Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384720 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional changes induced by over-expression of miR-27a-3p in C2C12 myoblasts.
| PRJNA384718 | ENA
Project description:Skeletal muscle has a central role in whole body metabolism with myofibers that represent its functional units. These are differentiated cells with different contraction power and metabolic traits. Faster contracting myofibers preferentially use glucose as substrate for energy production, while slower use lipids. Myofibers can plastically change phenotypic traits in response to pathophysiological stimuli. Since post-transcriptional mechanisms should administer the changes of these post-mitotic cells, we demonstrated that miR-142-3p influences myofiber fuel availability and mitochondrial morphology. In vitro and in vivo experiments demonstrate that miR-142-3p regulates lipids utilization. We used microarrays to characterize the global changes in gene expression in C2C12 myoblasts due to over-expression of miR-142-3p.
2019-12-20 | GSE98327 | GEO
Project description:Skeletal muscle has a central role in whole body metabolism with myofibers that represent its functional units. These are differentiated cells with different contraction power and metabolic traits. Faster contracting myofibers preferentially use glucose as substrate for energy production, while slower use lipids. Myofibers can plastically change phenotypic traits in response to pathophysiological stimuli. Since post-transcriptional mechanisms should administer the changes of these post-mitotic cells, we demonstrated that miR-27a-3p influences myofiber fuel availability and mitochondrial morphology. In vitro and in vivo experiments demonstrate that miR-27a-3p regulates glycogen utilization. We used microarrays to characterize the global changes in gene expression in C2C12 myoblasts due to over-expression of miR-27a-3p.
2019-12-20 | GSE98326 | GEO
Project description:This study compares changes in gene expression induced by four interrelated miRNAs with similar but staggered 5'-ends: miR-142-3p, miR-142-3p-1, miR-K10a, and miR-K10a+1. miR-K10a and miR-K10a+1 are co-expressed by the Kaposi's sarcoma-associated herpesvirus.
2015-07-31 | GSE66489 | GEO
Project description:This study compares changes in gene expression induced by four interrelated miRNAs with similar but staggered 5'-ends: miR-142-3p, miR-142-3p-1, miR-K10a, and miR-K10a+1. miR-K10a and miR-K10a+1 are co-expressed by the Kaposi's sarcoma-associated herpesvirus. Total RNA was harvested from HEK293 cells transfected with individual miRNAs including a negative control miRNA mimic.
2015-07-31 | E-GEOD-66489 | 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. Four replicates each of miR-142-3p-mimic transfection and apparied control mimic.
2011-05-30 | E-GEOD-28456 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs, micro ribonucleic acids) are pivotal post-transcriptional regulators of gene expression. These endogenous small non-coding RNAs play significant roles in tumorigenesis and tumor progression. miR-142-3p expression is dysregulated in several breast cancer subtypes. We aimed at investigating the role of miR-142-3p in breast cancer cell invasiveness. Supported by transcriptomic Affymetrix array analysis and confirmatory investigations at the mRNA and protein level, we demonstrate that overexpression of miR-142-3p in MDA-MB-231, MDA-MB-468 and MCF-7 breast cancer cells leads to downregulation of WASL (Wiskott-Aldrichsyndrome-like, protein: N-WASP), Integrin-aV, RAC1, and CFL2, molecules implicated in cytoskeletal regulation and cell motility. ROCK2, IL6ST, KLF4, PGRMC2 and ADCY9 were identified as additional targets in a subset of cell lines. Decreased matrigel invasiveness was associated with the miR-142-3p-induced expression changes. Confocal immunofluorescence microscopy, nanoscale atomic force microscopy and digital holographic microscopy revealed a change in cell morphology as well as a reduced cell volume and size. A more cortical actin distribution and a loss of membrane protrusions were observed in cells overexpressing miR-142-3p. Luciferase activation assays confirmed direct miR-142-3p-dependent regulation of the 3'-untranslated region of ITGAV and WASL. siRNA-mediated depletion of ITGAV andWASL resulted in a significant reduction of cellular invasiveness, highlighting the contribution of these factors to the miRNA-dependent invasion phenotype. While knockdown of WASL significantly reduced the number of membrane protrusions compared to controls, knockdown of ITGAV resulted in a decreased cell volume, indicating differential contributions of these factors to the miR-142-3p-induced phenotype. Our data identify WASL, ITGAV and several additional cytoskeleton associated molecules as novel invasion-promoting targets of miR-142-3p in breast cancer.
2015-11-16 | GSE50829 | 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:MicroRNAs (miRs), a group of small and non-coding RNAs, negatively regulate gene expression via promoting messenger RNA (mRNA) degradation or blocking mRNA translation. Many miRs have been recognized as biomarkers or possible targets for the diagnosis or therapy of some diseases. Among them, miR-142-3p was involved in the occurrences and progression of various cardiovascular diseases. Previous studies found that miR-142-3p upregulation could ameliorate myocardial ischemia/reperfusion (I/R)-induced transdifferentiation of fibroblasts to myofibroblasts and collagen deposition. miR-142-3p-mediacted autophagy was reported as a novel mechanism towards I/R-induced cardiac injure. Besides, miR-142-3p could mitigate myocardial mitochondrial dysfunction. Thus, it is worth studying whether silencing miR-142-3p may affect the pathological and physiological functions of cardiac fibroblasts.
2024-03-27 | GSE262000 | GEO
Project description:To identify target genes of miR-142-5p and miR-130a-3p that are involved in M2 polarization, we examined the mRNA expression profile changes after altering miR-142-5p or miR-130a-3p expression in IL-4-treated macrophages.
2014-07-12 | GSE59347 | GEO