Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227212 | ENA |
REPOSITORIES: ENA
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Project description:Human Peripheral blood mononuclear cells (PBMC) were isolated from healthy human whole blood by density gradient centrifugation using Histopaque®-1077 and cultured in RPMI (containing 10% FBS) with 10 ng/ml human recombinant GM-CSF at 37 °C for 7 days. These cells are confirmed as human macrophages. These macrophages were transfected with vector control, miR-466l,anti-miR-negative or anti-miR-466l (37 °C, 72h). After transfection, total RNA was extracted for reverse transcription. The product cDNA was collected for real-time PCR with respective primers. In the study presented here, lentiviral vector control (VC), miR-466l, anti-miR-negative (anti-miR-neg) or anti-miR-466l transfected human macrophages were used to acquire expression profiles of a total of 60 unique genes related to inflammation
2013-11-08 | E-GEOD-52174 | biostudies-arrayexpress
Project description:BACKGROUND: Obesity and diabetes are associated with elevated free fatty acids like palmitic acid (PA), which promote chronic inflammation and impaired inflammation resolution associated with cardiometabolic disorders. Long non-coding RNAs (lncRNAs) are implicated in inflammatory processes, however, their roles in PA-regulated inflammation and resolution are unclear. METHODS: We performed RNA-seq analysis to identify PA-regulated coding genes and novel lncRNAs in CD14+ monocytes from healthy volunteers. We investigated the regulation and function of an uncharacterized PA-induced lncRNA PARAIL (PA-regulated anti-inflammatory lncRNA). We examined its role in inflammation resolution employing knockdown and overexpression strategies in human and mouse macrophages. We also used RNA-pulldown coupled to mass spectrometry to identify PARAIL interacting nuclear proteins and their mechanistic involvement in PARAIL functions in human macrophages. RESULTS: Treatment of human CD14+ monocytes with PA induced several lncRNAs and genes associated with inflammatory phenotype. PA strongly induced lncRNA PARAIL expressed near RIPK2. PARAIL was also induced by cytokines and infectious agents in human monocytes/macrophages and was regulated by NF-kB. Time course studies showed PARAIL was induced during inflammation resolution phase in PA treated macrophages. Knockdown of PARAIL with antisense oligonucleotides upregulated key inflammatory genes and vice versa with PARAIL overexpression. We found that PARAIL interacts with Human Antigen R (HuR) protein via AU-rich elements (AREs). HuR knockdown inhibited the anti-inflammatory functions of PARAIL. Moreover, PARAIL knockdown increased cytosolic localization of HuR and increased the stability of ARE-containing inflammatory mRNAs. Mouse orthologous Parail was downregulated in macrophages from mice with diabetes and atherosclerosis. Parail overexpression attenuated pro-inflammatory genes in mouse macrophages. CONCLUSIONS: Upregulation of PARAIL under acute inflammatory conditions contributes to pro-resolution mechanisms via PARAIL-HuR interactions. Conversely, PARAIL downregulation in cardiometabolic diseases enhances HuR function and impairs inflammation resolution to further augment inflammation. Thus, inflammation-resolving lncRNAs like PARAIL represent novel tools to combat inflammatory cardiometabolic diseases.
2024-09-25 | GSE214160 | GEO
Project description:Gene expression profile upon miR-10b overexpression or knockdown
| PRJNA173052 | ENA
Project description:Chronic obstructive pulmonary disease (COPD) is a highly prevalent respiratory disease characterized by airflow limitation and chronic inflammation. MiR-155 is described as an ancient regulator of the immune system. Our objective was to establish a role for miR-155 in cigarette smoke (CS)-induced inflammation and COPD. We demonstrate increased miR-155 expression by RT-qPCR in lung tissue of smokers without airflow limitation and patients with COPD compared to never smokers and in lung tissue and alveolar macrophages of CS-exposed mice compared to air-exposed mice. In addition, we exposed wild type and miR-155 deficient mice to CS and show an attenuated inflammatory profile in the latter. Alveolar macrophages were sorted by FACS from the different experimental groups and their gene expression profile was analyzed by RNA sequencing. This analysis revealed increased expression of miR-155 targets (including the NF-κB inhibitor rassf6) and an attenuation of the CS-induced increase in inflammation-related genes in miR-155 deficient mice. Finally, intranasal instillation of a specific miR-155 inhibitor significantly attenuated the CS-induced pulmonary inflammation in mice. In conclusion, we highlight a role for miR-155 in CS-induced inflammation and the pathogenesis of COPD, implicating miR-155 as a new therapeutic target in COPD.
