Sleep deprivation impairs calcium signaling in mouse splenocytes and leads to a decreased immune response

Lungato, Lisandro; Gazarini, Marcos L.; Paredes‐Gamero, Edgar Julian; Tersariol, Ivarne L.S.; Tufik, Sérgio; D’Almeida, Vânia

doi:10.1016/j.bbagen.2012.09.010

Cited by 13 publications

(18 citation statements)

References 28 publications

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“…Our data show that SD impairs the cellular integrity and consequently its viability. Our previously study showed Ca 2+ overload, mitochondrial loss potential, disruption of cellular membrane, and lysosomes (Lungato et al, ) and these findings may strengthen our hypothesis about a necrotic‐like death pathway in these cells. Interestingly, 24 h of sleep recovery after prolonged SD seems to be insufficient for the recovery of the lymphocytic system, as showed by other studies using different experimental protocols involving other tissues and cell types (Guariniello et al, ; Hirotsu et al, ).…”

Section: Discussionsupporting

confidence: 87%

“…Biswas et al () showed that SD increased the number of apoptotic neurons in the rat brain. In a previous study, our group showed that SD impaired Ca 2+ —mediated intracellular signaling in organelles such as endoplasmic reticulum, mitochondria and lysosomes, causing stress and cell homeostatic disruption and, promoting necrotic‐like cell death (Lungato et al, ). An analysis of apoptotic B lymphocytes in the BM in the current study showed an increase in necrotic‐like B lymphocytes after 48 and 72 h of SD (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies in the field of sleep have shown the importance of this behavioral state for the homeostasis of the immune system. SD can result in many losses concerning the bidirectional communication of the immune system with the nervous and endocrine systems (Lange et al, , ; Motivala, ; Reis et al, ), reduction in the weight of the lymphoid organs (Zager et al, ) and disruption of the homeostasis of immune cells (Zager et al, ; Guariniello et al, ; Lungato et al, ; Maragno‐Correa et al, ). In this study, it was found that the total populations of B lymphocytes in the spleen tissue were reduced after 72 h of SD (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis

Lungato

Nogueira‐Pedro

Dias

et al. 2015

Journal Cellular Physiology

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B lymphocytes are immune cells crucial for the maintenance and viability of the humoral response. Sleep is an essential event for the maintenance and integrity of all systems, including the immune system (IS). Thus, sleep deprivation (SD) causes problems in metabolism and homeostasis in many cell systems, including the IS. In this study, our goal was to determine changes in B lymphocytes from the bone marrow (BM) and spleen after SD. Three-month-old male Swiss mice were used. These mice were sleep deprived through the modified multiple platform method for different periods (24, 48, and 72 h), whereas another group was allowed to sleep for 24 h after 72 h of SD (rebound group) and a third group was allowed to sleep normally during the entire experiment. After this, the spleen and BM were collected, and cell analyses were performed. The numbers of B lymphocytes in the BM and spleen were reduced by SD. Additionally, reductions in the percentage of lymphocyte progenitors and their ability to form colonies were observed. Moreover, an increase in the death of B lymphocytes from the BM and spleen was associated with an increase in oxidative stress indicators, such as DCFH-DA, CAT, and mitochondrial SOD. Rebound was not able to reverse most of the alterations elicited by SD. The reduction in B lymphocytes and their progenitors by cell death, with a concomitant increase in oxidative stress, showed that SD promoted a failure in B lymphopoiesis.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis

Lungato

Nogueira‐Pedro

Dias

et al. 2015

Journal Cellular Physiology

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“…Considering that we found increased levels of CuZnSOD activity in splenocytes of mice after 72 h of SD when compared with the CT group (Table ), it is possible that SD could also trigger cell death by related mechanisms. In fact, we recently showed a mitochondrial calcium gradient disruption after SD that could be another factor contributing to cell death .…”

Section: Discussionmentioning

confidence: 97%

Sleep Deprivation Alters Gene Expression and Antioxidant Enzyme Activity in Mice Splenocytes

