MicroRNA-148a regulated the development of inflammatory dendritic cells.
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ABSTRACT:
PROVIDER: PRJNA597295 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-12-23 | GSE142517 | GEO
Project description:Purpose: MicroRNA-148a regulates the differentiation of dendritic cells. The goals of this study are to identify genes and pathways invovled in the regulation. Methods: Monocytes isolated from wild type or microRNA-148a-/- BM were cultured with GM-CSF and IL-4, or not. Cells were collected at day 0 and day 3. Then, the next-generation libraries of mRNA were prepared using VAHTS mRNA-seq v2 Library Prep Kit for Illumina® (Vazyme, Nanjing, China). The Library quality was determined by Bioanalyzer 4200 (Agilent, Santa Clara, CA, USA). Then the mRNA-seq libraries were sequenced in HiSeq ⅹ10 system (Illumina, San Diego, CA, USA) on a 150bp paired-end run. The differentially expressed genes were selected as having more than 0.5 fold difference in their geometrical mean expression between the compared groups and a statistically significant p-value (<0.05) by analysis of DEseq2. The GO analysis on differentially expressed genes was performed with an R package: Clusterprofiler using a p<0.05 to define statistically enriched GO categories. Pathway analysis was used to determine the significant pathway of the differential genes according to Kyoto Encyclopedia of Genes and Genomes Database (http://www.genome.jp/kegg/) and DAVID Bioinformatics Resources 6.8 (https://david.ncifcrf.gov/). Results: Gene ontology analysis showed that obviously changed genes enriched in autoimmune disease related pathways, suggesting miR-148a is important in autoimmune responses. 990 protein-coding genes upregulated in their mRNA abundance in miR-148a-/- monocytes on day 0, and 1036 genes in miR-148a-/- monocytes on day 3. Among them, 136 genes were found upregulation on both day 0 and 3 in miR-148a-/- monocytes.
2019-12-23 | GSE142511 | GEO
Project description:A quantitative proteomics combined with stable isotope labeling was applied to identify the global profile of miR-148a-regulated downstream proteins in AGS cancer cells. For proteomic analysis, cells were treated with miR-148a mimic (Pre-miR-148a) or miR-148a negative control (miR-CTL) and the downstream protein expression level (Pre-miR-148a/miR-CTL) were quantified using iTRAQ approach. Bioinformatics pipeline: The peak list in the resultant MS/MS spectra were generated by Mascot Distiller v2.1.1.0 and searched using Mascot v2.2 against the International Protein Index (IPI) human database (v. 3.64, 84032 sequences). The Mascot search parameters were +-0.1 Da for MS tolerance, +-0.1 Da for MS/MS mass tolerance, allowances for two missed cleavages, and variable modifications of deamidation (NQ), oxidation (M), iTRAQ (N terminal), iTRAQ (K), and MMTS (C). Protein quantitation were calculated using the Multi-Q software v1.6.5.4 with a dynamic range filter of ion count > 30.
2013-07-24 | PXD000190 | Pride
Project description:Monocyte-derived DCs (moDCs) have been implicated in the pathogenesis of autoimmunity, but the molecular pathways determining the differentiation potential of these cells remain unclear. Here, we report that microRNA-148a (miR-148a) serves as a critical regulator for moDC differentiation. First, miR-148a deficiency impaired the moDC development in vitro and in vivo. A mechanism study showed that MAFB, a transcription factor that hampers moDC differentiation, was a direct target of miR-148a. In addition, a promoter study identified that miR-148a could be transcriptionally induced by PU.1, which is crucial for moDC generation. miR-148a ablation eliminated the inhibition of PU.1 on MAFB. Furthermore, we found that miR-148a increased in monocytes from patients with psoriasis, and miR-148a deficiency or intradermal injection of antagomir-148a immensely alleviated the development of psoriasis-like symptoms in a psoriasis-like mouse model. Therefore, these results identify a pivotal role for the PU.1-miR-148a-MAFB circuit in moDC differentiation and suggest a potential therapeutic avenue for autoimmunity.
| S-EPMC7205423 | biostudies-literature
Project description:Transcriptome analysis of five population of Antigen Presenting Cells: inflammatory macrophages, Inflammatory dendritic cells, Cd14+CD16- monocytes, CD14 dim Cd16+ monocytes and BDCA1+ Dendritic cells. We analyzed transcriptomic profiles from 5 differents DC populations: inflammatory DC and macrophages form inflammatory ascites (ovarian cancer, 4 different donors); CD14+CD16- monocytes, CD14dim CD16+ monocytes and BDCA1+ DC (from 3 different healthy donors) using the Affymetrix Human Gene 1.1 ST platform.
