Genomic Determinants of Gene Regulation by 1,25-Dihydroxyvitamin D3 During Osteoblast-Lineage Cell Differentiation
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ABSTRACT:
PROVIDER: PRJNA224717 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1106830.fastq.gz | Fastqsanger.gz | |||
| SRR1106840.fastq.gz | Fastqsanger.gz | |||
| SRR1106850.fastq.gz | Fastqsanger.gz | |||
| SRR1106860.fastq.gz | Fastqsanger.gz | |||
| SRR1106870.fastq.gz | Fastqsanger.gz |
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Project description:We have carried out global gene expression analysis to clarify the interrelationship between 1,25-dihydroxyvitamin D3 and differentiation-driven gene expression patterns in developing human monocyte-derived dendritic cells. Monocytes were treated with 10 nM 1,25-dihydroxyvitamin D3 or vehicle 14 hours after plating for 12 hours or 5 days. Monocytes, differentiating dendritic cells (+/-1,25-dihydroxyvitamin D3 for 12 hours) and immature dendritic cells (+/-1,25-dihydroxyvitamin D3 for 5 days) were harvested. This design allows one to identify genes regulated by differentiation and/or 1,25-dihydroxyvitamin D3 in human monocyte-derived dendritic cells.
2009-02-15 | GSE13762 | GEO
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts.
2014-06-02 | GSE51514 | GEO
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts.
2014-06-02 | GSE51513 | GEO
Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts. RNA was isolated and applied to gene expression microarrays in undifferentiated MC3T3-E1 cells as well as post 15 day osteogenic differentiation MC3T3-E1 cells, which were treated for 24 hours with 10-7M 1,25(OH)2D3. For the vehicle matched samples, please refer to study GSE41955. The samples were completed in biological triplicate.
2014-06-02 | E-GEOD-51514 | biostudies-arrayexpress
Project description:The biological effects of 1?,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBP?. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBP? on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts. 4 transcription factors and 5 histone modifications were examined in undifferentiated MC3T3-E1 cells as well as post 15 day osteogenic differentiation MC3T3-E1 cells, which were treated for 3 hours prior to ChIP assay with ethanol vehicle or with 10-7M 1,25(OH)2D3. For the vehicle matched samples for RUNX2, CEBP beta and histones, please refer to study GSE41955. The samples were completed in biological replicate and examined separately.
2014-06-02 | E-GEOD-51513 | biostudies-arrayexpress
Project description:Background: Epidemiology and experimental studies suggest 1,25-dihydroxyvitamin D3 plays a neuroprotective role in neurodegenerative diseases including Alzheimer's disease. Most of the experimental data on the genes regulated by this hormone in brain cells have been obtained with neuron and glial cells. Emerging evidence demonstrates pericyte plays a critical role in brain function that encompasses its classical function in the control and maintenance of the blood brain barrier. However, the gene response of brain pericyte to 1,25D remains to be investigated. Methods: The transcriptomic response of human brain pericytes to 1,25-dihydroxyvitamin D3 was analyzed. Results were confirmed by RT-qPCR for the genes of interest. Results: We demonstrate that human brain pericyte in culture responds to 1,25-dihydroxyvitamin D3 by regulating genes involved in the control of neuro-inflammation. We also showed that pericytes respond to the pro-inflammatory cytokines TNF-alpha and Interferon gamma by inducing the expression of the gene involved in the synthesis of 1,25-dihydroxyvitamin D3 named CYP27B1. Conclusion: Taken together these results suggest that neuro-inflammation could trigger the synthesis of 1,25-dihydroxyvitamin D3 by brain pericytes, which will in turn respond to the hormone by a global anti-inflammatory response.
2017-01-01 | GSE54765 | GEO
Project description:A major goal in prostate stem cell biology is to identify genes, pathways, or networks that control self-renewal and multilineage differentiation. We hypothesize that 1,25 dihydroxyvitamin D3 can induce differentiation of prostatic progenitor/stem cells, thus serving as an in vitro model with which to study the molecular mechanisms of stem cell differentiation by 1,25 dihydroxyvitamin D3. 1,25 dihydroxyvitamin D3 elicits its effects primarily through transcriptional regulation of genes, so microarray studies were used to gain insight into the cellular response to 1,25 dihydroxyvitamin D3. We used microarrays to detail the global gene expression changes that occur upon 1,25 dihydroxyvitamin D3 treatment of prostatic progenitor/stem cells.
2011-06-22 | GSE18993 | GEO
Project description:Transcriptomic response of mouse mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin D3 6 samples are analysed with three biological replicates in two conditions, control versus 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)
2013-03-25 | E-GEOD-41184 | biostudies-arrayexpress
Project description:Transcriptomic response of mouse mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin D3
2013-03-25 | GSE41184 | GEO
Project description:We have carried out global gene expression analysis to clarify the interrelationship between 1,25-dihydroxyvitamin D3 and differentiation-driven gene expression patterns in developing human monocyte-derived dendritic cells. Monocytes were treated with 10 nM 1,25-dihydroxyvitamin D3 or vehicle 14 hours after plating for 12 hours or 5 days. Monocytes, differentiating dendritic cells (+/-1,25-dihydroxyvitamin D3 for 12 hours) and immature dendritic cells (+/-1,25-dihydroxyvitamin D3 for 5 days) were harvested. This design allows one to identify genes regulated by differentiation and/or 1,25-dihydroxyvitamin D3 in human monocyte-derived dendritic cells. Experiment Overall Design: Human monocytes were obtained from buffy coats from healthy donors by Ficoll gradient centrifugation followed by immunomagnetic cell separation with anti-CD14-conjugated microbeads. Monocytes were cultured in RPMI-1640 supplemented with 10% FBS, 800 U/ml GM-CSF and 500 U/ml IL-4. Monocytes were treated with 10 nM 1,25-dihydroxyvitamin D3 or vehicle 14 hours after plating for 12 hours or 5 days. Monocytes, differentiating dendritic cells (+/-1,25-dihydroxyvitamin D3 for 12 hours) and immature dendritic cells (+/-1,25-dihydroxyvitamin D3 for 5 days) were harvested. Experiments were performed in biological triplicates representing samples from different donors. 15 samples were processed and hybridized to Human Genome U133 Plus 2.0 Arrays.
2009-02-21 | E-GEOD-13762 | biostudies-arrayexpress