Similar Datasets
Project description:Oligodendrocyte intrinsic miR-27a controls myelination and remyelination
| PRJNA558362 | ENA
Project description:Remyelination requires the generation of new oligodendrocytes (OLs), which are derived from oligodendrocyte progenitor cells (OPCs). Maturation of OPCs into OLs is a multi-step process. Here, we describe a microRNA expressed by OLs, miR-27a, as a regulator of OL development and survival. Increased levels of miR-27a were found in OPCs associated with multiple sclerosis (MS) lesions and in animal models of demyelination. Increased levels of miR-27a led to inhibition of OPC proliferation by cell-cycle arrest, as well as impaired differentiation of human OPCs (hOPCs) and myelination by dysregulating the Wnt-β-catenin signaling pathway. In vivo administration of miR-27a led to suppression of myelinogenic signals, leading to loss of endogenous myelination and remyelination. Our findings provide evidence supporting a critical role for a steady-state level of OL-specific miR-27a in supporting multiple steps in the complex process of OPC maturation and remyelination.
| S-EPMC6874400 | biostudies-literature
Project description:We have recently confirmed miR-27a-3p as a crucial regulator of human adipogenesis (Wu H, Pula T, Tews D, Amri E-Z, Debatin K-M, Wabitsch M, Fischer-Posovszky P, Roos J. microRNA-27a-3p but Not -5p Is a Crucial Mediator of Human Adipogenesis. Cells. 2021; 10(11):3205. https://doi.org/10.3390/cells10113205 ). MiR-27a-5p did not impair human adipogenesis. However, since several publications state that miR-27a ist also a crucial regulator of UCP1, we were interested if miR-27a-3p or miR-27a-5p regulatas UCP1 and other thermogenesis related genes. We found a strong regulation of UCP1 with functional relevance for the cellular metabolism by miR-27a-5p.To asesse the mRNA gene expression pattern, mRNA sequencing was performed.
2024-06-30 | GSE217629 | GEO
Project description:Whole transcriptome Identification of direct targets of miR-23b and miR-27a using biotinylated pull-downs found that both miRNAs have roles relevant to the mammalian cell cycle and cancer.
2014-12-31 | GSE40410 | GEO
Project description:Microarry analysis of mouse gene expression profile after transfected with miR-27a mimics (27a-7) and mimic NC (NC-9) Goal was to determine the effects of miR-27a transfection on global gene expression. Two-condition experiment, 27a-7 vs.NC-9.
2013-01-31 | E-GEOD-43910 | biostudies-arrayexpress
Project description:In infection with an adenovirus, it remains to be clarified whether host miRNAs affect Ad replication. We focused on miR-27 as an miRNA crucial for regulation of Ad infection because miR-27 has been reported to be involved in infection of other viruses, including MCMV and herpesvirus saimiri (HVS). We used microarrays to detail gene expression profiles in miR-27a/b-overexpressing HeLa cells and demonstarted that expression levels of various genes were down- or up-regulated following transfection with miR-27a/b mimics.
2017-04-03 | GSE85587 | GEO
Project description:Pancreatic β-cell dysfunction caused by obesity can be associated with alterations in the levels of microRNAs (miRNAs). However, the role of miRNAs in such processes remains elusive. Here, we show that pancreatic islet miR-27a-5p, which is markedly increased in obese mice and impairs insulin secretion, is mainly delivered by visceral adipocyte-derived extracellular vesicles (EVs). Depleting miR-27a-5p significantly improves insulin secretion and glucose intolerance in db/db mice. Supporting the function of EVs’ miR-27a-5p as a key pathogenic factor, intravenous injection of miR-27a-5p-containing EVs shows their distribution in mouse pancreatic islets. Tracing the injected AAV-miR-27a-5p (AAV-miR-27a) or AAV-FABP4-miR-27a-5p (AAV-FABP4-miR-27a) in visceral fat results in upregulating miR-27a-5p in EVs and serum, and elicits mouse pancreatic β-cell dysfunction. Mechanistically, miR-27a-5p directly targets L-type Ca2+ channel subtype CaV1.2 (Cacna1c) and reduces insulin secretion in β-cells. Overexpressing mouse CaV1.2 largely abolishes the insulin secretion injury induced by miR-27a-5p. These findings reveal a causative role of EVs’ miR-27a-5p in visceral adipocyte-mediated pancreatic β-cell dysfunction in obesity-associated type 2 diabetes mellitus.
2024-12-04 | GSE271706 | GEO
Project description:Microarry analysis of mouse gene expression profile after transfected with miR-27a mimics (27a-7) and mimic NC (NC-9) Goal was to determine the effects of miR-27a transfection on global gene expression.
2013-01-31 | GSE43910 | GEO
Project description:Comparison af adherent growing breast cancer cell lines versus mammospheres under serum-free conditions Background: In patients with breast cancer, subsets of long-lived cells tolerate chemotherapies. These chemoresistant cells can remain dormant at secondary sites, such as bone and lung, for years and decades. Cancer cells endowed with drug resistance are maintained in vivo in a quiescent slow-growing state that preserves them from anti-proliferative cancer drugs. The mechanism of conversion from dormancy to growth remains poorly understood. We aimed to identify microRNAs (miRNAs) as master regulators of cancer stem cells (CSCs) maintainance, because one of the characteristics of CSCs is their slow proliferation or dormancy. MiRNA targeting CSCs may be an effective therapy to improve the prognosis of breast cancer patients. Methods: We performed miRNA array analysis to identify differences miRNA expression profiles between adherent cells and mammospheres that contain higher number of breast cancer stem cells (BCSCs). In this approach, we focused on expression of hsa-miR-27a. Further, roles of hsa-miR-27a target genes in maintaining BCSC properties were analysed . Results: Here, we showed that hsa-miR-27a was downregulated in mammosphere cells. The formation of BCSCs was attenuated by transfection of hsa-miR-27a. We found that hsa-miR-27a targets F-box and WD-40 domain protein 7 (FBW7), a tumor suppressor gene, thereby inducing tumor dormancy. Additionally, we found that hsa-miR-27a targets genes involved in GSH synthesis, including xCT (encoded by SLC7A11), a heterodimeric protein of a transporter subunit of the xC(-) system, cystathionine gamma-lyase (CTH/CSE), and nuclear factor-erythroid 2-related factor 2 (Nrf2/NFE2L2), thereby increasing intracellular reactive oxygen species (ROS) levels. Upregulation of these genes by antisense (as)-miR-27a induced autophagy. Conclusions: Previous studies showed that expression of hsa-miR-27a is elevated in breast cancer. Here, we showed that expression of hsa-miR-27a was reduced in BCSC. CSCs in the dormant state are resistant to chemotherapy due to inhibition of ROS accumulation in these cells. These results demonstrate that hsa-miR-27a plays an essential role in maintaining the BCSCs phenotype via regulation of FBW7, ROS related genes and the Nrf2 pathway, as well as in the dormant-to-proliferative switch of breast cancer cells. Thus, hsa-miR-27a represents a novel strategy for various type of breast cancer.
2019-03-06 | GSE127849 | 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