Ol levels and promoted lung epithelial cell differentiation in lung organoids (enhanced SPC and CC10 expression). AFSC-EVs include 901 microRNAs, some of which are crucial for foetal lung development, for example miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs rescues impaired foetal lung improvement in experimental models of PH. AFSC-EV regenerative capacity is exerted via the release of miRNAs some 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.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 often a recognized reason for neonatal death. To date, there isn’t any helpful remedy that promotes foetal lung development and maturation. Herein, we describe a stem cell-based approach 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 Health-related Center Groningen, Groningen, NetherlandsOWP1.07=PS08.Exploration in the surface TFR-1/CD71 Proteins medchemexpress modification of outer membrane vesicles Maximilian Richtera, Eleonora Diamantib, Anna Hirschb, Gregor FuhrmanncaIntroduction/Background: Transition from isolated steatosis to non-alcoholic steatohepatitis is usually a crucial problem in non-alcoholic fatty liver disease (NAFLD). Current observations in individuals with obstructive sleep apnoea syndrome (OSAS), suggest that hypoxia may contribute to disease progression primarily through activation of hypoxia inducible factor 1 (HIF-1)-related pathways. Release of extracellular vesicles (EV) by injured hepatocytes may perhaps be involved in NAFLD progression. Aim: to discover whether hypoxia modulates the release of EV from cost-free fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk involving hepatocytes and LX-2 cells (human hepatic stellate cell line). Methods: HepG2 cells have been Frizzled Proteins Species 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 distinct groups and markers of pro-fibrogenic signalling were determined by quantitative PCR (qPCR), WB and immunofluorescence (IF). Results: FFA and CH-treatment of HepG2 cells enhanced gene expression of IL-1 and TGF-1 in HepG2 cells and elevated the release of EV in comparison to non-treated HepG2 cells. Remedy of LX-2 cells with EV from FFA-treated hypoxic HepG2 cells increased 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. In addition, EV from FFA-treated hypoxic HepG2 cells improved Collagen1A1 and -SMA protein.