2012-11-01 | E-GEOD-40484 | biostudies-arrayexpress
Project description:Purpose: To investigate the regulatory role of microRNA (miR)-148a-3p in mouse corpus cavernous pericyte (MCPs)-derived extracellular vesicles (EVs) in the treatment of diabetes-induced erectile dysfunction (ED). Materials and Methods: Mouse corpus cavernous tissue was used for MCPs primary culture and EVs isolation. Small RNA sequencing analysis was performed to assess the type and content of miRs in MCPs-EVs. Four groups of mice were used: control nondiabetic mice and streptozotocin-induced diabetic mice receiving two intracavernous injections (days -3 and 0) of phosphate buffered saline, MCPs-EVs transfected with regent control, or MCPs-EVs transfected with miR-148a-3p inhibitor. The function of miR-148a-3p in MCPs-EVs was evaluated by tube formation assay, migration assay, TUNEL assay, intracavernous pressure, immunofluorescence staining, and western blot experiments. Results: We extracted EVs from MCPs and by small RNA sequencing analysis we found that miR-148a-3p is enriched in MCPs-EVs. Exogenous administration of MCPs-EVs can effectively promote mouse cavernous endothelial cell (MCECs) tube formation, migration, proliferation, and reduce MCECs apoptosis under high-glucose conditions. However, these effects are significantly attenuated in miR-148a-3p-depleted MCPs-EVs, which is extracted after inhibiting miR-148a-3p expression in MCPs. Repeated intracavernous injections of MCPs-EVs improves erectile function by inducing cavernous neurovascular regeneration in diabetic mice. Through online bioinformatics databases and luciferase report assays, we predict Pyruvate dehydrogenase kinase-4 (PDK4) is a potential target gene of miR-148a-3p. Conclusions: Our findings provide new and reliable evidence that miR-148a-3p in MCPs-EVs significantly enhances cavernous neurovascular regeneration by inhibiting PDK4 in diabetic mice.
2023-12-19 | GSE195533 | GEO
Project description:Transcriptome analysis of five population of Antigen Presenting Cells: inflammatory macrophages, Inflammatory dendritic cells, Cd14+CD16- monocytes, CD14 dim Cd16+ monocytes and BDCA1+ Dendritic cells.
2012-11-01 | GSE40484 | GEO
Project description:Cholangitis mouse models were characterised by selective intrahepatic expansion of type 2 conventional dendritic cells, whereas plasmacytoid and type 1 conventional dendritic cells were not expanded. Expansion of type 2 conventional dendritic cells in human PSC lesions was confirmed by histology. Depletion studies revealed a pro-inflammatory role of type 2 conventional dendritic cells. Single-cell transcriptomics confirmed inflammatory maturation of the intrahepatic type 2 conventional dendritic cells and identified dendritic cell-derived inflammatory mediators.
2022-07-08 | E-MTAB-11821 | biostudies-arrayexpress
Project description:Expression profiling of miR-32 or miR-148a transfected LNCaP cells.
2012-03-29 | E-MEXP-2943 | biostudies-arrayexpress
Project description:Long-lived antibody-secreting plasma cells are essential to establish humoral memory against pathogens. While a plasma cell gene signature has been established, elaborate key regulators remain enigmatic.The plasma cell signature microRNA miR-148a favors in vitro differentiation of plasmablasts by repressing the germinal center transcription factor Bach2 and pro-apoptotic BIM and PTEN. To determine whether miR-148a fine-tunescontrols the in vivo development of B cells into long-lived plasma cells, we established mice with a genomic, conditional and inducible deletion of miR-148a. The analysis of miR-148a-deficient mice revealed reduced serum Ig, decreased numbers of newly formed plasmablasts and a reduced CD19-negative, CD93-positive long-lived plasma cells compartment. RNASeq and metabolic analysis showed an impaired glucose uptake and oxidative phosphorylation-based energy metabolism, altered abundance of homing receptors CXCR3 (increase) and CXCR4 (reduction) in miR-148a-deficient plasma cells. These findings establish the importance of miR-148a as a regulator of the differentiation and maintenance of late CD19-negative mature plasma cells by controlling their metabolism and retention in the bone marrow niche. clearly undermine our model of miR-148a as a regulator of the maintenance of long-lived plasma cells.
2021-05-21 | GSE156002 | GEO