Project description:Exosomes research has been strongly promoted by the discovery of different classes of RNAs, mainly miRNAs, which are transfered to target cells and modulate various simgnaling pathways in target cells. Inflamed endothelial cells derived exosomes, acting as carriers for intercellular information exchange in atherosclerosis, are worthy of further research to investigate the disease pathophysiological mechanisms. This study aimed to investigate the differentially microRNA expression between normal and inflamed endothelial cells derived exosomes.
Project description:This SuperSeries is composed of the following subset Series: GSE35387: Expression data from normal melanocyte, melanoma cells and their exosomes (microRNA) GSE35388: Expression data from normal melanocyte, melanoma cells and their exosomes (mRNA) Refer to individual Series
Project description:microRNA profiles of Exosomes from Pooled NPC Patients serum comparing Control Exosomes from Healthy donors serum Two-condition experiment, Exosomes from Pooled Healthy donors serum vs. Exosomes from Pooled NPC Patients serum. Biological replicates: 1 Exosomes from Pooled Healthy donors serum, 1 Exosomes from Pooled NPC Patients serum,
Project description:Signalling between endothelial cells, endothelial progenitor cells and stromal cells is crucial for the establishment and maintenance of vascular integrity and involves exosomes, among other signalling pathways. Exosomes are important mediators of intercellular communication in immune signalling, tumour survival, stress responses and angiogenesis. The ability of exosomes to incorporate and transfer mRNAs encoding for ‘acquired’ proteins or miRNAs repressing ‘resident’ mRNA translation suggests that they can influence the physiological behaviour of recipient cells. We here demonstrate that miR-214, a miRNA that controls endothelial cell function and angiogenesis, plays a dominant role in exosome-mediated signalling between endothelial cells. Endothelial cell-derived exosomes stimulated migration and angiogenesis in recipient cells, whereas exosomes from miR-214 depleted endothelial cells failed to stimulate these processes. Exosomes containing miR-214 repressed the expression of Ataxia Telangiectasia Mutated in recipient cells, thereby preventing senescence and allowing blood vessel formation. Concordantly, specific reduction of miR-214 content in exosome-producing endothelial cells abolishes the angiogenesis the angiogenesis stimulatory function of the resulting exosomes. Collectively our data indicate that endothelial cells release miR-214 containing exosomes to stimulate angiogenesis through silencing of Ataxia Telangiectasia Mutated in neighbouring target cells. Gene expression analysis of HMEC endothelial cells exposed to supernatant containing either HMEC derived exosomes (miR-214 high), HMEC derived exosomes depleted of miR-214 (miR-214 low) or containing no exosomes (no exosomes). Each sample was analysed in duplo.
Project description:Brain microvascular endothelial cell (BMEC) injury can affect neuronal survival by modulating immune responses through the microenvironment. We used microarrays to detail the miRNAs expression in the exosomes from normal and oxygen glucose deprivation (OGD)-cultured BMECs.
Project description:microRNA profiles of exosomes :Exosomes from two nasopharyngeal carcinoma cell line TW03M-oM-<M-^HEBV+M-oM-<M-^Iand TW03M-oM-<M-^HEBV-M-oM-<M-^I and Exosomes from nasopharyngeal epithelial cells NP69 Two-condition experiment, Exosomes from two nasopharyngeal carcinoma cell line vs.one normal epithelium cell line. Biological replicates:1 Exosomes from nasopharyngeal carcinoma cell line TW03M-oM-<M-^HEBV+M-oM-<M-^I, 1 Exosomes from nasopharyngeal carcinoma cell line TW03M-oM-<M-^HEBV-M-oM-<M-^I,1 Exosomes from nasopharyngeal epithelial cells NP69.
Project description:The goal of this study is to report that breast cancer associated exosomes contain microRNAs (miRNAs) associated with the RISC Loading Complex (RLC) and display cell-independent capacity to process precursor microRNAs (pre-miRNAs) into mature miRNAs. Pre-miRNAs, along with Dicer, AGO2, and TRBP, are present in exosomes of cancer cells. CD43 mediates the accumulation of Dicer specifically in cancer exosomes. Cancer exosomes mediate an efficient and rapid silencing of mRNAs to reprogram the target cell transcriptome. Exosomes derived from cells and sera of patients with breast cancer instigate non-tumorigenic epithelial cells to form tumors in a Dicer-dependent manner. These findings offer opportunities for the development of exosomes based biomarkers and therapies. Exosomes from cancer cells and non-tumorigenic cells were isolated using established ultracentrifugation methods. The global miRNA content of cancer exosomes and normosomes was investigated. Profiling of cells themselves was also used as a control. Exosomes with Dicer down regulation (MCF10AshDicer and MDA-MB-231shDicer exosomes), as well as MDA-MB-231 exosomes that contain a Dicer antibody inside were used to study the function Dicer protein in the microRNA biogenesis in exosomes.
Project description:Signalling between endothelial cells, endothelial progenitor cells and stromal cells is crucial for the establishment and maintenance of vascular integrity and involves exosomes, among other signalling pathways. Exosomes are important mediators of intercellular communication in immune signalling, tumour survival, stress responses and angiogenesis. The ability of exosomes to incorporate and transfer mRNAs encoding for ‘acquired’ proteins or miRNAs repressing ‘resident’ mRNA translation suggests that they can influence the physiological behaviour of recipient cells. We here demonstrate that miR-214, a miRNA that controls endothelial cell function and angiogenesis, plays a dominant role in exosome-mediated signalling between endothelial cells. Endothelial cell-derived exosomes stimulated migration and angiogenesis in recipient cells, whereas exosomes from miR-214 depleted endothelial cells failed to stimulate these processes. Exosomes containing miR-214 repressed the expression of Ataxia Telangiectasia Mutated in recipient cells, thereby preventing senescence and allowing blood vessel formation. Concordantly, specific reduction of miR-214 content in exosome-producing endothelial cells abolishes the angiogenesis the angiogenesis stimulatory function of the resulting exosomes. Collectively our data indicate that endothelial cells release miR-214 containing exosomes to stimulate angiogenesis through silencing of Ataxia Telangiectasia Mutated in neighbouring target cells.