Ol levels and promoted lung epithelial cell differentiation in lung organoids (elevated SPC and CC10 expression). AFSC-EVs include 901 microRNAs, a number of that are critical for foetal lung improvement, for example miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs rescues impaired foetal lung improvement in experimental models of PH. AFSC-EV regenerative capability is exerted by way of the release of miRNAs a number of which regulate genes involved in foetal lung development. AFSC-EVs represent a promising therapeutic technique for PH in foetuses. Funding: CIHR-SickKids Foundation.OWP1.06=PS01.Extracellular vesicles from Fat-laden hypoxic hepatocytes activates pro-fibrogenic signals in Hepatic Stellate Cells Alejandra Hernandeza, Yana Gengb, Daniel Cabrerac, Nancy Solisd, Han CD10/Neprilysin Proteins manufacturer Moshagee and Marco ArresedIntroduction: Incomplete lung improvement, also known as pulmonary hypoplasia (PH), is usually a recognized cause of neonatal death. To date, there’s no helpful therapy that promotes foetal lung development and maturation. Herein, we describe a stem cell-based method that enhances foetalJOURNAL OF EXTRACELLULAR VESICLESa Pontificia Universidad Cat ica de Chile; University Health-related Center of Groningen, Groningen, Netherlands; bUMCG, Groningen, Netherlands; c Pontificia Universidad Cat ica de Chile/Universidad Bernardo O iggins, SANTIAGO, Chile; dPontificia Universidad Cat ica de Chile, Santiago, Chile; eUniversity Health-related Center Groningen, Groningen, NetherlandsOWP1.07=PS08.Exploration from the surface modification of outer membrane vesicles Maximilian CD93 Proteins Biological Activity Richtera, Eleonora Diamantib, Anna Hirschb, Gregor FuhrmanncaIntroduction/Background: Transition from isolated steatosis to non-alcoholic steatohepatitis is usually a key problem in non-alcoholic fatty liver disease (NAFLD). Recent observations in sufferers with obstructive sleep apnoea syndrome (OSAS), recommend that hypoxia may contribute to disease progression primarily by way of activation of hypoxia inducible aspect 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes may be involved in NAFLD progression. Aim: to explore irrespective of whether hypoxia modulates the release of EV from free fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk among hepatocytes and LX-2 cells (human hepatic stellate cell line). Approaches: HepG2 cells had been treated with FFAs (250 M palmitic acid + 500 M oleic acid) and chemical hypoxia (CH) was induced with Cobalt (II) Chloride, which can be an inducer of HIF-1. Induction of CH was confirmed by Western blot (WB) of HIF-1. EV isolation and quantification was performed by ultracentrifugation and nanoparticle tracking evaluation respectively. EV characterization was performed by electron microscopy and WB of CD-81 marker. LX-2 cells have been treated with 15 g/ml of EV from hepatocytes obtained from distinctive groups and markers of pro-fibrogenic signalling have been determined by quantitative PCR (qPCR), WB and immunofluorescence (IF). Final results: FFA and CH-treatment of HepG2 cells improved gene expression of IL-1 and TGF-1 in HepG2 cells and improved the release of EV in comparison to non-treated HepG2 cells. Remedy of LX-2 cells with EV from FFA-treated hypoxic HepG2 cells elevated gene expression of TGF-1, CTGF, -SMA and Collagen1A1 when compared with LX-2 cells treated with EV from non-treated hepatocytes or LX-2 cells exposed to EV-free supernatant from FFA-treated hypoxic HepG2 cells. Additionally, EV from FFA-treated hypoxic HepG2 cells enhanced Collagen1A1 and -SMA protein.