Impact of miR-203-3p overexpression on human primary keratinocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE223523 | GEO | 2023/09/06
REPOSITORIES: GEO
Similar Datasets
Project description:miR-142-3p is highly expressed in peripheral blood mononuclear cells (PBMCs) and has been described as a hematopoietic-restricted lineage, suggesting immune functions (Chen, Li et al. 2004; Landgraf, Rusu et al. 2007; Merkerova, Belickova et al. 2008). In order to determine the roles of miR-142-3p in B lymphocytes, we over-expressed this miRNA in the Raji B-cell line using a synthetic mimic of miR-142-3p and analyzed gene expression 24 hours after the transfection. Four replicates each of miR-142-3p-mimic transfection and apparied control mimic.
2011-05-30 | E-GEOD-28456 | biostudies-arrayexpress
Project description:To identify putative novel specific targets of miR-199-5p, miR-199a-3p and miR-214-3p, we overexpressed these miRNAs in human MRC5 pulmonary fibroblasts (CCL-171) using synthetic pre-miRNAs or a synthetic “negative” pre-miRNA control (miR-Neg). RNA samples were harvested 48 hours post-transfection and 3 independent experiments were carried out.
2019-04-11 | GSE97824 | GEO
Project description:Tumor progression is accompanied by an altered myelopoiesis that causes the accumulation of cells inhibiting anti-tumor T lymphocytes. We previously reported that immunosuppressive cells can be generated in vitro from bone marrow cells (BM) after four days GM-CSF and IL-6 treatment. Here, we describe that miR-142-3p down-regulation directs macrophage differentiation and determines the acquisition of their immunosuppressive function in cancer. Enforced miR over-expression impaired monocyte to macrophage transition both in vitro and in vivo. Conversely, forced miR down-regulation promoted the generation of immunosuppressive macrophages even during G-CSF-induced granulocytic differentiation. To identify how miR-142-3p regulates MDSC generation and activity, we analyze the gene expression of BM cultures transfected with either CTRL- or miR 142-3p mimic oligo -transfected before four days GM-CSF and IL-6 treatment. Keywords: Expression profiling by array BM cells were transfected either CTRL- or miR 142-3p mimic oligo before GM-CSF and IL-6 treatment to generate in vitro MDSCs during enforced miR over-expression. A triplicate of each sample was considered.Total RNA from obtained in vitro BM-differentiated MDSCs was isolated by Trizol reagent, and cRNA samples were hybridized to the Affymetrix GeneChip MOE430 2.0.
2015-07-23 | E-GEOD-39803 | biostudies-arrayexpress
Project description:Background: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder, characterized by cardiomyocyte hypertrophy, cardiomyocyte disarray and fibrosis, which has a prevalence of ~1:200-500 and predisposes individuals to sudden death and heart failure. The mechanisms through which diverse HCM-causing mutations cause cardiac dysfunction remain mostly unknown and their identification may reveal new therapeutic avenues. MicroRNAs have emerged as critical regulators of gene expression and disease phenotype in various pathologies. We explored whether miRNAs could play a role in HCM pathogenesis and offer potential therapeutic targets. Methods and Results: Using high-throughput miRNA expression profiling and qPCR analysis in two distinct mouse models of HCM, we found that miR-199a-3p expression levels are upregulated in mutant mice compared to age- and treatment-matched wild-type mice. We also found that miR-199a-3p expression is enriched in cardiac non-myocytes compared to cardiomyocytes. When we expressed miR-199a-3p mimic in cultured primary cardiac non-myocytes and analyzed the conditioned media by proteomics, we found that several ECM proteins (e.g., TSP2, FBLN3, COL11A1, LYOX) were differentially expressed. We confirmed our proteomics findings by qPCR analysis of selected mRNAs and demonstrated that miR-199a-3p mimic expression in cardiac non-myocytes drives upregulation of ECM genes including Tsp2, Fbln3, Pcoc1, Col1a1 and Col3a1. To examine the role of miR-199a-3p in vivo, we inhibited its function using lock-nucleic acid (LNA)-based inhibitors (antimiR-199a-3p) in an HCM mouse model. Our results revealed that progression of cardiac fibrosis is attenuated when miR-199a-3p function is inhibited in mild-to-moderate HCM. Finally, guided by computational target prediction algorithms, we identified mRNAs Cd151 and Itga3 as direct targets of miR-199a-3p and have shown that miR-199a-3p mimic expression negatively regulates AKT activation in cardiac non-myocytes. Conclusions: Altogether, our results suggest that miR-199a-3p may contribute to cardiac fibrosis in HCM through its actions in cardiac non-myocytes. Thus, inhibition of miR-199a-3p in mild-to-moderate HCM may offer therapeutic benefit in combination with complementary approaches that target the primary defect in cardiac myocytes.
