Ol levels and promoted lung epithelial cell differentiation in lung organoids (enhanced SPC and CC10 expression). AFSC-EVs include 901 microRNAs, a few of which are important for foetal lung development, including 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 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 improvement, also called pulmonary hypoplasia (PH), can be a recognized reason for neonatal death. To date, there is absolutely no successful remedy that promotes foetal lung growth and maturation. Herein, we describe a stem cell-based method 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 FCGR2A/CD32a Proteins manufacturer 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 CD40 Proteins supplier non-alcoholic steatohepatitis is usually a important problem in non-alcoholic fatty liver illness (NAFLD). Current observations in individuals with obstructive sleep apnoea syndrome (OSAS), suggest that hypoxia could contribute to illness progression mainly by means of activation of hypoxia inducible aspect 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes might be involved in NAFLD progression. Aim: to discover whether hypoxia modulates the release of EV from free fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk between hepatocytes and LX-2 cells (human hepatic stellate cell line). Methods: HepG2 cells have 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 had been treated with 15 g/ml of EV from hepatocytes obtained from unique groups and markers of pro-fibrogenic signalling had been determined by quantitative PCR (qPCR), WB and immunofluorescence (IF). Benefits: FFA and CH-treatment of HepG2 cells increased gene expression of IL-1 and TGF-1 in HepG2 cells and increased the release of EV when compared with non-treated HepG2 cells. Therapy of LX-2 cells with EV from FFA-treated hypoxic HepG2 cells improved 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 enhanced Collagen1A1 and -SMA protein.