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

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

Autor Haak, L. L. Google Scholar
Grimaldi, M. Google Scholar
Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Russell, J. T. Google Scholar
Instituição NICHHD
Universidade Federal de São Paulo (UNIFESP)
Resumo Mitochondria 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.
Palavra-chave calcium wave
gelsolin
inositol trisphosphate
mitochondria
oligodendrocyte progenitor
PIP2
Idioma Inglês
Data de publicação 2002-02-01
Publicado em Journal of Neurochemistry. Oxford: Blackwell Publishing Ltd, v. 80, n. 3, p. 405-415, 2002.
ISSN 0022-3042 (Sherpa/Romeo, fator de impacto)
Publicador Blackwell Publishing Ltd
Extensão 405-415
Fonte http://dx.doi.org/10.1046/j.0022-3042.2001.00727.x
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000173618500005
Endereço permanente http://repositorio.unifesp.br/handle/11600/26735

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