Expression data from wild-type and cardiac specific miR-125b-1 knockout neonatal hearts
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE157746 | GEO | 2020/09/10
REPOSITORIES: GEO
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Project description:Expression data from wild-type and cardiac specific miR-125b-1 knockout neonatal hearts
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Project description:MiR-125b possible targets were identified after transfecting a miRNA-mimic (miR-125b) and a scramble miRNA (Negative control) in MCF7 cell line and analyzing gene expression modifications.
2013-12-02 | E-MTAB-1604 | biostudies-arrayexpress
Project description:The goal of this study is to define miR-125b-2 target genes in the hematopoietic system by genetic alteration of miR-125b expression levels. Here we report the identification of miR-125b-2 targets in the hematopoietic system by repressing miR125b in megakaryoblastic leukemia (AMKL) cell lines and overexpressing miR-125b-2 in hematopoietic stem and progenitor cells (CD34+-HSPCs)
2009-12-29 | GSE19680 | GEO
Project description:To better understand the mechanisms of blockage of myeloid differentiation and apoptosis and induction of proliferation by miR-125b, we preceded to identify miR-125b target genes involved in these pathways. We analyzed the total cellular gene expression pattern by RNA-sequencing of the parental 32Dclone3 myeloid cell line and that ectopically expressing miR-125b. We generated four cDNA libraries corresponding to duplicates of miR-125b and control cells. Compare the gene expression level in vector transduced 32Dclone3 cells with that in miR-125b transduced 32Dclone3 cells.
2012-04-04 | E-GEOD-37018 | biostudies-arrayexpress
Project description:To better understand the mechanisms of blockage of myeloid differentiation and apoptosis and induction of proliferation by miR-125b, we proceeded to identify miR-125b target genes involved in these pathways. We analyzed the total cellular gene expression pattern by RNA-sequencing of the parental NB4 myeloid cell line and that transiently transfected with miR-125b. We generated four cDNA libraries corresponding to duplicates of miR-125b and control cells. Compare the gene expression levels in miR control transfected cells with that in miR-125b transfected NB4 cells.
2012-04-06 | E-GEOD-37061 | biostudies-arrayexpress
Project description:Myofibroblasts (MFs) are crucial components of the fibrotic remodeling after myocardial infarction (MI). We have previously demonstrated the centrality of AMPKα1 in post-MI remodeling. Here, we investigate the effects of MF-specific deletion of AMPKα1 on left ventricular (LV) adaptation following MI, and the underlying molecular mechanisms. Importantly, MF-restricted AMPKα1 conditional knockout (cKO) hearts exhibit exacerbated post-MI adverse LV remodeling and are characterized by exaggerated fibrotic response, compared to wild-type (WT) hearts. Myofibroblast proliferation significantly increases in cKO infarcted hearts, coincident with a significant reduction of Connexin 43 (Cx43) expression in MFs. Mechanistically, lack of AMPKα1 in MFs enhances miR-125b expression, which, in turn, downregulates Cx43. Collectively, our data demonstrate a cardinal role for MF-AMPKα1 in cardiac remodeling, as its lineage-specific inactivation accentuates fibrosis and LV dilatation following MI. The deleterious effects of MF-specific AMPKα1 deletion are mediated via Cx43, and its post-transcriptional regulation by miR-125b.
2020-03-25 | GSE147470 | GEO
Project description:To better understand the mechanisms of blockage of myeloid differentiation and apoptosis and induction of proliferation by miR-125b, we proceeded to identify miR-125b target genes involved in these pathways. We analyzed the total cellular gene expression pattern by RNA-sequencing of the parental NB4 myeloid cell line and that transiently transfected with miR-125b. We generated four cDNA libraries corresponding to duplicates of miR-125b and control cells.
2012-04-06 | GSE37061 | GEO
Project description:To better understand the mechanisms of blockage of myeloid differentiation and apoptosis and induction of proliferation by miR-125b, we preceded to identify miR-125b target genes involved in these pathways. We analyzed the total cellular gene expression pattern by RNA-sequencing of the parental 32Dclone3 myeloid cell line and that ectopically expressing miR-125b. We generated four cDNA libraries corresponding to duplicates of miR-125b and control cells.
2012-04-05 | GSE37018 | GEO
Project description:Human vein umbilical endothelial cells (HUVEC) were transfected with pre-miR control and pre-miR 125b (Ambion) in order to identify targets (direct and indirect) downregulated by miR-125b in endothelial cells. 317 transcripts were downregulated with a fold change ≥ 1.5, among which 99 are predicted direct targets of mir-125b. Computional approach performed with Ingenuity Pathway Knowledge shows that movement of cell and cell-to-cell signalling are the top two biological functions affected bewteen control and transfected cells. Experiments performed in zebrafish and in HUVEC confirmed that mir-125b mainly affects genes involved in cellular movements and junctions. Total RNA was obtained from cells transfected in HUVEC with pre-miR control and pre-miR 125b. Three independent transfections were performed for each condition.
2011-04-30 | E-GEOD-21458 | biostudies-arrayexpress
Project description:Here, we have screened a miRNA expression library in a pre-B cell expression system to identify miRNAs with a potential oncogenic activity in early lymphocytes. We show that miR-125b is sufficient to transform B cell precursors in vitro as defined by growth factor independence, and demonstrate that continuous expression of miR-125b is necessary to keep cells in the transformed cells. Mechanistically, we find that expression of miR-125b protects against apoptosis induced by growth factor withdrawal, and that miR-125 interferes with the differentiation of pre-B to immature B cells. In consequence, transformed cells express the pre-BCR on the cell surface, which appears to provide signals for ongoing proliferation and survival. Using microarray analysis, we identified several previously known and novel putative target genes of miR-125b in B cell precursors. To evaluate their contribution to the miR-125b-mediated phenotype, transformed cells were reconstituted with expression constructs of validated target genes. Surprisingly, we only find that reconstitution of MAP3K11 interferes with the cellular fitness of transformed cells in vitro as well as in vivo. This indicates that MAP3K11 functions as an important tumor suppressor in the context of miR-125b. Gene expression in cells expressing a control vector or a vector encoding hsa-miR-125b-1 was measured either in the presence or 24 hours after withdrawal of the growth factor IL-7. Two independent experiments were performed, using independently generated cell clones for each repetition.
2015-01-01 | E-GEOD-59994 | biostudies-arrayexpress