Sleep Deprivation and Gene Expression

2015 ◽  
pp. 65-90 ◽  
Author(s):  
Annie da Costa Souza ◽  
Sidarta Ribeiro
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation

050 GENE EXPRESSION PROFILE AS A CONSEQUENCE OF SLEEP DEPRIVATION IN HUMANS

2009 ◽  
Vol 10 ◽  
pp. S14
Author(s):  
R. Pellegrino ◽  
C.S. Guindalini ◽  
D.Y. Sunaga ◽  
M.L. Andersen ◽  
R. Martins ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Gene Expression Profile ◽  
Expression Profile

scholarly journals Macromolecule biosynthesis: a key function of sleep

2007 ◽  
Vol 31 (3) ◽  
pp. 441-457 ◽  
Author(s):  
Miroslaw Mackiewicz ◽  
Keith R. Shockley ◽  
Micah A. Romer ◽  
Raymond J. Galante ◽  
John E. Zimmerman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Sleep Deprivation ◽  
Expression Patterns ◽  
State Level ◽  
Altered Expression ◽  
Mouse Cerebral Cortex ◽  
Genes Encoding ◽  
Function Of Sleep ◽  
Cellular Components

The function(s) of sleep remains a major unanswered question in biology. We assessed changes in gene expression in the mouse cerebral cortex and hypothalamus following different durations of sleep and periods of sleep deprivation. There were significant differences in gene expression between behavioral states; we identified 3,988 genes in the cerebral cortex and 823 genes in the hypothalamus with altered expression patterns between sleep and sleep deprivation. Changes in the steady-state level of transcripts for various genes are remarkably common during sleep, as 2,090 genes in the cerebral cortex and 409 genes in the hypothalamus were defined as sleep specific and changed (increased or decreased) their expression during sleep. The largest categories of overrepresented genes increasing expression with sleep were those involved in biosynthesis and transport. In both the cerebral cortex and hypothalamus, during sleep there was upregulation of multiple genes encoding various enzymes involved in cholesterol synthesis, as well as proteins for lipid transport. There was also upregulation during sleep of genes involved in synthesis of proteins, heme, and maintenance of vesicle pools, as well as antioxidant enzymes and genes encoding proteins of energy-regulating pathways. We postulate that during sleep there is a rebuilding of multiple key cellular components in preparation for subsequent wakefulness.

To what extent is sleep rebound effective in reversing the effects of paradoxical sleep deprivation on gene expression in the brain?

2009 ◽  
Vol 201 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Camila Guindalini ◽  
Monica L. Andersen ◽  
Tathiana Alvarenga ◽  
Kil Lee ◽  
Sergio Tufik
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Paradoxical Sleep ◽  
Paradoxical Sleep Deprivation ◽  
The Brain

scholarly journals Altered hippocampal transcriptome dynamics following sleep deprivation

2021 ◽  
Author(s):  
Marie E Gaine ◽  
Ethan Bahl ◽  
Snehajyoti Chatterjee ◽  
Jacob J Michaelson ◽  
Ted Abel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Rna Splicing ◽  
Public Health Problem ◽  
The United States ◽  
Postsynaptic Membrane ◽  
Protein Coding ◽  
Recovery Sleep ◽  
Behavioral Studies ◽  
Acute Sleep Deprivation

Widespread sleep deprivation is a continuing public health problem in the United States and worldwide affecting adolescents and adults. Acute sleep deprivation results in decrements in spatial memory and cognitive impairments. The hippocampus is vulnerable to acute sleep deprivation with changes in gene expression, cell signaling, and protein synthesis. Sleep deprivation also has long lasting effects on memory and performance that persist after recovery sleep, as seen in behavioral studies from invertebrates to humans. Although previous research has shown that acute sleep deprivation impacts gene expression, the extent to which sleep deprivation affects gene regulation remains unknown. Using an unbiased deep RNA sequencing approach, we investigated the effects of acute sleep deprivation on gene expression in the hippocampus. We identified 1,146 genes that were significantly dysregulated following sleep deprivation with 507 genes upregulated and 639 genes downregulated, including protein coding genes and long non-coding RNAs not previously identified as impacted by sleep deprivation. Notably, genes significantly upregulated after sleep deprivation were associated with RNA splicing and the nucleus. In contrast, downregulated genes were associated with cell adhesion, dendritic localization, the synapse, and postsynaptic membrane. These results clearly demonstrate that sleep deprivation differentially regulates gene expression on multiple transcriptomic levels to impact hippocampal function.