2019-12-16 | GSE137653 | GEO
Project description:Extracellular vesicles derived from induced pluripotent stem cells (iPSC EVs) have immunoregulatory potential with the ability to alter monocyte-derived macrophages. Macrophages function in the propagation and resolution of inflammation which is mediated by their phenotype. Macrophages are an ideal therapeutic target as modulating their phenotype towards an anti-inflammatory pro-resolving state may be beneficial in chronic inflammatory diseases such as atherosclerosis. Macrophages are naturally phagocytotic cells and readily take up iPSC EVs however the contents of iPSC EVs and their effects on macrophages are poorly understood. Here iPSC EVs were characterized and analysed by mass-spectrometry based proteomics and a targeted microRNA (miR) panel. Their immunomodulatory effects on macrophages were assessed and a monocyte transmigration assay was used to assess the chemotactic potency of the secretome from iPSC EV treated macrophages. Proteomic analysis on iPSC EVs identified Podocalyxin-like protein 1 (PODXL1), Insulin (INS) and Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) as the most abundant proteins unique to the iPSC EVs when compared to control NT-2 EVs. Notably, thioredoxin and peroxiredoxin related proteins were detected. miR-302d-3p was the most abundant miR in these iPSC EVs. miR-25-3p, previously reported to alter the macrophage phenotype, was significantly increased in comparison to the control NT-2 EVs. iPSC EVs increased expression of the anti-inflammatory associated MRC1 and miR-21 in human primary macrophages and decreased monocyte chemoattractant protein1 (MCP-1). Mass spectrometry based proteomics revealed that treated macrophages had decreased levels of secretory proteins, some of which have chemotactic properties, these included Azurocidin 1 (AZU1), Growth Differentiation Factor 15 (GDF15), and Ribosomal Protein S19 (RPS19). There was a decrease in monocyte transmigration towards conditioned media from macrophages treated with iPSC EVs. Collectively this study provides insights into the protein content and miR cargo of iPSC EVs and highlights their capacity to inhibit chemotactic proteins in macrophages and upregulate MRC1.
2025-09-08 | PXD067567 | Pride
Project description:Extracellular vesicles derived from induced pluripotent stem cells (iPSC EVs) have immunoregulatory potential with the ability to alter monocyte-derived macrophages. Macrophages function in the propagation and resolution of inflammation which is mediated by their phenotype. Macrophages are an ideal therapeutic target as modulating their phenotype towards an anti-inflammatory pro-resolving state may be beneficial in chronic inflammatory diseases such as atherosclerosis. Macrophages are naturally phagocytotic cells and readily take up iPSC EVs however the contents of iPSC EVs and their effects on macrophages are poorly understood. Here iPSC EVs were characterized and analysed by mass-spectrometry based proteomics and a targeted microRNA (miR) panel. Their immunomodulatory effects on macrophages were assessed and a monocyte transmigration assay was used to assess the chemotactic potency of the secretome from iPSC EV treated macrophages. Proteomic analysis on iPSC EVs identified Podocalyxin-like protein 1 (PODXL1), Insulin (INS) and Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 3 (SLC2A3) as the most abundant proteins unique to the iPSC EVs when compared to control NT-2 EVs. Notably, thioredoxin and peroxiredoxin related proteins were detected. miR-302d-3p was the most abundant miR in these iPSC EVs. miR-25-3p, previously reported to alter the macrophage phenotype, was significantly increased in comparison to the control NT-2 EVs. iPSC EVs increased expression of the anti-inflammatory associated MRC1 and miR-21 in human primary macrophages and decreased monocyte chemoattractant protein1 (MCP-1). Mass spectrometry based proteomics revealed that treated macrophages had decreased levels of secretory proteins, some of which have chemotactic properties, these included Azurocidin 1 (AZU1), Growth Differentiation Factor 15 (GDF15), and Ribosomal Protein S19 (RPS19). There was a decrease in monocyte transmigration towards conditioned media from macrophages treated with iPSC EVs. Collectively this study provides insights into the protein content and miR cargo of iPSC EVs and highlights their capacity to inhibit chemotactic proteins in macrophages and upregulate MRC1.
2025-09-08 | PXD067612 | Pride
Project description:To profile gene expression in human HeLa cells follwing the knockdown of miR-574-5p, as compared to control HeLa cells Gene ontology and clustering analyses revealed that the differentially-expressed genes were highly enriched for the immune system and its related signal transduction pathways.
2023-07-04 | GSE235926 | GEO
Project description:From a previous microarray study we developed a small chondrogenesis model. We performed qPCR and measured how knockdown of miR-199a-5p or miR-199b-5p could modulate chondrogenesis. Several experiments were used to determine the parameters of this model. We utilised parameter scan and manual sliding to refine the model. Within are two models - an initial model which only comprises of genes which we have data for, and an enhanced model which expands of the initial model to make more predictions - e.g. how miR-140-5p is indirectly regulated by miR-199a-5p and miR-199b-5p.
2023-06-06 | MODEL2305010001 | BioModels
Project description:miR-490 is robustly downregulated in GBM tumour samples. This study identifies the genes differentially expressed upon miR-490 overexpression in U87MG glioblastoma cell line. GeneChip PrimeView Human Gene Expression Array was used to assess mRNA expression profile in response to miR-490 overexpression in U87MG cell line.
2018-08-24 | GSE118983 | GEO
Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride