriptome shotgun sequencing (RNA-seq) in fish treated with picomolar concentrations of the VDR ligand and hormonal form of vitamin D3, 1a,25-dihydroxyvitamin D3 (1a,25(OH)2D3). We observed significant changes in RNAs encoding proteins of fatty acid, amino acid, and xenobiotic metabolism pathways, and RNAs of transcription factors, leptin, peptide hormones, receptor-activator of NFkB ligand (RANKL), and calcitonin-like ligand receptor pathways. Early small, and subsequent massive changes in >10% of expressed cellular RNAs were observed. At day 2 (24h 1a,25(OH)2D3-treatment), only 5 RNAs were differentially expressed (hormone vs. vehicle). On day 4 (72h-treatment), 78 RNAs; on day 6 (120h-treatment) 1040 RNAs; and on day 7 (144h-treatment), 1755 RNAs were differentially expressed in response to 1a,25(OH)2D3. Fewer RNAs (n = 482) were altered in day 7 embryos treated for 24h with 1a,25(OH)2D3 vs. those treated with hormone for 144h. At 7 days, in 1a,25(OH)2D3-treated embryos, pharyngeal cartilage was larger and mineralization was greater. Changes in expression of RNAs for transcription factors, peptide hormones, and RNAs encoding proteins integral to fatty acid, amino acid, leptin, calcitonin-like ligand receptor, RANKL and xenobiotic metabolism pathways, demonstrate heretofore unrecognized mechanisms by which 1a,25(OH)2D3 functions in vivo in developing eukaryotes. Zebrafish embryos were obtained from mating of Segrest wild-type (SWT) parents under controlled barrier conditions, in the Mayo Clinic Zebrafish Core Facility, in Instant Ocean media . Zebrafish embryos (25-30) were placed in 20 mL embryo medium (pH 7.2) containing 1-phenyl-2-thiourea (PTU) (0.003% (w/v) and were maintained at 28-30 oC. At 24 hpf (1 day post fertilization, dpf), 10 microliters of 1a,25(OH)2D3 in ethanol was added to embryos maintained in 20 mL fresh embryo medium with PTU. The final concentration of 1a,25(OH)2D3 was 300 pM. Control zebrafish were treated with 10 microliters ethanol alone (vehicle controls). The medium containing either 300 pM 1a,25(OH)2D3 or vehicle was changed every 24 h . In experiment 1, at 2, 4, 6 and 7 dpf embryos/larvae were removed and immediately frozen at -80 0C for later RNA preparations. 25-30 embryos per set were used for preparation on RNA. At the same times, 7-12 embryos were fixed in 4% paraformaldehyde in 0.75 X DulbeccoM-bM-^@M-^Ys phosphate buffered saline (DPBS). In experiment 2, 6 dpf larvae were treated with 1a,25(OH)2D3 (300 pM) or vehicle for 24 h. RNA was prepared from three sets of larvae.
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2014-07-01 | GSE57028 | GEO
Project description:In this study, we compared the modulation of the transcriptome of human PBMCs by the vitamin D metabolites 25-hydroxyvitamin D3 (25(OH)D3), 25(OH)D2 and 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3).
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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 1?,25-dihydroxyvitamin D3 has a role in lipid metabolism control, we tested whether the link between 1?,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 1?,25-dihydroxyvitamin D3 at the time of infection. To investigate the mechanism of 1?,25-dihydroxyvitamin D3 modulation of LD formation, we analyzed the transcriptome of M. tuberculosis-infected THP-1 cells with and without 1?,25-dihydroxyvitamin D3 treatment. THP-1 cells were cultured in 24-well flat bottom plates, pre-treated with 20ng/ml PMA for 24 h, and incubated with M. tuberculosis H37Rv. After 4 hours of infection, cells were washed to remove extracellular bacteria and treated with 100 nM of 1?,25-dihydroxyvitamin D3. THP-1 cells were collected and analyzed at 24h. 3 biological replicates in each of the 4 groups were prepared: Infected, Infected plus 1?,25-dihydroxyvitamin D3, Non-infected, Non-infected plus 1?,25-dihydroxyvitamin D3.
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Project description:Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.
2021-02-25 | GSE167412 | GEO
Project description:Pregnancy 25-hydroxyvitamin D (25(OH)D) concentrations are associated with maternal and fetal health outcomes, but the underlying mechanisms have not been elucidated. Using physiological human placental perfusion approaches and intact villous explants we demonstrate a role for the placenta in regulating the relationships between maternal 25(OH)D concentrations and fetal physiology. Here, we demonstrate active placental uptake of 25(OH)D3 by endocytosis and placental metabolism of 25(OH)D3 into 24,25-dihydroxyvitamin D3 and active 1,25-dihydroxyvitamin D [1,25(OH)2D3], with subsequent release of these metabolites into both the fetal and maternal circulations. Active placental transport of 25(OH)D3 and synthesis of 1,25(OH)2D3 demonstrate that fetal supply is dependent on placental function rather than solely the availability of maternal 25(OH)D3. We demonstrate that 25(OH)D3 exposure induces rapid effects on the placental transcriptome and proteome. These map to multiple pathways central to placental function and thereby fetal development, independent of vitamin D transfer, including transcriptional activation and inflammatory responses. Our data suggest that the underlying epigenetic landscape helps dictate the transcriptional response to vitamin D treatment. This is the first quantitative study demonstrating vitamin D transfer and metabolism by the human placenta; with widespread effects on the placenta itself. These data show complex and synergistic interplay between vitamin D and the placenta, and inform possible interventions to optimise placental function to better support fetal growth and the maternal adaptations to pregnancy.
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