Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules

Extracellular vesicles (EVs) mediate cell-to-cell crosstalk whose content can induce changes in acceptor cells and their microenvironment. MLP29 cells are mouse liver progenitor cells that release EVs loaded with signaling cues that could affect cell fate. In the current work, we incubated 3T3-L1 mo...

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Detalles Bibliográficos
Autores: Royo, Felix, Azkargorta, Mikel, Lavin, Jose L.|||0000-0003-0914-3211, Clos-Garcia, Marc|||0000-0002-0208-1372, Cortazar, Ana Rosa|||0000-0002-7082-5695, Gonzalez-Lopez, Monika, Barcena, Laura, Del Portillo, Hernando A.|||0000-0002-5278-3452, Yáñez-Mó, María|||0000-0001-7484-2866, Marcilla, Antonio|||0000-0003-0004-0531, Borràs i Serres, Francesc Enric|||0000-0003-4038-1912, Peinado, Héctor|||0000-0002-4256-3413, Guerrero, Isabel, Váles-Gómez, Mar|||0000-0001-7424-3206, Cereijo, Unai|||0000-0003-1557-8836, Sardon, Teresa|||0000-0002-5935-9312, Aransay, Ana M.|||0000-0002-8271-612X, Elortza, Felix|||0000-0001-8839-5438, Falcón-Pérez, Juan M.|||0000-0003-3133-0670
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:252334
Acceso en línea:https://ddd.uab.cat/record/252334
https://dx.doi.org/urn:doi:10.3389/fcell.2020.613583
Access Level:acceso abierto
Palabra clave:Extracellular vesicles (EVs)
Exosomes
MLP29
Fibroblast
Cell crosstalk
Immune response
Descripción
Sumario:Extracellular vesicles (EVs) mediate cell-to-cell crosstalk whose content can induce changes in acceptor cells and their microenvironment. MLP29 cells are mouse liver progenitor cells that release EVs loaded with signaling cues that could affect cell fate. In the current work, we incubated 3T3-L1 mouse fibroblasts with MLP29-derived EVs, and then analyzed changes by proteomics and transcriptomics. Results showed a general downregulation of protein and transcript expression related to proliferative and metabolic routes dependent on TGF-beta. We also observed an increase in the ERBB2 interacting protein (ERBIN) and Cxcl2, together with an induction of ribosome biogenesis and interferon-related response molecules, suggesting the activation of immune system signaling.

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