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Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition

Epithelial to mesenchymal transition (EMT) has emerged as a key process in the development of renal fibrosis. In fact, EMT-derived fibroblasts contribute to the progression of chronic renal disease. In addition, anti-inflammatory M2 macrophages have exhibited a great influence on renal fibrosis. How...

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Autores principales: Sola, Anna, Saenz del Burgo, Laura, Ciriza, Jesús, Hernandez, Rosa Maria, Orive, Gorka, Martin Cordero, Jorge, Calle, Priscila, Pedraz, Jose Luis, Hotter, Georgina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058712/
https://www.ncbi.nlm.nih.gov/pubmed/29250977
http://dx.doi.org/10.1080/10717544.2017.1413449
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author Sola, Anna
Saenz del Burgo, Laura
Ciriza, Jesús
Hernandez, Rosa Maria
Orive, Gorka
Martin Cordero, Jorge
Calle, Priscila
Pedraz, Jose Luis
Hotter, Georgina
author_facet Sola, Anna
Saenz del Burgo, Laura
Ciriza, Jesús
Hernandez, Rosa Maria
Orive, Gorka
Martin Cordero, Jorge
Calle, Priscila
Pedraz, Jose Luis
Hotter, Georgina
author_sort Sola, Anna
collection PubMed
description Epithelial to mesenchymal transition (EMT) has emerged as a key process in the development of renal fibrosis. In fact, EMT-derived fibroblasts contribute to the progression of chronic renal disease. In addition, anti-inflammatory M2 macrophages have exhibited a great influence on renal fibrosis. However, because of the high impact that the inputs of different environmental cytokines have on their phenotype, macrophages can easily lose this property. We aim to known if microencapsulated macrophages on M2-inducing alginate matrices could preserve macrophage phenotype and thus release factors able to act on epithelial cells to prevent the epithelial differentiation towards mesenchymal cells. We reproduced an in vitro model of EMT by treating adipose-derived stem cells with all-trans retinoic acid (ATRA) and induced their transformation toward epithelia. Dedifferentiation of epithelial cells into a mesenchymal phenotype occurred when ATRA was retired, thus simulating EMT. Results indicate that induction of M2 phenotype by IL-10 addition in the alginate matrix produces anti-inflammatory cytokines and increases the metabolic activity and the viability of the encapsulated macrophages. The released conditioned medium modulates EMT and maintains healthy epithelial phenotype. This could be used for in vivo cell transplantation, or alternatively as an external releaser able to prevent epithelial to mesenchymal transformation for future anti-fibrotic therapies.
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spelling pubmed-60587122018-08-17 Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition Sola, Anna Saenz del Burgo, Laura Ciriza, Jesús Hernandez, Rosa Maria Orive, Gorka Martin Cordero, Jorge Calle, Priscila Pedraz, Jose Luis Hotter, Georgina Drug Deliv Research Article Epithelial to mesenchymal transition (EMT) has emerged as a key process in the development of renal fibrosis. In fact, EMT-derived fibroblasts contribute to the progression of chronic renal disease. In addition, anti-inflammatory M2 macrophages have exhibited a great influence on renal fibrosis. However, because of the high impact that the inputs of different environmental cytokines have on their phenotype, macrophages can easily lose this property. We aim to known if microencapsulated macrophages on M2-inducing alginate matrices could preserve macrophage phenotype and thus release factors able to act on epithelial cells to prevent the epithelial differentiation towards mesenchymal cells. We reproduced an in vitro model of EMT by treating adipose-derived stem cells with all-trans retinoic acid (ATRA) and induced their transformation toward epithelia. Dedifferentiation of epithelial cells into a mesenchymal phenotype occurred when ATRA was retired, thus simulating EMT. Results indicate that induction of M2 phenotype by IL-10 addition in the alginate matrix produces anti-inflammatory cytokines and increases the metabolic activity and the viability of the encapsulated macrophages. The released conditioned medium modulates EMT and maintains healthy epithelial phenotype. This could be used for in vivo cell transplantation, or alternatively as an external releaser able to prevent epithelial to mesenchymal transformation for future anti-fibrotic therapies. Taylor & Francis 2017-12-17 /pmc/articles/PMC6058712/ /pubmed/29250977 http://dx.doi.org/10.1080/10717544.2017.1413449 Text en © 2017 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Sola, Anna
Saenz del Burgo, Laura
Ciriza, Jesús
Hernandez, Rosa Maria
Orive, Gorka
Martin Cordero, Jorge
Calle, Priscila
Pedraz, Jose Luis
Hotter, Georgina
Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title_full Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title_fullStr Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title_full_unstemmed Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title_short Microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
title_sort microencapsulated macrophages releases conditioned medium able to prevent epithelial to mesenchymal transition
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058712/
https://www.ncbi.nlm.nih.gov/pubmed/29250977
http://dx.doi.org/10.1080/10717544.2017.1413449
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