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.
Project description:EVs were isolated from primary human aortic endothelial cells (ECs) (+/- IL-1b activation) grown on transwells, quantified, and analysed by miRNA transcriptomics.
Project description:EVs were isolated from primary human aortic endothelial cells (ECs) (+/- IL-1b activation), quantified, and analysed by miRNA transcriptomics and proteomics.
Project description:Metastasis, the spread of malignant cells from the primary tumour to distant sites is in 90% of the cases, the ultimate cause cancer related death. The integrin ITGB3 has been previously described to play an essential role in breast cancer metastasis, but the precise mechanisms remain undefined. We have now uncovered essential and thus far unknown roles of ITGB3 in vesicle uptake and exosome biogenesis. The functional requirement on ITGB3 is founded in its described interactions with heparan sulphated glyco-proteins (HSPGs) and the process of integrin recycling, allowing the capture of extracellular vesicles and their endocytosis-mediated internalisation. Key for the function of ITGB3 is the interaction and activation of the focal adhesion kinase (FAK), which is required for endocytosis of this vesicles and the entry of the endocytosis derived early endosomes into the exosome biogenesis pathway. Thus, ITGB3 has a central role in intracellular communication via extracellular vesicles, proposed to be critical for cancer metastasis.