Versity, Hasselt, ADAMTS Like 4 Proteins Synonyms Belgium; 2Peripheral Neuropathy Group, VIB-Department of Molecular Genetics, HIV-1 gp160 Proteins Recombinant Proteins University of Antwerp, Antwerpen, Belgium; 3Biomedical analysis institute (BIOMED), Hasselt University, Hasselt, Belgium; 4Bionanotechnology group, Biomedical analysis institute (BIOMED), Hasselt University, Hasselt, Belgium; 5Neurofunctional genomics Group, Biomedical Study Institute (BIOMED), Hasselt University, Diepenbeek, BelgiumPF07.Exosomes and neuroinflammatory microRNAs: cytokine-specific profiles Ashley Russell1; Sujung Jun2; Sara Lewis1; Stephanie Rellick1; James Simpkins1 West Virginia University, Morgantown, WV, USA; University College of Medicine, Baltimore, MD, USAJohns HopkinsBackground: Proof suggests that exosomes take part in the spread of pathology by transferring misfolded proteins and aberrant microRNAs (miR) from diseased to healthier cells. Lots of neurodegenerative ailments are related with chronic neuroinflammation, characterized by improved levels of immunomodulatory molecules, including tumour necrosis factor-alpha (TNF-) and interferon-gamma (IFN-). Methods: We investigated the effects of those cytokines on exosome secretion, miR expression and mitochondrial function. We exposed a neuronal cell line to varying concentrations of TNF- or IFN- for 24 h, isolated exosomes and applied the NanoSight NS300 to figure out if enriched vesicles have been constant in size with exosomes after cytokine exposure. Using qRT-PCR we profiled the exosomal and intracellular levels of 3 miRs linked with neuroinflammation (miR-34a, -146a and -155), and also assessed mitochondrial function right after exposure to these cytokines straight or after exposing na e cells to exosomes isolated from the conditioned media of cytokine exposed cells. Ultimately, we performed Western blot analyses to figure out alterations in miR-34a mRNA target protein expression. Outcomes: Exposure to either cytokine substantially increased exosome secretion in comparison with handle. Exposure to TNF- induced a dosedependent raise in all three miRs, with variations in intracellular profiles (miR-34a unchanged, miR-145a and -155 considerably upregulated). Information suggest IFN- exposure induces various miR expression patterns than does TNF-. Exposure to either cytokine does not appear to induce mitochondrial dysfunction. Interestingly, exposing na e cells to isolated exosomes in the media of cytokine-exposed cells increases the respiratory capacity of mitochondria. Imaging studies confirm na e cells take up the exosomes.Background: Currently, the repair mechanisms of numerous sclerosis (MS) are nonetheless unknown. Having said that, it can be recognized that tiny heat-shock proteins (HSPBs), which have protective functions, are upregulated in MS lesions. During MS lesion development, HSPB1 and 8 are upregulated in astrocytes but downregulated in oligodendrocytes and microglia cells. In addition, it really is shown that mutations in HSPB1 and 8 bring about peripheral neurodegeneration. While the protective intracellular functions of HSPBs are identified, the extracellular functions are unclear. One way cells secrete HSPBs is by releasing extracellular vesicles (EV). We hypothesize that extracellular HSPBs exhibit neuroprotective roles that are altered upon inflammation in oligodendrocytes. Solutions: To determine the protective activity of intracellular and extracellular HSPBs in oligodendrocytes, we establish HSPB overexpressing cell-lines for the production and characterization of HSPB-positive EV below standard and.