In order to assess whether culturing adipose-derived adult stem cells (ADASCs) affect their gene expression (see Sample Growth Condition Protocol), we wanted to identify possible genes that were differentially expressed between cultured polyclonal CD31- ADASCs and freshly isolated (uncultured) polyclonal CD31- ADASCs. To that end, RNA was isolated from cultured and uncultured ADASCs from three different donors and analyzed using the Affymetrix Microarray HG-U133A. Then, using the Affymetrix program MAS 5.0 we performed three comparisons and could identify differentially expressed transcripts common between the three donors, using the Affymetrix program DMT 3.0.
Isolation and transcription profiling of purified uncultured human stromal stem cells: alteration of gene expression after in vitro cell culture.
Sex, Age, Specimen part, Disease, Disease stage, Cell line, Subject
View SamplesFetal and adult -globin gene expression is tightly regulated during human development. Fetal globin genes are transcriptionally silenced during embryogenesis through the process of hemoglobin switching. Efforts to understand the transcriptional mechanism(s) behind fetal globin silencing have led to novel strategies to derepress fetal globin expression in the adult, which could alleviate symptoms in hereditary b-globin disorders including sickle cell disease (SCD) and -thalassemia. We identified a novel zinc finger protein, pogo transposable element with zinc finger domain (Pogz), expressed in mouse and human hematopoietic stem and progenitor cells, which represses embryonic b-like globin gene expression in mice. Ablation of Pogz expression in adult hematopoietic cells in vivo results in persistence of embryonic b-like globin expression without significantly affecting erythroid development or mouse survival. Elevated embryonic -like globin expression correlates with reduced expression of Bcl11a, a known repressor of embryonic -like globin expression, in Pogz-/- fetal liver cells. Pogz binds to the Bcl11a promoter, and, to erythroid specific intragenic regulatory regions. Importantly, Pogz+/- mice develop normally, but show elevated embryonic b-like globin expression in peripheral blood cells, demonstrating that reducing Pogz levels results in persistence of embryonic b-like globin expression. Finally, knockdown of POGZ in primary human CD34+ hematopoietic stem and progenitor cell derived erythroblasts, reduces BCL11A expression and increases fetal hemoglobin expression. These findings are significant since new therapeutic targets and strategies are needed to treat the increasing global burden of b-globin disorders.
POGZ Is Required for Silencing Mouse Embryonic β-like Hemoglobin and Human Fetal Hemoglobin Expression.
Specimen part
View SamplesmRNA, sncRNA and lncRNA show a clear difference in expression between proliferative phase and 7–9 days after ovulation, thorough described together with lncRNA, snoRNA and snRNA not previously reported in healthy human endometrium Overall design: 7 small RNA and 7 total RNA samples sequenced from endmometrial tissue from two time points of the menstrual cycle. Gene expression from the two time points compared. Additionally 12 small RNA from stromal cells was sequenced.
Comprehensive RNA sequencing of healthy human endometrium at two time points of the menstrual cycle.
No sample metadata fields
View SamplesIt has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Overall design: Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000
The age and genomic integrity of neurons after cortical stroke in humans.
No sample metadata fields
View SamplesWe discovered a rare missense mutation in NR1H4 (R436H), which encodes the farnesoid X receptor (FXR), associating with lower levels of total cholesterol in the Icelandic population. To explore the effects of R436H we used CRISPR-Cas9 to generate homozygous NR1H4 R436H and NR1H4 knockout human iPSC lines which we differentiated to hepatocytes. Hepatocytes were treated with an FXR agonist for 24 hours and transcript abundance measured by RNA-seq. The global response to FXR activation in NR1H4 R436H cells was very similar to that of wild-type cells showing that it is not a loss-of-function mutation. However, we did observe subtle gene expression differences compatible with an effect on lipids when we compared R436H agonist treated hepatocytes to wild-type agonist treated hepatocytes. Overall design: RNA-seq was performed on wild-type, NR1H4 knockout and NR1H4 R436H iPSC-derived hepatocytes treated with FXR agonist GW4064.
Predicted loss and gain of function mutations in ACO1 are associated with erythropoiesis.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.
Specimen part
View SamplesAn investigation of the global gene expression signatures of murine hematopoietic stem cell differentiation during steady state hematopoiesis.
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.
Specimen part
View SamplesPharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in thoracic aorta from SP467L mice and their control littermates using the Affymetrix Mouse Genome 430 2.0 array.
Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.
Specimen part
View SamplesTranscriptional analysis of identified DRG subpopulations.
Scaling proprioceptor gene transcription by retrograde NT3 signaling.
Specimen part
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