Expression data from livers in wildtype and Sox17+/-mice at 17dpc
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33106 | GEO | 2013/01/09
SECONDARY ACCESSION(S): PRJNA149509
REPOSITORIES: GEO
Similar Datasets
Project description:The onset of the liver inflamentation in the Sox17+/- embryos. The expression of Cxcl10, Cxcl2, Cxcl1 and stress-induced heat shock protein Hspa1a and Hspa1b were elevated in Sox17+/- livers at 17dpc, as compared with the wildtype livers. Total RNAs from liver tissues of wildtype and Sox17+/- mice at 17dpc were subjected to microarray analyses. Two biological replicates of each genotype were analyzed.
2013-01-09 | E-GEOD-33106 | biostudies-arrayexpress
Project description:We previously showed that the proteasome inhibitor bortezomib (Velcade) induces cell death in a subset of human bladder cancer cell lines. Heat shock protein 72 kDa (Hsp72) is the major cytosolic stress-inducible molecular chaperone, and is thought to protect cells from proteasome inhibition. Here, using whole genome mRNA expression profiling, we identify isoform-specific expression of Hsp72 within a heterogeneous panel of bladder cancer cell lines. Bortezomib induced strong upregulation of both the HSPA1A and HSPA1B isoforms of Hsp72 in 253J B-V and SW780 (HSPA1A-high) cells, whereas only HSPA1B isoform expression was induced in UM-UC10 and UM-UC13 (HSPA1A-low) cells. Bortezomib stimulated the binding of heat shock factor-1 (HSF1) to the HSPA1A promoter much more efficiently in 253JB-V cells than in UM-UC13, but other HSF1 transcriptional targets were induced in all of the cell lines, implicating a specific defect in HSPA1A induction. Methylation-specific PCR revealed that the HSPA1A promoter was selectively methylated in the HSPA1A-low cell lines (UM-UC10 and UM-UC13), and exposure to the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA1A expression. Overexpression of Hsp72 promoted bortezomib resistance in the UM-UC10 and UM-UC13 cells, whereas transient knockdown of HSPA1B sensitized these cells to bortezomib. Exposure to the chemical HSF1 inhibitor KNK-437 promoted bortezomib sensitivity in the 253J B-V cells. Finally, shRNA-mediated stable knockdown of Hsp72 in 253J B-V promoted sensitivity to bortezomib both in vitro and in vivo. Together, our results suggest that a subset of human bladder cancer cells possess epigenetic modifications that shut off the HSPA1A promoter and increases dependency on the HSPA1B isoform to maintain Hsp72 expression. Our data also support the targeting of HSF1 or Hsp72 for use as tools to enhance bortezomib sensitivity in solid tumors.
2013-08-01 | GSE46132 | GEO
Project description:We previously showed that the proteasome inhibitor bortezomib (Velcade) induces cell death in a subset of human bladder cancer cell lines. Heat shock protein 72 kDa (Hsp72) is the major cytosolic stress-inducible molecular chaperone, and is thought to protect cells from proteasome inhibition. Here, using whole genome mRNA expression profiling, we identify isoform-specific expression of Hsp72 within a heterogeneous panel of bladder cancer cell lines. Bortezomib induced strong upregulation of both the HSPA1A and HSPA1B isoforms of Hsp72 in 253J B-V and SW780 (HSPA1A-high) cells, whereas only HSPA1B isoform expression was induced in UM-UC10 and UM-UC13 (HSPA1A-low) cells. Bortezomib stimulated the binding of heat shock factor-1 (HSF1) to the HSPA1A promoter much more efficiently in 253JB-V cells than in UM-UC13, but other HSF1 transcriptional targets were induced in all of the cell lines, implicating a specific defect in HSPA1A induction. Methylation-specific PCR revealed that the HSPA1A promoter was selectively methylated in the HSPA1A-low cell lines (UM-UC10 and UM-UC13), and exposure to the chromatin demethylating agent 5-aza-2'-deoxycytidine restored HSPA1A expression. Overexpression of Hsp72 promoted bortezomib resistance in the UM-UC10 and UM-UC13 cells, whereas transient knockdown of HSPA1B sensitized these cells to bortezomib. Exposure to the chemical HSF1 inhibitor KNK-437 promoted bortezomib sensitivity in the 253J B-V cells. Finally, shRNA-mediated stable knockdown of Hsp72 in 253J B-V promoted sensitivity to bortezomib both in vitro and in vivo. Together, our results suggest that a subset of human bladder cancer cells possess epigenetic modifications that shut off the HSPA1A promoter and increases dependency on the HSPA1B isoform to maintain Hsp72 expression. Our data also support the targeting of HSF1 or Hsp72 for use as tools to enhance bortezomib sensitivity in solid tumors. RNA was isolated from cells using the TRIzol Reagent (Invitrogen/ Life Technologies, Grand Island, NY), followed by cleanup with RNeasy Mini kits (Qiagen, Germantown, MD). RNA was used for the synthesis of biotin-labeled cRNA, which was prepared using the Illumina RNA amplification kit (Ambion/ Life Technologies), and then hybridized to Illumina Human-HT12 (Illumina, Inc., Hayward, CA) chips. Washed chips were scanned with BeadStation 500x (Illumina) and the signal intensities quantified with BeadStudio (Illumina).
