Mitochondria regulate Ca2+ wave initiation and inositol trisphosphate signal transduction in oligodendrocyte progenitors

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dc.contributor.authorHaak, L. L.
dc.contributor.authorGrimaldi, M.
dc.contributor.authorSmaili, Soraya Soubhi [UNIFESP]
dc.contributor.authorRussell, J. T.
dc.contributor.institutionNICHHD
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:33:14Z
dc.date.available2016-01-24T12:33:14Z
dc.date.issued2002-02-01
dc.description.abstractMitochondria in oligodendrocyte progenitor cells (OPs) Dtake up and release cytosolic Ca2+ during agonist-evoked Ca2+ waves, but it is not clear whether or how they regulate Ca2+ signaling in OPs. We asked whether mitochondria. play an active role during agonist-evoked Ca2+ release from intracellular stores. Ca2+ puffs, wave initiation, and wave propagation were measured in fluo-4 loaded OP processes using linescan confocal microscopy. Mitochondrial depolarization, measured by tetramethyl rhodamine ethyl ester (TMRE) fluorescence, accompanied Ca2+ puffs and waves. in addition, waves initiated only where mitochondria were localized. To determine whether energized mitochondria were necessary for wave generation, we blocked mitochondrial function with the electron transport chain inhibitor antimycin A (AA) in combination with oligomycin. AA decreased wave speed and puff probability. These effects were not due to global changes in ATP. We found that AA increased cytosolic Ca2+ markedly reduced agonist-evoked inositol trisphosphate (IP3) production, and also enhanced phosphatidylinositol 4,5-bisphosphate (PIP2) binding to the Ca2+ dependent protein gelsolin. Thus, the reduction in puff probability and wave speed after AA treatment may be explained by competition for PIP2 between phospholipase C and gelsolin. Energized mitochondria and low cytosolic Ca2+ concentration may be required to maintain PIP2, a substrate for IP3 signal transcluction.en
dc.description.affiliationNICHHD, LCSN, NIH, Bethesda, MD 20892 USA
dc.description.affiliationUniversidade Federal de São Paulo, Dept Farmacol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Farmacol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent405-415
dc.identifierhttp://dx.doi.org/10.1046/j.0022-3042.2001.00727.x
dc.identifier.citationJournal of Neurochemistry. Oxford: Blackwell Publishing Ltd, v. 80, n. 3, p. 405-415, 2002.
dc.identifier.doi10.1046/j.0022-3042.2001.00727.x
dc.identifier.issn0022-3042
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/26735
dc.identifier.wosWOS:000173618500005
dc.language.isoeng
dc.publisherBlackwell Publishing Ltd
dc.relation.ispartofJournal of Neurochemistry
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectcalcium waveen
dc.subjectgelsolinen
dc.subjectinositol trisphosphateen
dc.subjectmitochondriaen
dc.subjectoligodendrocyte progenitoren
dc.subjectPIP2en
dc.titleMitochondria regulate Ca2+ wave initiation and inositol trisphosphate signal transduction in oligodendrocyte progenitorsen
dc.typeinfo:eu-repo/semantics/article
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