Ontology highlight
ABSTRACT:
PROVIDER: PRJNA772154 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16388444_1.fastq.gz | Fastqsanger.gz | |||
| SRR16388444_2.fastq.gz | Fastqsanger.gz | |||
| SRR16388445_1.fastq.gz | Fastqsanger.gz | |||
| SRR16388445_2.fastq.gz | Fastqsanger.gz | |||
| SRR16388446_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Expression profiling was used to explore the potential impact of VDR signaling in TGF?1 and TGF?1+1,25(OH)2D3-treated primary rat HSCs. Notably, 1,25(OH)2D3 treatment attenuated the culture-induced activation of HSCs, such that the transcriptome of treated cells closely resembled that of freshly isolated quiescent cells (Figure 2A), and co-treatment of 1,25(OH)2D3 together with TGF? resulted in considerable repression of a large set of TGF? induced genes. We also demonstrated that in primary mouse HSCs, calcipotriol potently repressed fibrotic gene expression, suggesting that the anti-TGF? properties of VDR agonists are likely conserved across mammalian species. Total RNA from primary rat HSCs were isolated and treated 1,25(OH)2D3 (100nM) for 24 hours to determine how Vitamin D ligands can impact the activated stellate cell state.
2013-04-29 | E-GEOD-41579 | biostudies-arrayexpress
Project description:Heterogeneous nuclear ribonucleoprotein (hnRNP) C1/C2 plays a pivotal role in vitamin D receptor (VDR) signaling by acting as a vitamin D response element (VDRE)-binding protein (VDRE-BP). Transcriptional regulation by active 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) involves occupancy of VDRE by VDRE-BP or 1,25(OH)2D3 bound-VDR. This relationship is disrupted by over-expression of VDRE-BP and can cause a form of human hereditary vitamin D-resistant rickets (HVDRR). DNA array analyses using B-cells from an HVDRR patient and matched control defined a sub-cluster of genes where 1,25(OH)2D3-regulated transcription was abrogated by over-expression of VDRE-BP. Amongst these, the DNA-damage-inducible transcript 4 (DDIT4), an inhibitor of mammalian target of rapamycin (mTOR) signaling, was also induced by 1,25(OH)2D3 in human osteoblasts. Chromatin immunoprecipitation using 1,25(OH)2D3-treated osteoblasts confirmed that liganded VDR and VDRE-BP compete for binding to the proximal promoter of the DDIT4 gene in a similar fashion to other known 1,25(OH)2D3-target genes. Treatment of osteoblasts with 1,25(OH)2D3 induced DDIT4 expression and suppressed phosphorylated S6K1T389 protein (a downstream target of mTOR). The functional importance of this for 1,25(OH)2D3 responses in osteoblasts was underlined by the fact that siRNA knockdown of DDIT4 expression suppressed antiproliferative and cell growth responses to 1,25(OH)2D3. These data confirm that VDRE-BP is required for normal 1,25(OH)2D3-mediated transcription and cell function in osteoblasts. Conversely over-expression of VDRE-BP exerts a dominant-negative effect on transcription of 1,25(OH)2D3-target genes. Characterization of VDRE-BP action in 1,25(OH)2D3-treated osteoblasts highlights an entirely novel role for vitamin D as a regulator of mTOR – a known ‘master regulator’ of cell function.
2010-11-19 | GSE22523 | GEO
Project description:Heterogeneous nuclear ribonucleoprotein (hnRNP) C1/C2 plays a pivotal role in vitamin D receptor (VDR) signaling by acting as a vitamin D response element (VDRE)-binding protein (VDRE-BP). Transcriptional regulation by active 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) involves occupancy of VDRE by VDRE-BP or 1,25(OH)2D3 bound-VDR. This relationship is disrupted by over-expression of VDRE-BP and can cause a form of human hereditary vitamin D-resistant rickets (HVDRR). DNA array analyses using B-cells from an HVDRR patient and matched control defined a sub-cluster of genes where 1,25(OH)2D3-regulated transcription was abrogated by over-expression of VDRE-BP. Amongst these, the DNA-damage-inducible transcript 4 (DDIT4), an inhibitor of mammalian target of rapamycin (mTOR) signaling, was also induced by 1,25(OH)2D3 in human osteoblasts. Chromatin immunoprecipitation using 1,25(OH)2D3-treated osteoblasts confirmed that liganded VDR and VDRE-BP compete for binding to the proximal promoter of the DDIT4 gene in a similar fashion to other known 1,25(OH)2D3-target genes. Treatment of osteoblasts with 1,25(OH)2D3 induced DDIT4 expression and suppressed phosphorylated S6K1T389 protein (a downstream target of mTOR). The functional importance of this for 1,25(OH)2D3 responses in osteoblasts was underlined by the fact that siRNA knockdown of DDIT4 expression suppressed antiproliferative and cell growth responses to 1,25(OH)2D3. These data confirm that VDRE-BP is required for normal 1,25(OH)2D3-mediated transcription and cell function in osteoblasts. Conversely over-expression of VDRE-BP exerts a dominant-negative effect on transcription of 1,25(OH)2D3-target genes. Characterization of VDRE-BP action in 1,25(OH)2D3-treated osteoblasts highlights an entirely novel role for vitamin D as a regulator of mTOR – a known ‘master regulator’ of cell function. We performed gene expression microarray analysis in HVDRR EBV-transformed B-cells and control cells in the presence or absence of vitamin D.
2010-11-19 | E-GEOD-22523 | biostudies-arrayexpress
Project description:We report the effects of 1,25(OH)2D3 treatment on the mRNA expression in human muscle cells Primary cultures of human muscle cells were treated with 1,25(OH)2D3 or vehicle for 48 hours.
