Directional endothelial communication by polarized extracellular vesicle release
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE230246 | GEO | 2024/01/02
REPOSITORIES: GEO
Similar Datasets
Project description:EVs were isolated from primary human aortic endothelial cells (ECs) (+/- IL-1b activation) grown on transwells, quantified, and analysed by miRNA transcriptomics.
2024-01-02 | GSE230289 | GEO
Project description:EVs were isolated from primary human aortic endothelial cells (ECs) (+/- IL-1b activation), quantified, and analysed by miRNA transcriptomics and proteomics. Compared to quiescent ECs, activated ECs increased EV release, with miRNA and protein cargo that were related to atherosclerosis pathways. RNA sequencing of EV-treated monocytes and vascular smooth muscle cells (VSMCs) revealed that EVs from activated ECs altered pathways that were pro-inflammatory and atherogenic.
2024-01-02 | GSE231715 | GEO
Project description:Small extracellular vesicles (EVs) are released by cells and deliver biologically active payloads important in the intercellular signaling that coordinates the response of multiple cell types in cutaneous wound healing. Here we focus on the use of EV reporters to address cell type specificity and central questions regarding EV source cells, target cells, heterogeneity, payload, and activity using a combination of molecular approaches to address some of the barriers to translation in the use of engineered EVs. We identify a role for EVs released by resident macrophages present in adipose tissue and dermis to stimulate proliferation of overlying basal layer of keratinocytes. For these studies we use an allograft model, where donor EVs are harvested from subcutaneous implants, then purified for transplantation into the wound bed of recipient mice with a defined impaired wound healing phenotype. We demonstrate that EVs isolated from diabetic obese mice decreased keratinocyte proliferation and delayed wound closure, and that EVs loaded with specific miRNAs like miR-425-5p increased proliferation and accelerated wound closure. Utilizing a CD9-GFP reporter system, we show that fibroblasts uptake macrophage-derived EVs. In this work, we show that cell type-specific approaches can be used to unravel the biochemical activity of EVs in the complex microenvironment of the wound bed and form the basis for developing targeted pro-reparative EV payloads.
2024-02-16 | GSE242497 | GEO
Project description:Comparative RNA profiling between tumor cells and their secreted extracellular vesicles. Results revealed enrichment in genes involved in cellular migration and metastasis in extracellular vesicles, in agreement with their role as mediators of tumor progression. Mice were orthotoplically transplanted with MDA-MB-231 Breast Adenocarcinoma cells. Cells and extracellular vesicles (EVs) from the resulting tumors were isolated. EVs were characterized by electron microscopy and Nanoparticle Tracking Analysis before total RNA isolation for comparative analysis with cellular RNA. Three biological replicates were analyzed in (technical) duplicate.
2015-03-05 | E-GEOD-66488 | biostudies-arrayexpress
Project description:The nematode Caenorhabditis elegans has evolutionarily conserved EV signaling pathways. In this study, we apply a recently published method for high specificity purification of EVs from C. elegans to carry out target-independent proteomic and RNA analysis of EVs from C. elegans. Our experiments uncovered diverse coding and non-coding RNA transcripts as well as protein cargo types commonly found in human EVs.
2020-08-05 | GSE146973 | GEO
Project description:Extracellular vesicles (EVs) are involved in intercellular communication in health and disease and affect processes including immune and antiviral responses. We have previously demonstrated that ultracentrifuged serum is depleted of EVs and, when used in cell culture media, is associated with declines in growth and viability of numerous cultured cell types. Although EVs had been reported to enhance or interfere with HIV-1 infection, depending on the setting, the effects of EVs on HIV-1 production and infectivity of released virions were unknown. In this study, we examined the effects of EV-depleted serum on HIV-1 replication in primary cells and cell lines, including two HIV-1 latency models. Cell culture media were prepared with EV-replete fetal bovine serum (FBS) or serum depleted of EVs via ultracentrifugation or a proprietary method (ThermoFisher/Gibco). T-cell and myeloid-lineage cell lines, including ACH-2 and U1 HIV-1 latency models, and primary cells were grown in 10% FBS-based culture media. Cell counts, viability, and proliferation were assessed throughout. HIV-1 production and infectivity were measured by p24 ELISA and luciferase reporter cell lines, respectively. Flow cytometry, Seahorse assays, and miRNA and mRNA expression arrays were done to assess cellular responses to EV-depleted conditions. Significant increases in HIV-1 production were observed in EV-depleted conditions, along with, in some cases, morphology changes and decreased cell viability. Add-back of pelleted EVs reduced HIV-1 production almost to baseline. Primary cells appeared to be less susceptible to EV depletion. ACH-2 and U1 latency models also produced more HIV-1 under EV-depleted conditions. Virus produced under EV-depleted conditions was more infectious. Changes in cellular metabolism and gene expression were associated with EV-depleted culture. The EV environment of HIV-1 infected cells appears to have a significant effect on virus production and infectivity. In cell lines of HIV-latency, significantly higher concentrations of p24 were observed in those cells cultured in EVD conditions. EV-dependence of cell cultures should be examined carefully prior to examining additional experimental variables. However, we also sound a cautionary note that direct actions of EVs may be accompanied by the effects of other, closely associated factors.
