Ol levels and promoted lung epithelial cell differentiation in lung organoids (increased SPC and CC10 expression). AFSC-EVs contain 901 microRNAs, some of which are important for foetal lung improvement, for instance miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs CD28 Proteins Species rescues impaired foetal lung development in experimental models of PH. AFSC-EV regenerative potential is exerted through the release of miRNAs a number of which regulate genes involved in foetal lung development. AFSC-EVs represent a promising therapeutic strategy for PH in foetuses. Funding: CIHR-SickKids Foundation.OWP1.06=PS01.CD185/CXCR5 Proteins Formulation 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 referred to as pulmonary hypoplasia (PH), is usually a recognized reason for neonatal death. To date, there is no effective remedy 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 in 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 key challenge in non-alcoholic fatty liver illness (NAFLD). Recent observations in individuals with obstructive sleep apnoea syndrome (OSAS), recommend that hypoxia may contribute to illness progression mainly by way of activation of hypoxia inducible issue 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes could be involved in NAFLD progression. Aim: to explore whether hypoxia modulates the release of EV from no cost fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk in between hepatocytes and LX-2 cells (human hepatic stellate cell line). Techniques: 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 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 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 diverse groups and markers of pro-fibrogenic signalling have 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 improved the release of EV in comparison with 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. Furthermore, EV from FFA-treated hypoxic HepG2 cells enhanced Collagen1A1 and -SMA protein.
