“Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress”

Pandey, Anshuman; Kar, Sasmita

doi:10.1101/375683

Cited by 7 publications

(11 citation statements)

References 44 publications

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“…Based on our histopathology results, we hypothesized and tested that REMSD might will cause cell death in hepatocytes. Our hypothesis was further supported by report of cell death in the peripheral organs and tissues due to total and selective sleep loss in rats [44], and our recent reports suggesting REMSD induced increased acute phase response in serum and ROS in hepatocytes [20,47]. We labeled hepatocytes with Annexin V and TUNEL to estimate the cell death.…”

Section: Resultssupporting

confidence: 82%

“…Our recent finding suggested that REMSD of rats increased iNOS expression. While, this higher NO production in hepatocytes leads the ROS production and augmented susceptibility of hepatocytes towards oxidative stress [60]. This allowed us to hypothesize that might be caspases are involved in the REMSD driven apoptotic process?…”

Section: Resultsmentioning

confidence: 98%

“…Our previous reports, we had shown that REMSD induces acute phase response in the liver, increasing the synthesis of pro-inflammatory cytokines like IL1β, IL-6 and IL-12 and increasing the levels of liver toxicity marker enzymes, alanine transaminase (ALT) and aspartic transaminase (AST) which circulates in the blood [19]. Whereas, we also found that REMSD can induce the ROS level and NO production in the hepatocytes along with making them more susceptible to oxidative stress [20]. Recent, reports also suggest the effect of REMSD on the new born baby's sleep [21].…”

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confidence: 74%

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The flower pot method of REM sleep deprivation causes apoptotic cell death in the hepatocytes of rat

Pandey

Kumar

Ray

et al. 2018

Preprint

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Short running title: REM sleep deprivation causes liver cell death. Highlights of the study• We observed significant apoptosis in the hepatocytes of REMSD group of rats.• Our expression analysis confirmed altered expression for genes p53, Bcl2, Bax, and Caspase-3 after REMSD.• Protein level analysis supported our gene expression results for p53, Bcl2, Bax, Caspase 3 and Caspase 9 after REMSD.• Sleep recovery improved the respective genes and protein expression levels towards normalcy, signifying the functional role of REM sleep. Abstract Introduction:The rapid eye movement sleep deprivation (REMSD) of rats relates with increased inflammations, acute phase response, oxidative damage, neuronal cell loss, and neurodegenerative diseases. Whereas, its role outside brain are not well studied. This study tried to explore the causal effect of REM sleep loss on hepatocytes. Methods: We deprived the rats of REM sleep using standard flower pot method. We focused on liver to see the REMSD affects which controls most of the metabolic processes of the body. Results: We report here that flower pot induced REMSD causes apoptotic cell death of hepatocytes (~10% by Annexin Assay & ~20% by TUNEL assay). This were further got alleviated up to extent after sleep recovery of 5 days (recovered approximately 8.0% by Annexin Assay & 14% by TUNEL assay). The gene expression and protein level profiling revealed the up-regulation of p53, Bax, Cytochrome c, Caspase 3, and Caspase 9. While, Bcl2 which is an anti-apoptotic protein were down-regulated in response to REMSD. Relentless recovery of 5 days affected the expression pattern of these genes/proteins. Conclusions: Our study offer great pathological and physiological significance for sleep loss, by inferring the apoptotic celldeath in the hepatocytes of rat. This further signifies the functional and preventive role of REM sleep which is unique to mammals and avians with certain exceptions, as its loss can affect the natural well-being and survival of the individuals. IntroductionSleep is an important evolutionary physiological and behavioral process required for the survival and well-being of animals studied, although no predominant hypothesis has emerged to explain its functions [1,2]. In mammals, it is categorize as two types, non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. Evolutionary REM sleep is present in mammals and birds with essential functions related to physiological and ecological success. REM sleep, also called as paradoxical sleep in general associates with memory consolidation, brain maturation, spatial memory acquisition, muscle regeneration and maintenance of body physiology [3][4][5][6][7][8][9]. Functional aspect of REM sleep can inferred by its effect on amygdala activity in response to previous emotional experiences, reorganizing the hippocampal excitability, pruning and maintenance of new synapses in development and learning [10][11][12]. Its prolonged loss can alter blood brain barrier functions and can be fatal [13][14][15]. Some recent stu...

