Similar Datasets
Project description:To analyze the function of miR-223 in steady-state myelopoiesis.
2022-01-01 | GSE33917 | GEO
Project description:To analyze the function of miR-223 in ex-vivo cultured bone marrow.
2022-01-01 | GSE33914 | GEO
Project description:We used a multi-omics approach combining transcriptomics, proteomics and metabolomics to study the impact of over-expression and inhibition of the microRNA miR-223, a pleiotropic regulator of metabolic-related disease, in the RAW monocyte-macrophage cell line. We analyzed the levels of proteins, mRNAs, and metabolites in order to identify genes involved in miR-223 regulation, to determine candidate disease biomarkers and potential therapeutic targets. We observed that both up- and down-regulation of miR-223 induced profound changes in the mRNA, protein and metabolite profiles in RAW cells. Microarray-based transcriptomics evidenced a change in 120 genes that were linked predominantly to histone acetylation, bone remodeling and RNA regulation. In addition, 30 out the 120 genes encoded long noncoding RNAs. The nanoLC-MS/MS revealed that 52 proteins were significantly altered when comparing scramble, pre- and anti-miR-223 treatments. Sixteen out of the mRNAs coding these proteins genes are predicted to have binding sites for miR-223. CARM-1, Ube2g2, Cactin and Ndufaf4 were confirmed to be miR-223 targets by western blotting. Analyses using Gene Ontology annotations evidenced association with cell death, splicing and stability of mRNAs, bone remodeling and cell metabolism. miR-223 alteration changed the expression of CARM-1, Ube2g2, Cactin and Ndufaf4 during osteoclastogenesis and macrophage, indicating that these genes are potential biomarkers of these processes. The most important discriminant metabolites found in the metabolomics study were found to be hydrophilic amino acids, carboxylic acids linked to metabolism and pyrimidine nucleotides, indicating that changes in miR-223 expression alter the metabolic profile of cells, and may affect their apoptotic and proliferative state.
2021-03-29 | PXD009844 | Pride
Project description:miR-223 is step-wise increasingly up-regulated in the normal esophagus - Barrett's esophagus -esophageal adenocarcinoma carcinoma sequence. In this study, we aimed to determine the function of miR-223 in esophageal adenocarcinoma carcinogenesis.
2013-02-07 | GSE44120 | GEO
Project description:Gene expression profiling of bone marrow derived eosinophils from miR-223 wildtype or miR-223 deficient mice
2012-08-25 | E-MEXP-3350 | biostudies-arrayexpress
Project description:miR-223 is step-wise increasingly up-regulated in the normal esophagus - Barrett's esophagus -esophageal adenocarcinoma carcinoma sequence. In this study, we aimed to determine the function of miR-223 in esophageal adenocarcinoma carcinogenesis. miR-223 was transfected in OE33 cells using 10nM pre-miR hsa-miR-223 miRNA precursor (Ambion, Life Technologies, Grand Island, NY) and lipofectamin 2000 (OE33_223_1 and OE33_223_2). Mock control OE33 cells were transfected with a negative control pre-miR miRNA (OE33_NEG_1 and OE33_NEG_2). HumanHT-12 v4 Expression BeadChip arrays (Illumina, San Diego, CA) were used for microarray hybridizations to examine the global gene expression of two biological replicated experiments (four samples in total). The array targets more than 25,000 annotated genes with 47,323 unique probes derived from the National Center for Biotechnology Information (NCBI) Reference Sequence (RefSeq) Release 38 and UniGene (Build 199) databases.
2013-02-07 | E-GEOD-44120 | biostudies-arrayexpress
Project description:miR-223 is a novel regulator of murine hemogenic endothelial cell specification and endothelial-to-hematopoietic transition. miR-223-deficient mouse embryos exhibit significant increase in hemogenic endothelial cells and HSPCs.
2023-05-12 | GSE193579 | GEO
Project description:This array analysis is to study the regulation of target messages’ expression in murine neutrophils versus miR-223 null neutrophils.
2008-07-31 | GSE12001 | GEO
Project description:The control of cell cycle progression mostly relays on the concerted activity of cyclins, CDKs and CDKs inhibitor. Recent data demonstrated that microRNAs, by regulating the expression of these proteins, contribute to the control of cell cycle progression. Here we provide evidences that the CDK inhibitor p27Kip1 directly regulates microRNAs stability thereby influencing cell cycle exit following contact inhibition. By the use of wild type and p27 knock-out cells we uncovered several microRNAs whose expression is linked to the cell cycle exit in a p27-dependent manner. By studying one of this microRNA, miR-223, we provide evidence that p27 is an RNA binding protein able to bind miR-223 to stabilize its expression. High miR-223 levels participate in the control of cell proliferation.
2015-12-31 | GSE45538 | GEO
Project description:The molecular mechanisms that control innate cell recruitment during chronic infection and inflammation, such as tuberculosis (TB), are incompletely understood. During TB, myeloid cells infiltrate the lung and sustain local inflammation. We identified microRNA (miR)-223 as one of the most abundant noncoding RNAs in lung parenchyma of TB patients and susceptible mice. MiR-223 controlled lung recruitment of myeloid cells, and consequently, neutrophil-driven lethal inflammation, by directly targeting the chemoattractants CXCL2, CCL3 and IL-6. Our study reveals an essential role for a single miR in TB. Moreover, we identify new targets for and assign novel biological functions to miR-223. By regulating leukocyte chemotaxis via chemoattractants, miR223 is critical for control of TB and probably other nonresolving inflammatory diseases.
2014-04-21 | GSE39163 | GEO