MRNA expression profile in IL-4-treated macrophages transfected with miR-142-5p ASO or miR-130a-3p mimics
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59347 | GEO | 2014/07/12
SECONDARY ACCESSION(S): PRJNA255114
REPOSITORIES: GEO
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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. Macrophages were transfected with control ASO, miR-142-5p ASO, control mimics or miR-130-3p mimics using lentiviral vectors. After 24 hr, the cells were treated with IL-4 for 24h.mRNA was purified from total RNA after removal of rRNA (mRNA-ONLY™ Eukaryotic mRNA Isolation Kit, Epicentre). Then, each sample was amplified and transcribed into fluorescent cRNA along the entire length of the transcripts without 3’ bias utilizing a random priming method. The labeled cRNAs were hybridized onto the Human RNA Array v2.0 (8 x 60K, Arraystar). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505B.
2014-07-12 | E-GEOD-59347 | biostudies-arrayexpress
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2023-02-06 | GSE217971 | 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 is dynamically expressed and plays a regulatory role in hematopoiesis. Based on the simple observation that miR-142 levels are significantly lower in CD34+CD38- cells from blast crisis (BC) chronic myeloid leukemia (CML). CML patients compared with chronic phase (CP) CML patients (p=0.002), we hypothesized that miR-142 deficit plays a role in BC transformation. To test this hypothesis, we generated a miR-142 KO BCR-ABL (i.e., miR-142−/−BCR-ABL) mouse by crossing a miR-142−/− mouse with a miR-142+/+BCR-ABL mouse. While the miR-142+/+BCR-ABL mice developed and died of CP CML, the miR-142−/−BCR-ABL mice developed a BC-like phenotype in the absence of any other acquired gene mutations and died significantly sooner than miR-142+/+BCR-ABL CP controls (p=0.001). Leukemic stem cell (LSC)-enriched Lineage-Sca-1+c-Kit+ cells (LSKs) from diseased miR-142−/−BCR-ABL mice transplanted into congenic recipients, recapitulated the BC features thereby suggesting stable transformation of CP-LSCs into BC-LSCs in the miR-142 KO CML mouse. Single cell (sc) RNA-seq profiling showed that miR-142 deficit changed the cellular landscape of the miR-142−/−BCR-ABL LSKs compared with miR-142+/+BCR-ABL LSKs with expansion of myeloid-primed and loss of lymphoid-primed factions. Bulk RNA-seq analyses along with unbiased metabolomic profiling and functional metabolic assays demonstrated enhanced fatty acid β-oxidation (FAO) and oxidative phosphorylation (OxPhos) in miR-142−/−BCR-ABL LSKs vs miR-142+/+BCR-ABL LSKs. MiR-142 deficit enhanced FAO in miR-142−/−BCR-ABL LSKs by increasing the expression of CPT1A and CPT1B, that controls the cytosol-to-mitochondrial acyl-carnitine transport, a critical step in FAO. MiR-142 deficit also enhanced OxPhos in miR-142−/−BCR-ABL LSKs by increasing mitochondrial fusion and activity. As the homeostasis and activity of LSCs depend on higher levels of these oxidative metabolism processes, we then postulate that miR-142 deficit is a potentially druggable target for BC-LSCs. To this end, we developed a novel CpG-miR-142 mimic oligonucleotide (ODN; i.e., CpG-M-miR-142) that corrected the miR-142 deficit and alone or in combination with a tyrosine kinase inhibitor (TKI) significantly reduced LSC burden and prolonged survival of miR-142−/−BCR-ABL mice. The results from murine models were validated in BC CD34+CD38- primary blasts and patient-derived xenografts (PDXs). In conclusion, an acquired miR-142 deficit sufficed in transforming CP-LSCs into BC-LSCs, via enhancement of bioenergetic oxidative metabolism in absence of any additional gene mutations, and likely represent a novel therapeutic target in BC CML.
2023-01-13 | ST002446 | MetabolomicsWorkbench
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.
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Project description:MicroRNAs (miRNAs or miRs) play essential roles in the initiation and progression of human tumors, including cervical cancer. However, the mechanisms underlying their actions in cervical cancer remain unclear. The present study aimed to evaluate the functional role of miR‑130a‑3p in cervical cancer. Cervical cancer cells were transfected with a miRNA inhibitor (anti‑miR‑130a‑3p) and a negative control. Adhesion‑independent cell proliferation, migration and invasion were evaluated. The findings presented herein demonstrated that miR‑130a‑3p was overexpressed in HeLa, SiHa, CaSki, C‑4I and HCB‑514 cervical cancer cells. The inhibition of miR‑130a‑3p significantly reduced the proliferation, migration and invasion of cervical cancer cells. The canonical delta‑like Notch1 ligand (DLL1) was identified as a possible direct target of miR‑103a‑3p. The DLL1 gene was further found to be significantly downregulated in cervical cancer tissues. On the whole, the present study demonstrates that miR‑130a‑3p contributes to the proliferation, migration and invasion of cervical cancer cells. Therefore, miR‑130a‑3p may be used as a biomarker to determine cervical cancer progression.
2023-03-10 | GSE224301 | GEO
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:hematopoiesis and myelopoiesis was tightly controled by microRNAs. In the zebrafish adult kidney, specific sets of genes were dysregulated in myelomonocytes or whole kidney marrow after deletion of miR-142-3p. microarrays were used to clarified the miR-142-3p regulatory network in myelopoiesis in miR-142-3p knockout zebrafish kidney and we identified distinct classes of up-regulated genes in zebrafish myelopoiesis or hematopoiesis after deletion of miR-142-3p.
2014-07-01 | GSE58944 | GEO
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.
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