Sleep deprivation impairs calcium signaling in mouse splenocytes and leads to a decreased immune response
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 af...
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| Published in | Biochimica et biophysica acta Vol. 1820; no. 12; pp. 1997 - 2006 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier B.V
01.12.2012
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| Abstract | 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).
Adult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72h) 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 evaluated
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.
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.
► Sleep deprivation impairs calcium signaling in mice splenocytes. ► Sleep deprivation results in decrease in calcium stores in endoplasmic reticulum. ► Mitochondrial membrane potential in splenocytes is lost after sleep deprivation. ► Sleep deprivation results in splenocytes lysosomal integrity leakage. ► STIM expression is augmented after sleep deprivation in mice spleen. |
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| AbstractList | 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).
Adult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72h) 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 evaluated
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.
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.
► Sleep deprivation impairs calcium signaling in mice splenocytes. ► Sleep deprivation results in decrease in calcium stores in endoplasmic reticulum. ► Mitochondrial membrane potential in splenocytes is lost after sleep deprivation. ► Sleep deprivation results in splenocytes lysosomal integrity leakage. ► STIM expression is augmented after sleep deprivation in mice spleen. Sleep is a physiological event that directly influences health by affecting the immune system, in which calcium (Ca(2+)) plays a critical signaling role. We performed live cell measurements of cytosolic Ca(2+) mobilization to understand the changes in Ca(2+) signaling that occur in splenic immune cells after various periods of sleep deprivation (SD). Adult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72h) and Ca(2+) intracellular fluctuations were evaluated in splenocytes by confocal microscopy. We also performed spleen cell evaluation by flow cytometry and analyzed intracellular Ca(2+) mobilization in endoplasmic reticulum and mitochondria. Additionally, Ca(2+) channel gene expression was evaluated Splenocytes showed a progressive loss of intracellular Ca(2+) maintenance from endoplasmic reticulum (ER) stores. Transient Ca(2+) 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) Ca(2+) channels. These novel data suggest that SD impairs Ca(2+) signaling, most likely as a result of ER stress, leading to an insufficient Ca(2+) 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. 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 72h) 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 evaluated RESULTS: 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. Sleep is a physiological event that directly influences health by affecting the immune system, in which calcium (Ca(2+)) plays a critical signaling role. We performed live cell measurements of cytosolic Ca(2+) mobilization to understand the changes in Ca(2+) signaling that occur in splenic immune cells after various periods of sleep deprivation (SD).BACKGROUNDSleep is a physiological event that directly influences health by affecting the immune system, in which calcium (Ca(2+)) plays a critical signaling role. We performed live cell measurements of cytosolic Ca(2+) mobilization to understand the changes in Ca(2+) signaling that occur in splenic immune cells after various periods of sleep deprivation (SD).Adult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72h) and Ca(2+) intracellular fluctuations were evaluated in splenocytes by confocal microscopy. We also performed spleen cell evaluation by flow cytometry and analyzed intracellular Ca(2+) mobilization in endoplasmic reticulum and mitochondria. Additionally, Ca(2+) channel gene expression was evaluatedMETHODSAdult male mice were subjected to sleep deprivation by platform technique for different periods (from 12 to 72h) and Ca(2+) intracellular fluctuations were evaluated in splenocytes by confocal microscopy. We also performed spleen cell evaluation by flow cytometry and analyzed intracellular Ca(2+) mobilization in endoplasmic reticulum and mitochondria. Additionally, Ca(2+) channel gene expression was evaluatedSplenocytes showed a progressive loss of intracellular Ca(2+) maintenance from endoplasmic reticulum (ER) stores. Transient Ca(2+) 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) Ca(2+) channels.RESULTSSplenocytes showed a progressive loss of intracellular Ca(2+) maintenance from endoplasmic reticulum (ER) stores. Transient Ca(2+) 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) Ca(2+) channels.These novel data suggest that SD impairs Ca(2+) signaling, most likely as a result of ER stress, leading to an insufficient Ca(2+) 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.CONCLUSIONS AND GENERAL SIGNIFICANCEThese novel data suggest that SD impairs Ca(2+) signaling, most likely as a result of ER stress, leading to an insufficient Ca(2+) 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. |
| Author | Gazarini, Marcos L. Tufik, Sergio D'Almeida, Vânia Tersariol, Ivarne l.S. Lungato, Lisandro Paredes-Gamero, Edgar J. |
| Author_xml | – sequence: 1 givenname: Lisandro surname: Lungato fullname: Lungato, Lisandro organization: Department of Psychobiology, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil – sequence: 2 givenname: Marcos L. surname: Gazarini fullname: Gazarini, Marcos L. organization: Department of Biosciences, Universidade Federal de São Paulo-UNIFESP, Santos, SP, Brazil – sequence: 3 givenname: Edgar J. surname: Paredes-Gamero fullname: Paredes-Gamero, Edgar J. organization: Department of Biochemistry, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil – sequence: 4 givenname: Ivarne l.S. surname: Tersariol fullname: Tersariol, Ivarne l.S. organization: Department of Biochemistry, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil – sequence: 5 givenname: Sergio surname: Tufik fullname: Tufik, Sergio organization: Department of Psychobiology, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil – sequence: 6 givenname: Vânia surname: D'Almeida fullname: D'Almeida, Vânia email: vaniadalmeida@uol.com.br organization: Department of Psychobiology, Universidade Federal de São Paulo-UNIFESP, São Paulo, SP, Brazil |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23000491$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | adults Animals Ca2 + signaling calcium Calcium - metabolism calcium channels calcium signaling Calcium Signaling - physiology confocal microscopy endoplasmic reticulum Endoplasmic Reticulum - metabolism flow cytometry gene expression immune response Lysosomes - metabolism Male males Membrane Potential, Mitochondrial Membrane Proteins - genetics Membrane Proteins - metabolism Mice mitochondria Mitochondria - immunology Mitochondria - metabolism Mitochondrial dysfunction Neoplasm Proteins - genetics Neoplasm Proteins - metabolism sleep Sleep deprivation Sleep Deprivation - immunology Sleep Deprivation - metabolism Sleep Deprivation - pathology spleen Spleen - cytology Spleen - immunology Spleen - metabolism Splenocytes Stromal Interaction Molecule 1 |
| Title | Sleep deprivation impairs calcium signaling in mouse splenocytes and leads to a decreased immune response |
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