Ol levels and promoted lung epithelial cell differentiation in lung organoids (improved SPC and CC10 expression). AFSC-EVs include 901 microRNAs, a number of which are crucial for IgA Proteins site foetal lung development, such as miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs rescues impaired foetal lung SIRP alpha/CD172a Proteins Species development in experimental models of PH. AFSC-EV regenerative potential is exerted through the release of miRNAs a few of which regulate genes involved in foetal lung improvement. AFSC-EVs represent a promising therapeutic strategy 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 Moshagee and Marco ArresedIntroduction: Incomplete lung development, also called pulmonary hypoplasia (PH), is a recognized cause of neonatal death. To date, there isn’t any helpful treatment that promotes foetal lung development and maturation. Herein, we describe a stem cell-based strategy that enhances foetalJOURNAL OF EXTRACELLULAR VESICLESa Pontificia Universidad Cat ica de Chile; University Medical 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 Healthcare Center Groningen, Groningen, NetherlandsOWP1.07=PS08.Exploration on the surface modification of outer membrane vesicles Maximilian Richtera, Eleonora Diamantib, Anna Hirschb, Gregor FuhrmanncaIntroduction/Background: Transition from isolated steatosis to non-alcoholic steatohepatitis is a crucial issue in non-alcoholic fatty liver illness (NAFLD). Current observations in individuals with obstructive sleep apnoea syndrome (OSAS), recommend that hypoxia might contribute to disease progression primarily through activation of hypoxia inducible element 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes might be involved in NAFLD progression. Aim: to explore no matter whether hypoxia modulates the release of EV from free of charge fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk amongst hepatocytes and LX-2 cells (human hepatic stellate cell line). Methods: HepG2 cells were treated with FFAs (250 M palmitic acid + 500 M oleic acid) and chemical hypoxia (CH) was induced with Cobalt (II) Chloride, that is 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 analysis respectively. EV characterization was performed by electron microscopy and WB of CD-81 marker. LX-2 cells had been treated with 15 g/ml of EV from hepatocytes obtained from different 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 increased the release of EV in comparison to non-treated HepG2 cells. Remedy of LX-2 cells with EV from FFA-treated hypoxic HepG2 cells enhanced gene expression of TGF-1, CTGF, -SMA and Collagen1A1 in comparison 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. Furthermore, EV from FFA-treated hypoxic HepG2 cells increased Collagen1A1 and -SMA protein.