Ol levels and promoted lung epithelial cell differentiation in lung organoids (increased SPC and CC10 expression). AFSC-EVs include 901 microRNAs, some of which are important for SphK2 drug foetal lung development, including miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs rescues impaired foetal lung development in experimental models of PH. AFSC-EV regenerative ability is exerted by means of the release of miRNAs a few of which regulate genes involved in foetal lung development. AFSC-EVs represent a promising therapeutic method for PH in foetuses. Funding: CIHR-SickKids Foundation.OWP1.06=PS01.Extracellular vesicles from Fat-laden hypoxic XIAP MedChemExpress 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 known as pulmonary hypoplasia (PH), can be a recognized reason for neonatal death. To date, there’s no productive treatment that promotes foetal lung growth and maturation. Herein, we describe a stem cell-based approach 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 Medical Center Groningen, Groningen, NetherlandsOWP1.07=PS08.Exploration from the surface modification of outer membrane vesicles Maximilian Richtera, Eleonora Diamantib, Anna Hirschb, Gregor FuhrmanncaIntroduction/Background: Transition from isolated steatosis to non-alcoholic steatohepatitis can be a key concern in non-alcoholic fatty liver illness (NAFLD). Current observations in sufferers with obstructive sleep apnoea syndrome (OSAS), recommend that hypoxia may contribute to illness progression primarily by way of activation of hypoxia inducible issue 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes may perhaps be involved in NAFLD progression. Aim: to explore no matter if 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). Solutions: 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, 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 were treated with 15 g/ml of EV from hepatocytes obtained from various groups and markers of pro-fibrogenic signalling were determined by quantitative PCR (qPCR), WB and immunofluorescence (IF). Outcomes: FFA and CH-treatment of HepG2 cells increased gene expression of IL-1 and TGF-1 in HepG2 cells and enhanced the release of EV compared 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 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. Moreover, EV from FFA-treated hypoxic HepG2 cells elevated Collagen1A1 and -SMA protein.