2013-08-01 | E-GEOD-46132 | biostudies-arrayexpress
Project description:We identified Sox17 as a novel angiogenic transcription factor in the context of tumor. Our data revealed that Sox17 promotes tumor angiogenesis and tumor vessel abnormality. We found that Sox17 is specifically expressed in tumor endothelial cells within tumors. Our study elucidates a novel transcriptional regulation for tumor angiogenesis Control HUVECs vs. Sox17 knockdown HUVECs. Biological replicates: 3 control replicates, 3 transfected replicates.
2012-12-17 | E-GEOD-37395 | biostudies-arrayexpress
Project description:This experiment has been done to understand the dynamics of gene expression in Sox17.Epi and Endo cells using multiplex RNA-Seq technology. Sox17.Epi (Sox17^GFP+EpCAM+) and Sox17.Endo (Sox17^GFP+EpCAM-) cells were isolated by FACS from E9.5 mouse embryos. The spatial comparison between Sox17.Epi versus Sox17.Endo provides insight into which genes are differentially of specifically expressed in two populations.
2012-07-20 | E-MTAB-970 | biostudies-arrayexpress
Project description:The transcription factor SOX17 is expressed by fetal, but not adult hematoipoietic stem cells (HSCs), and is required for the maintenance of fetal and neonatal, but not adult, HSCs. In the current study we show that ectopic expression of Sox17 in adult HSCs and transiently reconstituting multipotent progenitors was sufficient to confer increased self-renewal potential and the expression of fetal HSC genes including fetal HSC surface markers. To assess the acute effects of ectopic Sox17 expression on global gene expression in adult HSCs, we performed microarray analysis to compare the gene expression profile of adult Sox17-trangenic and control HSCs after short induction of Sox17-transgene expression. Total RNA were isolated from 5 independent, freshly isolated aliquots of 10,000 HSCs isolated from 8-week old Sox17-transgenic ((tetO)7CMVSox17-IRES-NucEGFP;B6.Cg-Gt(ROSA)26Sortm1(rtTA*M2)Jae/J double transgenic) or littermate control mice that were treated with doxycycline for 5 days to induce transgene expression. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Pico RNA Amplification system (NuGEN Technologies) following the manufacturer’s instructions. Sense strand cDNA was generated using WT-Ovation™ Exon Module (NuGEN), then fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.
2011-07-14 | E-GEOD-30445 | biostudies-arrayexpress
Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.
2023-03-15 | GSE192649 | GEO
Project description:The transcription factor SOX17 is expressed by fetal, but not adult hematoipoietic stem cells (HSCs), and is required for the maintenance of fetal and neonatal, but not adult, HSCs. In the current study we show that ectopic expression of Sox17 in adult HSCs and transiently reconstituting multipotent progenitors was sufficient to confer increased self-renewal potential and the expression of fetal HSC genes including fetal HSC surface markers. To assess the acute effects of ectopic Sox17 expression on global gene expression in adult HSCs, we performed microarray analysis to compare the gene expression profile of adult Sox17-trangenic and control HSCs after short induction of Sox17-transgene expression.
2011-07-15 | GSE30445 | GEO
Project description:To determine the effect of Sox17 overexpression in mouse embryonic stem (ES) cells, we performed gain-of-function analysis by generating ES cell lines carrying a doxycycline inducible FLAG-tagged Sox17 transgene. We treated Sox17-inducible ES cells with doxycycline, collected RNA and performed genome-wide transcriptional analysis. We found that genes invovled in adhesion function and basement membrane establishment were transcriptionally upregulated in ES cells upon induction of Sox17. We also observed downregulation in the transcription of genes involved in pathways known to be functionally important for ES cell pluripotency and self-renewal. However, Sox17 expression was not sufficient to rapidly down-regulate Sox2, Nanog, and Oct4. Two independent doxycycline inducible Sox17-overexpressing mouse embryonic stem cells were derived. The genes expression changes in the Sox17-induced cells were compared to untreated (no doxycycline) controls and to control cells treated with or without doxycycline. The total RNA from these samples were amplified using Ambion Illumina TotalPrep RNA Amplification kit and arrayed on Illumina MouseRef8 v2 chips.
2010-03-31 | E-GEOD-19028 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE30444: Retroviral Sox17 over-expression adult hematopoietic stem/progenitor cells microarray GSE30445: Sox17-transgenic hematopoietic stem cell microarray Refer to individual Series
2011-07-14 | E-GEOD-30446 | biostudies-arrayexpress