2015-11-24 | E-GEOD-68323 | biostudies-arrayexpress
Project description:We report the effects of 1,25(OH)2D3 treatment on the microRNA expression in human muscle cells Primary cultures of human muscle cells were treated with 1,25(OH)2D3 or vehicle for 48 hours.
2015-11-24 | E-GEOD-70933 | biostudies-arrayexpress
Project description:Vitamin D deficiency is associated with high risk of colon cancer and a variety of other diseases. The active vitamin D metabolite 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) regulates gene transcription via its nuclear receptor (VDR), and posttranscriptional regulatory mechanisms of gene expression have also been proposed. We have identified microRNA-22 (miR-22) and several other miRNA species as 1,25(OH)2D3 targets in human colon cancer cells. Remarkably, miR-22 is induced by 1,25(OH)2D3 in a time-, dose-, and VDR-dependent manner. In SW480-ADH and HCT116 cells, miR-22 loss-of-function by transfection of a miR-22 inhibitor (anti-miR-22) suppresses the effect of 1,25(OH)2D3. Additionally, miR-22 inhibition increases cell migration per se and decreases the antimigratory effect of 1,25(OH)2D3 in both cell types. In silico analysis shows a significant overlap between genes suppressed by 1,25(OH)2D3 and miR-22 putative target genes. Consistently, miR-22 inhibition abrogates the reduction by 1,25(OH)2D3–mediated suppression of NELL2, OGN, HNRPH1, and NFAT5 genes. In 39 out of 50 (78%) human colon cancer patients, miR-22 expression was found lower in the tumor than in the matched normal tissue and correlated directly with that of VDR. Our results indicate that miR-22 is induced by 1,25(OH)2D3 in human colon cancer cells and it may contribute to its antitumor action against this neoplasia. We have analysed a human colon cancer cell line, SW480-ADH, treated with 1,25(OH)2D3 or isopropanol (vehicle) at three different time points (24, 48 and 96 hours). Each experiment was replicated 2 times by dye swap.
2011-12-20 | E-GEOD-34564 | biostudies-arrayexpress
Project description:Vitamin D deficiency is associated with high risk of colon cancer and a variety of other diseases. The active vitamin D metabolite 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) regulates gene transcription via its nuclear receptor (VDR), and posttranscriptional regulatory mechanisms of gene expression have also been proposed. We have identified microRNA-22 (miR-22) and several other miRNA species as 1,25(OH)2D3 targets in human colon cancer cells. Remarkably, miR-22 is induced by 1,25(OH)2D3 in a time-, dose-, and VDR-dependent manner. In SW480-ADH and HCT116 cells, miR-22 loss-of-function by transfection of a miR-22 inhibitor (anti-miR-22) suppresses the effect of 1,25(OH)2D3. Additionally, miR-22 inhibition increases cell migration per se and decreases the antimigratory effect of 1,25(OH)2D3 in both cell types. In silico analysis shows a significant overlap between genes suppressed by 1,25(OH)2D3 and miR-22 putative target genes. Consistently, miR-22 inhibition abrogates the reduction by 1,25(OH)2D3–mediated suppression of NELL2, OGN, HNRPH1, and NFAT5 genes. In 39 out of 50 (78%) human colon cancer patients, miR-22 expression was found lower in the tumor than in the matched normal tissue and correlated directly with that of VDR. Our results indicate that miR-22 is induced by 1,25(OH)2D3 in human colon cancer cells and it may contribute to its antitumor action against this neoplasia.
2011-12-20 | GSE34564 | GEO
Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Expression profiling was used to explore the potential impact of VDR signaling in TGFβ1 and TGFβ1+1,25(OH)2D3-treated primary rat HSCs. Notably, 1,25(OH)2D3 treatment attenuated the culture-induced activation of HSCs, such that the transcriptome of treated cells closely resembled that of freshly isolated quiescent cells (Figure 2A), and co-treatment of 1,25(OH)2D3 together with TGFβ resulted in considerable repression of a large set of TGFβ induced genes. We also demonstrated that in primary mouse HSCs, calcipotriol potently repressed fibrotic gene expression, suggesting that the anti-TGFβ properties of VDR agonists are likely conserved across mammalian species.
2013-04-29 | GSE41579 | GEO
Project description:To profile the changes in the pattern of gene expression in human OCa cells induced by 1,25(OH)2D3, OVCAR3 cells were treated with 0.1 pM 1,25(OH)2D3 for 0, 8, 24 and 72 h. The cells were harvested, RNA was extracted, and Affmetrix microarrays were hybridized.
2011-01-28 | GSE26903 | GEO
Project description:To profile the changes in the pattern of gene expression in human OCa cells induced by 1,25(OH)2D3, OVCAR3 cells were treated with 0.1 pM 1,25(OH)2D3 for 0, 8, 24 and 72 h. The cells were harvested, RNA was extracted, and Affmetrix microarrays were hybridized. OVCAR3 cells were treated with 0.1 pM 1,25(OH)2D3 for 0, 8, 24 and 72 hours. 1,25(OH)2D3 was added at different times to allow the treated cells to be harvested at the same time. Ethanol was included as vehicle controls and all cells were exposed to the same amount of ethanol for the same length of time. Total RNA was extracted using Trizol reagent (Invitrogen) and purified using Qiagen Rneasy kit as recommended by Affymetrix. In the initial set of array analysis with U95 chips, GADD45 was identified to be a VD-induced gene in OVCAR3 cells, which was confirmed by a follow-up study to be a primary target gene. For the array analyses with U133A chips, the response to 1,25(OH)2D3 of the cells used for RNA isolation was ensured by Northern blotting analysis of GADD45. Three independent experiments were performed.
2011-01-28 | E-GEOD-26903 | biostudies-arrayexpress