ATP is required and advances cytokine-induced gap junction formation in microglia in vitro

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dc.contributor.authorSaez, Pablo
dc.contributor.authorShoji, Kenji
dc.contributor.authorRetamal, Mauricio
dc.contributor.authorHarcha, Paloma
dc.contributor.authorRamirez, Gigliola
dc.contributor.authorJiang, Jean
dc.contributor.authorvon Bernhardi, Rommy
dc.contributor.authorSaez, Juan
dc.date.accessioned2017-04-07T14:59:48Z
dc.date.available2017-04-07T14:59:48Z
dc.date.issued2013
dc.descriptionCentro de Fisiología Celular e Integrativa
dc.description.abstractMicroglia 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-/IFN--induced dye coupling, probably through the induction of IL-1 release. Moreover, TNF-/IFN-, but not TNF- plus ATP, increased dye uptake in EOC20 cells. Blockade of Cx43 and Panx1 HCs prevented dye coupling induced by TNF-/IFN-, but not TNF- plus ATP. In addition, IL-6 prevented the induction of dye coupling and HC activity induced by TNF-/IFN- 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.
dc.format.extent17
dc.identifier.citationMediators of Inflammation, 2013, 2013:216402
dc.identifier.urihttp://hdl.handle.net/11447/1107
dc.identifier.urihttp://dx.doi.org/10.1155/2013/216402
dc.language.isoen_US
dc.publisherHindawi Publishing Corp.
dc.subjectcentral nervous system
dc.subjectMicroglia
dc.subjectATP
dc.subjecthemichannels
dc.subjectimmune response
dc.titleATP is required and advances cytokine-induced gap junction formation in microglia in vitro
dc.typeArtículo

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