Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/35515
Title: Sleep deprivation impairs calcium signaling in mouse splenocytes and leads to a decreased immune response
Authors: Lungato, Lisandro [UNIFESP]
Gazarini, Marcos Leoni [UNIFESP]
Paredes-Gamero, Edgar Julian [UNIFESP]
Tersariol, Ivarne Luis dos Santos [UNIFESP]
Tufik, Sergio [UNIFESP]
D'Almeida, Vania [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Keywords: Ca2+ signaling
Splenocytes
Sleep deprivation
Mitochondrial dysfunction
Mice
Issue Date: 1-Dec-2012
Publisher: Elsevier B.V.
Citation: Biochimica Et Biophysica Acta-general Subjects. Amsterdam: Elsevier B.V., v. 1820, n. 12, p. 1997-2006, 2012.
Abstract: Background: Sleep is a physiological event that directly influences health by affecting the immune system, in which calcium (Ca2+) plays a critical signaling role. We performed live cell measurements of cytosolic Ca2+ mobilization to understand the changes in Ca2+ signaling that occur in splenic immune cells after various periods of sleep deprivation (SD).Methods: Adult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72 h) and Ca2+ intracellular fluctuations were evaluated in splenocytes by confocal microscopy. We also performed spleen cell evaluation by flow cytometry and analyzed intracellular Ca2+ mobilization in endoplasmic reticulum and mitochondria. Additionally. Ca2+ channel gene expression was evaluatedResults: Splenocytes showed a progressive loss of intracellular Ca2+ maintenance from endoplasmic reticulum (ER) stores. Transient Ca2+ buffering by the mitochondria was further compromised. These findings were confirmed by changes in mitochondrial integrity and in the performance of the store operated calcium entry (SOCE) and stromal interaction molecule 1 (STIM1) Ca2+ channels.Conclusions and general significance: These novel data suggest that SD impairs Ca2+ signaling, most likely as a result of ER stress, leading to an insufficient Ca2+ supply for signaling events. Our results support the previously described immunosuppressive effects of sleep loss and provide additional information on the cellular and molecular mechanisms involved in sleep function. (C) 2012 Elsevier B.V. All rights reserved.
URI: http://repositorio.unifesp.br/handle/11600/35515
ISSN: 0304-4165
Other Identifiers: http://dx.doi.org/10.1016/j.bbagen.2012.09.010
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Artigo

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