scholarly journals Sleep deprivation and diet affect human GH gene expression in transgenic mice in vivo

2020 ◽  
Vol 9 (12) ◽  
pp. 1135-1147
Author(s):  
Jessica S Jarmasz ◽  
Yan Jin ◽  
Hana Vakili ◽  
Peter A Cattini
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Sleep Deprivation ◽  
Chow Diet ◽  
Negative Effects ◽  
Production Studies ◽  
First Time ◽  
Rna Levels

Human (h) growth hormone (GH) production studies are largely limited to effects on secretion. How pituitary hGH gene (hGH-N/GH1) expression is regulated is important in our understanding of the role hGH plays in physiology and disease. Here we assess for the first time the effect of sleep deprivation (SD) and high-fat diet (HFD) on hGH-N expression in vivo using partially humanized 171hGH/CS transgenic (TG) mice, and attempted to elucidate a role for DNA methylation. Activation of hGH-N expression requires interactions between promoter and upstream locus control region (LCR) sequences including pituitary-specific hypersensitive site (HS) I/II. Both SD and diet affect hGH secretion, but the effect of SD on hGH-N expression is unknown. Mice fed a HFD or regular chow diet for 3 days underwent SD (or no SD) for 6 h at Zeitgeber time (ZT) 3. Serum and pituitaries were assessed over 24 h at 6-h intervals beginning at ZT 14. SD and HFD caused significant changes in serum corticosterone and insulin, as well as hGH and circadian clock-related gene RNA levels. No clear association between DNA methylation and the negative effects of SD or diet on hGH RNA levels was observed. However, a correlation with increased methylation at a CpG (cytosine paired with a guanine) in a putative E-box within the hGH LCR HS II was suggested in situ. Methylation at this site also increased BMAL1/CLOCK-related nuclear protein binding in vitro. These observations support an effect of SD on hGH synthesis at the level of gene expression.

Invited Review: How sleep deprivation affects gene expression in the brain: a review of recent findings

2002 ◽  
Vol 92 (1) ◽  
pp. 394-400 ◽  
Author(s):  
Chiara Cirelli
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Neural Plasticity ◽  
Hormone Receptors ◽  
Sleep Regulation ◽  
Cellular Mechanisms ◽  
Systematic Screening ◽  
Behavioral States ◽  
Shock Proteins ◽  
The Brain

The identification of the molecular correlates of sleep and wakefulness is essential to understand the restorative processes occurring during sleep, the cellular mechanisms underlying sleep regulation, and the functional consequences of sleep loss. To determine what molecular changes occur in the brain during the sleep-waking cycle and after sleep deprivation, our laboratory is performing a systematic screening of brain gene expression in rats that have been either sleeping or spontaneously awake for a few hours and in rats that have been sleep deprived for different periods of time ranging from a few hours to several days. So far, ∼10,000 transcripts expressed in the cerebral cortex have been screened. The expression of the vast majority of these genes does not change either across behavioral states or after sleep deprivation, even when forced wakefulness is prolonged for several days. A few hours of wakefulness, either spontaneous or forced by sleep deprivation, increase the expression of the same small groups of genes: immediate-early genes/transcription factors, genes related to energy metabolism, growth factors/adhesion molecules, chaperones/heat shock proteins, vesicle- and synapse-related genes, neurotransmitter/hormone receptors, neurotransmitter transporters, and enzymes. Sleep, on the other hand, induces the expression of a few unknown transcripts whose characterization is in progress. Thus, although the characterization of the molecular correlates of behavioral states is not yet complete, it is already apparent that the transition from sleep to waking can affect basic cellular functions such as RNA and protein synthesis, neural plasticity, neurotransmission, and metabolism. The pattern of changes in gene expression after long periods of sleep deprivation is unique and does not resemble that of short-term sleep deprivation or spontaneous wakefulness. A notable exception is represented, however, by the enzyme arylsulfotransferase, whose induction appears to be proportional to the duration of previous wakefulness. Arylsulfotransferase in rodents plays a major role in the catabolism of catecholamines, suggesting that an important role for sleep may be that of interrupting the continuous activity, during wakefulness, of brain catecholaminergic systems.

scholarly journals Changes in brain gene expression after long-term sleep deprivation

2006 ◽  
Vol 98 (5) ◽  
pp. 1632-1645 ◽  
Author(s):  
Chiara Cirelli ◽  
Ugo Faraguna ◽  
Giulio Tononi
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Brain Gene Expression
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