2016-10-23 | GSE89067 | GEO
Project description:Osteolineage cell-derived extracellular vesicles (EVs) play a regulatory role in hematopoiesis and have been shown to promote the ex vivo expansion of human hematopoietic stem and progenitor cells (HSPCs). Here, we demonstrate that EVs from different human osteolineage sources do not have the same HSPC expansion promoting potential. Comparison of stimulatory and non-stimulatory osteolineage EVs by next-generation sequencing and mass spectrometry analyses revealed distinct microRNA (miRNA) and protein signatures identifying EV-derived candidate regulators of ex vivo HSPC expansion. Accordingly, the treatment of umbilical cord blood-derived CD34+ HSPCs with stimulatory EVs altered HSPC transcriptome, including genes with known roles in cell proliferation. An integrative bioinformatics approach, which connects the HSPC gene expression data with the candidate cargo in stimulatory EVs, delineated the potentially targeted biological functions and pathways during hematopoietic cell expansion and development. In conclusion, our study gives novel insights into the complex biological role of EVs in osteolineage cell-HSPC crosstalk and promotes the utility of EVs and their cargo as therapeutic agents in regenerative medicine.
2020-03-01 | GSE143613 | GEO
Project description:Liver fibrosis is characterized by the activation of hepatic stellate cells (HSCs) and the release of fibrogenic nano-sized extracellular vesicles (EVs). Activated HSCs increase their glucose metabolism via glycolysis to satisfy high energy demands. Nevertheless, the mechanism of how glycolysis in HSCs coordinates fibrosis amplification in the fibrogenic zones in the liver is elusive and is the scope of this study. Single cell RNA sequencing (scRNAseq) and bulk RNAseq demonstrated that several glycolysis enzymes, including hexokinase 2 (HK2), were upregulated in activated HSCs. HSC-selective glycolysis-deficient mice (HK2ΔHSC) showed abrogated CCl4-mediated fibrosis as compared to littermate controls (HK2fl/fl). Spatial transcriptomics revealed an upregulation of several EV-related pathways in the fibrotic pericentral zone during liver fibrosis in control HK2fl/fl mice. However, glycolysis-deficient HK2ΔHSC mice showed downregulation of these EV-related pathways in the pericentral zone. Consistently, induction of glycolysis in HSCs in vitro, either by glucose or platelet-derived growth factor B (PDGF), upregulated the expression of several extracellular vesicle (EV)-related genes, including RAB31. Glycolysis in HSCs epigenetically enhanced RAB31 expression through histone-3 lysine-9 acetylation (H3K9ac) on the promoter region, leading to increased EV release. Functionally, glycolysis-dependent EVs were enriched with fibrogenic molecules and increased the expression of fibrotic markers in recipient HSCs. Finally, EVs derived from glycolysis-deficient HK2ΔHSC mice abrogated liver fibrosis amplification as compared to EVs derived from littermate control HK2fl/fl mice. In summary, glycolysis in HSCs amplifies liver fibrosis by promoting fibrogenic EV release in the pericentral fibrotic regions in the liver.
2024-03-20 | GSE259363 | GEO
Project description:The coding transcriptomes of filamentous cultures of the maize smut fungus Ustilago maydis and their extracellular vesicles (EVs) were compared. Protein-coding transcripts relatively enriched in EVs versus filament cells were identified and examined to identify potentially functional mRNA cargos of U. maydis EVs.
2021-06-08 | GSE176292 | GEO
Project description:Given that different diets could alter cow milk yield and composition, the effects of different feed formula on milk extracellular vesicle (EV) miRNAs were detected. Cow milk EVs contained various small RNAs, including miRNAs, snRNAs, tiRNAs, Cis-regulatory elements, and piRNAs. Two hundred and seventy-six known bos taurus miRNAs were identified by sequencing in bovine milk EVs. There were 13 immune-related miRNAs in the top 20 miRNAs in milk EVs. Nine differently expressed known miRNAs were detected in responding to different feed formulations. Cow milk EVs are abundant of small RNAs, especially miRNAs, which might be closely related to the development of maternal mammary gland and neonatal immune maturity.
2019-12-17 | GSE142145 | GEO