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Section: Resultssupporting

confidence: 82%

Section: Resultsmentioning

confidence: 98%

mentioning

confidence: 74%

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The flower pot method of REM sleep deprivation causes apoptotic cell death in the hepatocytes of rat

Pandey

Kumar

Ray

et al. 2018

Preprint

Self Cite

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“…generating new molecules such as free radicals [26], increasing the permeability of the BBB [27], inducing pulse pressure surges [28], and increasing vascular stiffness and altering cerebral perfusion [29]. In the present study, subjects with a higher ArI showed more severe PWMHs, which supports the hypothesis that non breathing-related sleep fragmentation could be related to the pathological mechanism of WMHs.…”

Section: Discussionsupporting

confidence: 83%

Non breathing-related sleep fragmentation and imaging markers in patients with atherosclerotic cerebral small vessel disease (CSVD): a cross-sectional case-control study

wang¹,

Chen²,

Liao³

et al. 2019

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Objective : Sleep fragmentation was shown to be positively associated with cognitive impairment in patients with cerebral small vessel disease (CSVD); however, the underlying mechanisms are not well characterized. In this study, we sought to clarify this issue by investigating the relationship between non breathing-related sleep fragmentation and brain imaging markers in patients with CSVD. Methods : Eighty-four CSVD patients and 24 age-and sex-matched healthy controls were prospectively recruited. All subjects underwent 3.0 T superconducting magnetic resonance imaging and overnight polysomnography. Polysomnography parameters including sleep onset latency (SOL), total sleep time (TST); sleep efficiency (SE), wake after sleep onset (WASO), percentage of each sleep stage (N1, N2, N3 and rapid eye movement REM), arousal index (ArI), periodic limb movement in sleep index (PLSMI) and periodic limb movement related arousal index (PLMAI) were compared between CSVD patients and healthy controls. The relationship between arousal index and CSVD markers was explored in the CSVD group. Results : On polysomnography, CSVD patients showed significantly higher ArI, WASO, PLSMI, and PLMAI, and lower sleep efficiency and N-3 ratio compared to healthy controls ( p < 0.05). On ordinal logistic regression, higher ArI showed a positive association with the severity of periventricular white matter hyperintensity (odds ratio OR 1.121, 95% confidence interval CI 0.138-2.185) and perivascular space (OR 2.108, 95% CI 1.032-4.017) in CSVD patients, after adjusting for potential confounding variables. Conclusions : These preliminary results indicate that non breathing-related sleep fragmentation is common and related to the pathological markers of CSVD patients. Future prospective research is required to determine the causal relationship between sleep parameters and CSVD pathology. PSQI: Pittsburgh sleep quality index SE: sleep efficiency WASO: wake after sleep onset WMH: white matter hyperintensity PLMSI, periodic limb movement in sleep index PLMAI, periodic limb movement related arousal index Declarations Ethics approval and consent to participateThe protocol and informed consent documents were approved by the ethics committee of the Third Affiliated Hospital, Sun Yat-sen University. All participants provided written, informed consent. Consent for publicationNot applicable.

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“…Outside of the brain, deprivation of the REM sleep was found to be associated with acute phase response in the liver, increased synthesis of pro-inflammatory cytokines such as IL1β, IL-6, and IL-12, and an increase in liver enzymes, alanine transaminase and aspartic transaminase [ 46 ]. In addition, REM sleep deprivation induces the production of reactive oxygen species (ROS) and causes inflammation [ 47 ] and an increase in nitric oxide (NO) in hepatocytes, along with an increase in sensitivity to oxidative stress by the hepatocytes [ 48 ]. REM loss also affected the weight and content of nucleic acid in the liver [ 49 ].…”

Section: Introductionmentioning

confidence: 99%

Differential Gene Expression in Brain and Liver Tissue of Wistar Rats after Rapid Eye Movement Sleep Deprivation

2020

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Sleep is essential for the survival of most living beings. Numerous researchers have identified a series of genes that are thought to regulate “sleep-state” or the “deprived state”. As sleep has a significant effect on physiology, we believe that lack of total sleep, or particularly rapid eye movement (REM) sleep, for a prolonged period would have a profound impact on various body tissues. Therefore, using the microarray method, we sought to determine which genes and processes are affected in the brain and liver of rats following nine days of REM sleep deprivation. Our findings showed that REM sleep deprivation affected a total of 652 genes in the brain and 426 genes in the liver. Only 23 genes were affected commonly, 10 oppositely, and 13 similarly across brain and liver tissue. Our results suggest that nine-day REM sleep deprivation differentially affects genes and processes in the brain and liver of rats.

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“Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress”

Cited by 7 publications

References 44 publications

The flower pot method of REM sleep deprivation causes apoptotic cell death in the hepatocytes of rat

The flower pot method of REM sleep deprivation causes apoptotic cell death in the hepatocytes of rat

Non breathing-related sleep fragmentation and imaging markers in patients with atherosclerotic cerebral small vessel disease (CSVD): a cross-sectional case-control study

Differential Gene Expression in Brain and Liver Tissue of Wistar Rats after Rapid Eye Movement Sleep Deprivation

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