Ol levels and B7-H6 Proteins medchemexpress promoted lung epithelial cell differentiation in lung organoids (enhanced SPC and CC10 expression). AFSC-EVs contain 901 microRNAs, a number of which are important for foetal lung development, for instance miR17 92 cluster. Summary/Conclusion: Administration of AFSC-EVs rescues impaired foetal lung development in experimental models of PH. AFSC-EV regenerative capability is exerted by way of the release of miRNAs a number of which regulate genes involved in foetal lung development. AFSC-EVs represent a promising therapeutic tactic 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), is usually a recognized reason for neonatal death. To date, there is absolutely no efficient therapy that promotes foetal lung development and maturation. Herein, we describe a stem cell-based strategy that enhances foetalJOURNAL OF EXTRACELLULAR VESICLESa CD49d/Integrin alpha 4 Proteins Purity & Documentation 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 Healthcare 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 is usually a essential concern in non-alcoholic fatty liver illness (NAFLD). Recent observations in patients with obstructive sleep apnoea syndrome (OSAS), recommend that hypoxia may possibly contribute to illness progression primarily via 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 no cost fatty acid (FFA)-exposed hepatocytes and assess cellular crosstalk in between hepatocytes and LX-2 cells (human hepatic stellate cell line). Strategies: 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 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 distinctive groups and markers of pro-fibrogenic signalling had been 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 improved the release of EV in comparison to non-treated HepG2 cells. Remedy of LX-2 cells with EV from FFA-treated hypoxic HepG2 cells improved gene expression of TGF-1, CTGF, -SMA and Collagen1A1 in comparison to 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 enhanced Collagen1A1 and -SMA protein.
