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ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro
Microglia are the immune cells in the central nervous system. After injury microglia release bioactive molecules, including cytokines and ATP, which modify the functional state of hemichannels (HCs) and gap junction channels (GJCs), affecting the intercellular communication via extracellular and int...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655668/ https://www.ncbi.nlm.nih.gov/pubmed/23737642 http://dx.doi.org/10.1155/2013/216402 |
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author | Sáez, Pablo J. Shoji, Kenji F. Retamal, Mauricio A. Harcha, Paloma A. Ramírez, Gigliola Jiang, Jean X. von Bernhardi, Rommy Sáez, Juan C. |
author_facet | Sáez, Pablo J. Shoji, Kenji F. Retamal, Mauricio A. Harcha, Paloma A. Ramírez, Gigliola Jiang, Jean X. von Bernhardi, Rommy Sáez, Juan C. |
author_sort | Sáez, Pablo J. |
collection | PubMed |
description | Microglia are the immune cells in the central nervous system. After injury microglia release bioactive molecules, including cytokines and ATP, which modify the functional state of hemichannels (HCs) and gap junction channels (GJCs), affecting the intercellular communication via extracellular and intracellular compartments, respectively. Here, we studied the role of extracellular ATP and several cytokines as modulators of the functional state of microglial HCs and GJCs using dye uptake and dye coupling techniques, respectively. In microglia and the microglia cell line EOC20, ATP advanced the TNF-α/IFN-γ-induced dye coupling, probably through the induction of IL-1β release. Moreover, TNF-α/IFN-γ, but not TNF-α plus ATP, increased dye uptake in EOC20 cells. Blockade of Cx43 and Panx1 HCs prevented dye coupling induced by TNF-α/IFN-γ, but not TNF-α plus ATP. In addition, IL-6 prevented the induction of dye coupling and HC activity induced by TNF-α/IFN-γ in EOC20 cells. Our data support the notion that extracellular ATP affects the cellular communication between microglia through autocrine and paracrine mechanisms, which might affect the timing of immune response under neuroinflammatory conditions. |
format | Online Article Text |
id | pubmed-3655668 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-36556682013-06-04 ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro Sáez, Pablo J. Shoji, Kenji F. Retamal, Mauricio A. Harcha, Paloma A. Ramírez, Gigliola Jiang, Jean X. von Bernhardi, Rommy Sáez, Juan C. Mediators Inflamm Research Article Microglia are the immune cells in the central nervous system. After injury microglia release bioactive molecules, including cytokines and ATP, which modify the functional state of hemichannels (HCs) and gap junction channels (GJCs), affecting the intercellular communication via extracellular and intracellular compartments, respectively. Here, we studied the role of extracellular ATP and several cytokines as modulators of the functional state of microglial HCs and GJCs using dye uptake and dye coupling techniques, respectively. In microglia and the microglia cell line EOC20, ATP advanced the TNF-α/IFN-γ-induced dye coupling, probably through the induction of IL-1β release. Moreover, TNF-α/IFN-γ, but not TNF-α plus ATP, increased dye uptake in EOC20 cells. Blockade of Cx43 and Panx1 HCs prevented dye coupling induced by TNF-α/IFN-γ, but not TNF-α plus ATP. In addition, IL-6 prevented the induction of dye coupling and HC activity induced by TNF-α/IFN-γ in EOC20 cells. Our data support the notion that extracellular ATP affects the cellular communication between microglia through autocrine and paracrine mechanisms, which might affect the timing of immune response under neuroinflammatory conditions. Hindawi Publishing Corporation 2013 2013-04-23 /pmc/articles/PMC3655668/ /pubmed/23737642 http://dx.doi.org/10.1155/2013/216402 Text en Copyright © 2013 Pablo J. Sáez et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Sáez, Pablo J. Shoji, Kenji F. Retamal, Mauricio A. Harcha, Paloma A. Ramírez, Gigliola Jiang, Jean X. von Bernhardi, Rommy Sáez, Juan C. ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title | ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title_full | ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title_fullStr | ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title_full_unstemmed | ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title_short | ATP Is Required and Advances Cytokine-Induced Gap Junction Formation in Microglia In Vitro |
title_sort | atp is required and advances cytokine-induced gap junction formation in microglia in vitro |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655668/ https://www.ncbi.nlm.nih.gov/pubmed/23737642 http://dx.doi.org/10.1155/2013/216402 |
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