Versity, Hasselt, Belgium; 2Peripheral Neuropathy Group, VIB-Department of Molecular Genetics, University of Antwerp, Antwerpen, Belgium; 3Biomedical study institute (BIOMED), Hasselt University, Hasselt, Belgium; 4Bionanotechnology group, Biomedical analysis institute (BIOMED), Hasselt University, Hasselt, Belgium; 5Neurofunctional genomics Group, Biomedical Investigation 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 participate in the spread of pathology by transferring misfolded proteins and aberrant microRNAs (miR) from diseased to wholesome cells. Several neurodegenerative diseases are connected with chronic neuroinflammation, characterized by improved UCH Proteins Biological Activity expression and mitochondrial function. We exposed a neuronal cell line to varying concentrations of TNF- or IFN- for 24 h, isolated exosomes and used the NanoSight NS300 to identify if enriched vesicles had been constant in size with exosomes right after cytokine exposure. Making use of qRT-PCR we profiled the exosomal and intracellular levels of 3 miRs associated with neuroinflammation (miR-34a, -146a and -155), and also assessed mitochondrial function just after exposure to these cytokines directly or immediately after exposing na e cells to exosomes isolated from the conditioned media of cytokine exposed cells. Lastly, we performed Western blot analyses to determine adjustments in miR-34a mRNA target protein expression. Benefits: Exposure to either cytokine substantially increased exosome secretion when compared with control. Exposure to TNF- induced a dosedependent raise in all three miRs, with differences in intracellular profiles (miR-34a unchanged, miR-145a and -155 significantly upregulated). Data recommend IFN- exposure induces distinctive 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 from the media of cytokine-exposed cells increases the respiratory capacity of mitochondria. Imaging research confirm na e cells take up the exosomes.Background: At present, the repair mechanisms of numerous sclerosis (MS) are still unknown. Having said that, it is recognized that modest heat-shock proteins (HSPBs), which have protective functions, are upregulated in MS lesions. Throughout MS lesion improvement, HSPB1 and eight are upregulated in astrocytes but downregulated in oligodendrocytes and microglia cells. Additionally, it is actually shown that mutations in HSPB1 and eight lead to peripheral neurodegeneration. Despite the fact that 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. Procedures: 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 beneath standard and.