Lungato¹,

Marques²,

Pereira³

et al. 2013

Scand J Immunol

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Cellular defence against the formation of reactive oxygen species (ROS) involves a number of mechanisms in which antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD) play an important role. The relation between sleep deprivation and oxidative stress has not yet been completely elucidated. Although some authors did not find evidence of this relationship, others found alterations in some oxidative stress markers in response to sleep deprivation. Thus, the objective of this study was to identify changes induced by sleep deprivation in the activity and gene expression of antioxidant enzymes in mice splenocytes, ideally corroborating a better understanding of the observed effects related to sleep deprivation, which could be triggered by oxidative imbalance. Splenocytes from mice sleep deprived for 72 h showed no significant difference in CAT and CuZnSOD gene expression compared with normal sleep mice. However, sleep-deprived mice did show higher MnSOD gene expression than the control group. Concerning enzymatic activity, CuZnSOD and MnSOD significantly increased after sleep deprivation, despite the expression in CuZnSOD remained unchanged. Moreover, CAT activity was significantly lower after sleep deprivation. The data suggest that the antioxidant system is triggered by sleep deprivation, which in turn could influence the splenocytes homoeostasis, thus interfering in physiological responses.

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“…The primary function of sleep remains unknown, but the fact that prolonged sleep deprivation results in the death of experimental animals indicates that it is essential for survival (Rechtschaffen, 1998). Reinforcing the importance of sleep, poor sleep quality is associated in humans with an increased risk of developing metabolic syndrome, and in experimental animals with infectious diseases and changes in sexual motivation Knutson, Spiegel, Penev, & Van Cauter, 2007;Lungato et al, 2012;Ruiz, Andersen, Zager, Martins, & Tufik, 2007). The first two studies linking sleep deprivation to pregnancy loss were published by Pigareva (2006) and by Calegare et al (2010), both in experimental animals.…”

Section: Discussionmentioning

confidence: 99%

Sleep deprivation decreases the reproductive capacity by affecting the arrival of morulas in the uterus

Calegare

Azzolini

Vallim

et al. 2019

Genesis

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Summary A previous animal study by our group found that sleep deprivation during preimplantation was associated with decreased pregnancy maintenance. Given its impact on human society, we aimed in the current study to assess whether sleep deprivation affects blastocyst gene expression and/or the implantation process. For this, pregnant mice (gestational day 0 [GD 0]) were assigned into paradoxical sleep deprivation (SD, 72 hr; multiple platform method) and, a control (CT) group. Animals were euthanized on GD 3.5 and blood, uterus (embryos) and fallopian tube were collected. Then, 89% of CT presented blastocysts in the uterus versus 25% from SD group. Compared to CT, SD presented lighter relative uterus weight, increased plasma concentrations of corticosterone and testosterone, decreased concentrations of progesterone and luteinizing hormone, but no statistical differences in plasma concentrations of 17β‐estradiol and follicle stimulating hormone. There were no differences in uterus and blastocyst gene expression related to embryo implantation and development, and no alteration in blastocysts global DNA methylation. Considering this, the decreased pregnancy maintenance after sleep deprivation seems not to be associated with implantation losses or developmental problems related to the blastocysts. It is likely that complications in morula development and/or its movement through the fallopian tubes affect the pregnancy rate, since only 25% of SD females presented a blastocyst on the GD 3.5. In fact, three out of four females without blastocysts in the uterus presented morula in the fallopian tubes due to a phase delay. Additionally, we suggest that the observed hormonal changes may play a role in this outcome.

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Sleep deprivation impairs calcium signaling in mouse splenocytes and leads to a decreased immune response

Cited by 13 publications

References 28 publications

Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis

Effects of Sleep Deprivation on Mice Bone Marrow and Spleen B Lymphopoiesis

Sleep Deprivation Alters Gene Expression and Antioxidant Enzyme Activity in Mice Splenocytes

Sleep deprivation decreases the reproductive capacity by affecting the arrival of morulas in the uterus

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