2024-01-26 | PXD042904 | Pride
Project description:The goal of this experiment was to determine gene expression changes during IFNα treatment as the result of expression or inhibition of miR-203 in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, IFNα treated, IFNα treated in the presence of exogenous miR-203, and IFNα treated in the presence of miR-203 inhibitor) with 3 biological replicates for each group. Total RNA was purified from A549 cells that were untreated of treated with IFNα (1000 units/mL) alone or in the presence of miR-203 mimic or inhibitor for 10 hours.
2013-06-20 | E-GEOD-47866 | biostudies-arrayexpress
Project description:To identify putative novel specific targets of miR-143-3p and miR-145-5p, we overexpressed these miRNAs in BRAFV600E mutant human M238P melanoma cells using synthetic mimics or a synthetic “negative” control mimic (miR-Neg). RNA samples were harvested 48 hours post-transfection and 2 independent experiments were carried out.
2021-12-29 | GSE171880 | GEO
Project description:Hypertrophic scar (HS) is a skin fibroproliferative disease currently having no truly effective therapy. PIK3CA is a catalytic subunit of PI3K able to promote collagen synthesis in benign fibrotic diseases and to regulate cell survival, proliferation, and adhesion in malignancies. To explore PIK3CA’s functions in HS formation, we performed transcriptome sequencing and experimental validation. PIK3CA were overexpressed in HS tissues, and positively correlated with fibrosis. We then screened out miR-203a-3p as the most suitable endogenous inhibitor of PIK3CA through bioinformatics. Intriguingly, miR-203a-3p suppressed the proliferation, migration, collagen synthesis, and contractility, as well as trans-differentiation of fibroblasts into myofibroblasts in vitro, improved the morphology and histology of HS in vivo. Mechanistically, miR-203a-3p attenuated fibrosis by inactivating PI3K/AKT/mTOR pathway via directly targeting PIK3CA. In conclusion, Our findings identified that PIK3CA and PI3K/AKT/mTOR pathway were actively involved in HS formation and demonstrated that miR-203a-3p might serve as a potential strategy for HS therapy through targeting PIK3CA and inactivating PI3K/AKT/mTOR pathway.
2023-07-15 | GSE236983 | GEO
Project description:The goal of this experiment was to determine gene expression changes during Sendai virus infection as the result of expression or inhibition of miR-203 in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, Sendai virus infected, Sendai virus infeceted in the presence of exogenous miR-203, and Sendai virus infected in the presence of miR-203 inhibitor) with 3 biological replicates for each group. Total RNA was purified from A549 cells that were mock infected or infected with Sendai virus (Cantell strain, 5pfu/cell) alone or in the presence of miR-203 mimic or inhibitor for 10 hours.
2013-06-20 | E-GEOD-47865 | biostudies-arrayexpress
Project description:miR-142-3p is highly expressed in peripheral blood mononuclear cells (PBMCs) and has been described as a hematopoietic-restricted lineage, suggesting immune functions (Chen, Li et al. 2004; Landgraf, Rusu et al. 2007; Merkerova, Belickova et al. 2008). In order to determine the roles of miR-142-3p in B lymphocytes, we over-expressed this miRNA in the Raji B-cell line using a synthetic mimic of miR-142-3p and analyzed gene expression 24 hours after the transfection.
2011-05-30 | GSE28456 | GEO
Project description:MicroRNAs (miRNAs) regulate developmental events such as branching morphogenesis, epithelial to mesenchymal transition (EMT) and its reverse process mesenchymal to epithelial transition (MET). In this study, we performed small RNA sequencing of a breast epithelial progenitor cell line (D492), and its mesenchymal derivative (D492M) cultured in three-dimensional reconstituted basement membrane (3D-rBM) matrix. Large differences in miRNA expression were seen between D492 and D492M. Among the most downregulated miRNAs in D492M was miR-203a, a miRNA that plays an important role in epithelial differentiation. When analyzed over time (21 days) in 3D culture, increased expression of miR-203a was seen in D492, concomitant with increased complexity of the branching structures. When miR-203a was overexpressed in D492M (D492MmiR-203a), a partial reversion towards epithelial phenotype was seen. Gene expression analysis of D492M and D492MmiR-203a revealed that peroxidasin (PXDN), a collagen IV cross-linker was one of the most significantly downregulated genes in D492MmiR-203a. Bioinformatic analysis revealed that PXDN has three putative binding sites for miR-203a in its 3-prime UTR. When a miR-203a mimic was transfected into D492M, reduced PXDN expression was seen. Conversely, inhibition of miR-203a in D492MmiR-203a with a miR-203a inhibitor increased PXDN expression, demonstrating that miR-203a acts as a repressor of PXDN. To verify the binding of miR-203a to the 3’-UTR of PXDN we set up a luciferase reporter assay that confirmed the binding. Collectively, we have demonstrated that miR-203a expression temporally correlates with branching morphogenesis in 3D-rBM and is suppressed in the mesenchymal state. Overexpression of miR-203a in D492M induces a partial MET and reduces the expression of PXDN. Furthermore, we demonstrate that miR-203a is a novel repressor of PXDN. MiR-203-PXDN axis may be an important regulator in branching morphogenesis, EMT and basement membrane remodeling. \
2020-03-01 | GSE112306 | GEO