Here we report the gene expression profile of in vitro cultured human endometrial stromal cells treated with siRNA targeting FOXO1 piror to eutherian differentiation media exposure. The eutherian differentiation media contains cyclic AMP (cAMP) analogue 8-Br-cAMP and the progesterone (P4) analogue medroxyprogesterone acetate (MPA). Overall design: RNA-seq on decidualizing human endometrial stromal cells treated with siRNA targeting FOXO1.
The mammalian decidual cell evolved from a cellular stress response.
Specimen part, Treatment, Subject
View SamplesObjective
A subset of metastatic pancreatic ductal adenocarcinomas depends quantitatively on oncogenic Kras/Mek/Erk-induced hyperactive mTOR signalling.
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View SamplesOBJECTIVE:
Foam cell specific LXRα ligand.
Sex, Specimen part, Cell line
View SamplesMiRNAs have the potential to regulate cellular differentiation programs. However, miRNA-deficiency in primary hematopoietic stem cells (HSCs) results in HSC depletion in mice, leaving the question of whether miRNAs play a role in early-lineage decisions unanswered. To address this issue, we deleted Dicer1, which encodes an essential RNaseIII enzyme for miRNA biogenesis, in murine CCAAT/enhancer-binding protein alpha (C/EBPA)-positive myeloid-committed progenitors in vivo. In contrast to the results in HSCs, we found that miRNA depletion affected neither the number of myeloid progenitors nor the percentage of C/EBPA-positive progenitor cells. Analysis of gene-expression profiles from wild type and Dicer1-deficient granulocyte-macrophage progenitors (GMPs) revealed that 20 miRNA families were active in GMPs. Of the derepressed miRNA targets in Dicer1-null GMPs, 27% are normally exclusively expressed in HSCs or are specific for multi-potent progenitors and erythropoiesis, indicating an altered gene-expression landscape. Dicer1-deficient GMPs were defective in myeloid development in vitro and exhibited an increased replating capacity, indicating a regained self-renewal potential of these cells. In mice, Dicer1 deletion blocked monocytic differentiation, depleted macrophages and caused myeloid dysplasia with morphological features of Pelger-Hut anomaly. These results provide evidence for a miRNA-controlled switch for a cellular program of self-renewal and expansion towards myeloid differentiation in GMPs.
Dicer1 deletion in myeloid-committed progenitors causes neutrophil dysplasia and blocks macrophage/dendritic cell development in mice.
Specimen part
View SamplesOverexpression of miR-9 and miR-9* in 32D cells, cells grown under IL-3 conditions and miR-9 and miR-9* were introduced with retroviral vectors containing about ~150 bp up and downstream of mmu-mir-9-2.
Aberrant expression of miR-9/9* in myeloid progenitors inhibits neutrophil differentiation by post-transcriptional regulation of ERG.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Disruption of histone methylation in developing sperm impairs offspring health transgenerationally.
Specimen part
View SamplesA fathers lifetime experiences can be transmitted to his offspring to affect
Disruption of histone methylation in developing sperm impairs offspring health transgenerationally.
Specimen part
View SamplesWith a model mimicking GBM tumor cell dispersal, transcriptome changes between core (immotile) and dispersive (motile) cells were analyzed. Many genes are differentially expressed between these populations. This study focused on the genes that are significantly upregulated in dispersive cells. Besides gene sets related with the cell cycle and cell survival, epithelial to mesenchymal transition gene set is upregulated in dispersive cells. In this gene set, this study identified SERPINE1 gene as an important regulator of GBM cell dispersal. Overall design: Examination of core and dispersive populations' transcriptome during U373 cell spheroid dispersal. 2 sets of samples were prepared each for core and dispersive cells.
Identification of <i>SERPINE1</i> as a Regulator of Glioblastoma Cell Dispersal with Transcriptome Profiling.
Cell line, Subject
View SamplesTo identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d).
ICL-induced miR139-3p and miR199a-3p have opposite roles in hematopoietic cell expansion and leukemic transformation.
Age, Specimen part
View SamplesThe microbial population that live within the gut of animals influences their physiology. We used axenic and recolonized flies to identify genes whose expression is modulated by the presence of a bacterial flora in the gut.
Drosophila microbiota modulates host metabolic gene expression via IMD/NF-κB signaling.
Specimen part, Treatment
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