Ontology highlight
ABSTRACT:
PROVIDER: PRJNA659278 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12516449_1.fastq.gz | Fastqsanger.gz | |||
| SRR12516449_2.fastq.gz | Fastqsanger.gz | |||
| SRR12516450_1.fastq.gz | Fastqsanger.gz | |||
| SRR12516450_2.fastq.gz | Fastqsanger.gz | |||
| SRR12516451_1.fastq.gz | Fastqsanger.gz |
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Project description:Study Objectives: Sleep deprivation is highly prevalent and caused by conditions such as night shift work or illnesses like obstructive sleep apnea. Compromised sleep is proposed to play a role in several cardiovascular, immune related and neurodegenerative disorders. We recently published human serum proteome changes after a simulated night shift. This study aimed to further explore changes in the human blood serum after 6h of sleep deprivation at night by proteomics and systems biological databases. Methods: Human blood serum samples from 8 self-declared healthy females were analyzed using mass spectrometry and high-pressure liquid chromatography. Each subject was their own control, and two samples were taken from each subject, the first one after 6h of sleep at night and the second one after 6h of sleep deprivation the following night. Biological databases and bioinformatic software were used for systems biological analyzes and comparative analysis with other published sleep-related datasets. Results: Of 494 proteins, 66 were found to be differentially expressed after 6h of sleep deprivation at night. Functional enrichment analysis revealed associations of these proteins with several biological functions related to the regulation of cellular processes like protein- and ion-binding connected to platelet degranulation and blood coagulation, as well as associations with different curated gene sets. Conclusions: This study presents serum proteomic changes after 6h of sleep deprivation, supports previous findings that only 6h of sleep deprivation affects several biological processes and revealed a molecular signature of protein changes related to pathological conditions like altered coagulation and platelet function, impaired lipid and immune function and cancer. Keywords: Human blood serum, proteomics, sleep deprivation, cellular stress, functional enrichment analysis
2024-06-27 | PXD045729 | Pride
Project description:Background: Age-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption’s well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep’s relationship to cognitive aging. Methodology: We measured sleep stages in young adult and aged F344 rats during inactive (enhanced sleep) and active (enhanced wake) periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken. Principal Findings: Water maze performance was impaired, and inactive period deep sleep was decreased with age. However, increased deep sleep during the active period was most strongly correlated to maze performance. Transcriptional profiles were strongly associated with behavior and age, and were validated against prior studies. Bioinformatic analysis revealed increased translation and decreased myelin/ neuronal pathways. Conclusions: The F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep. Microarray analysis suggests that the processes engaged by this sleep are consistent with its function. Thus, active period deep sleep appears temporally misaligned but mechanistically intact, leading to the following: first, aged brain tissue appears capable of generating the slow waves necessary for deep sleep, albeit at a weaker intensity than in young. Second, this activity, presented during the active period, seems disruptive rather than beneficial to cognition. Third, this active period deep sleep may be a cognitively pathologic attempt to recover age-related loss of inactive period deep sleep. Finally, therapeutic strategies aimed at reducing active period deep sleep (e.g., by promoting active period wakefulness and/or inactive period deep sleep) may be highly relevant to cognitive function in the aging community. KEYWORDS: frontal cortex, rat, young or aged We implanted young and aged Fischer 344 rats (n = 6/ group) with wireless EEG, EMG and movement monitoring devices to measure sleep architecture. Animals were trained in the Morris water maze to assess cognitive function, and frontal cortices were removed for microarray analysis.sleep disruption and cognitive decline.
2011-04-21 | E-GEOD-24515 | biostudies-arrayexpress
Project description:Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total acute sleep deprivation (TSD) on the genome wide methylation profile in blood compared to normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations (neutrophil/leukocyte ratio). Additionally, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of ten healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69bp upstream of ING5, which has been shown to be differentially expressed following sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.
2016-06-30 | E-MTAB-4664 | biostudies-arrayexpress
Project description:CD163+ macrophages monitor enhanced permeability at the blood–dorsal root ganglion barrier
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Project description:Sleep is an evolutionarily conserved physiological process implicated in the consolidation of learning and memory. In our study, sleep deprivation-induced cognitive deficits in zebrafish are mediated through reduction in glucose metabolism to the hexosamine biosynthetic pathway. Therefore, we perform the microarray to confirm glucose metabolic pathway- and nerve system-related genes expression using mRNA from brains of control, sleep-deprived and fear-conditioned zebrafish groups.
2019-03-14 | GSE128217 | GEO
Project description:Obstructive sleep apnea syndrome (OSA) is a common sleep disorder. OSA is an independent risk factor for cognitive impairment. Chronic intermittent hypoxia (CIH) is the main characteristic of OSA and the main potential culprit of OSA-induced hippocampal damage. The mechanism of CIH in the development of cognitive impairment remains unclear The microarray was used to investigate the differentially expressed long non-coding RNAs(lncRNAs), microRNAs (miRNAs) and mRNAs in the hippocampus of control and CIH-exposed rats. The rats in control group and CIH group were exposed to normoxia for 4 weeks and CIH for 4 weeks, respectively.
2025-08-17 | GSE211586 | GEO
Project description:Cognitive impairment due to cancer and its therapy is a major concern among cancer survivors. Extracellular vesicles (EVs) composition altered by cancer and chemotherapy may affect neurological processes such as neuroplasticity, potentially impacting the cognitive abilities of cancer survivors. We investigated the EV proteome of breast cancer patients with and without cognitive impairment following anthracycline-based chemotherapy from longitudinally collected plasma. EVs were cup-shaped and positive for Flotillin-1 and TSG-101. We identified 517 differentially expressed EV proteins between the cognitive impaired and non-impaired groups during and post-chemotherapy. The observed decreased expression of p2X purinoceptor, cofilin-1, ADAM 10, and dynamin-1 in the plasma EVs of cognitive impaired group may suggest alterations in mechanisms underlying synaptic plasticity. The reduced expression of tight junction proteins among cognitive-impaired patients may imply weakening of the blood-brain barrier. These EV protein signatures may serve as a fingerprint that underscore the mechanisms underlying cognitive impairment in cancer survivors.
2021-05-27 | PXD021395 | Pride
Project description:The precise regulation of blood-brain-barrier (BBB) permeability for immune cells and blood-borne substances is essential to maintain brain homeostasis. Sphingosine-1-phosphate (S1P), a lipid signaling molecule enriched in plasma, is known to affect BBB permeability. Previous studies focussed on endothelial S1P receptors 1 and 2, reporting a barrier-protective effect of S1P1 and a barrier-disruptive effect of S1P2. Here we present novel data characterizing the expression, localization and function of the hitherto exclusively immunce cell-associated S1P receptor 4 (S1P4) on primary brain microvascular endothelial cells (BMECs). We detected a robust expression of S1P4 in homeostatic BMECs and pinpointed its localization to abluminal endothelial membranes by electron microscopy. Basolateral S1P treatment of BMECs led to increased permeability in vitro associated with S1P4 downregulation. Likewise, downregulation of S1P4 was observed in mouse brain microvessels after stroke, a neurological disease associated with BBB impairment. RNA sequencing analysis of BMECs suggested involvement of S1P4 in endothelial homeostasis, apicobasal polarity and barrier function. Using siRNA, pharmacological agonists and antagonists of S1P4 both in vitro and in vivo, we demonstrate a barrier-protective function of S1P4. We therefore suggest S1P4 as a novel target regulating BBB permeability and propose its therapeutic targeting in CNS diseases associated with BBB dysfunction.
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Project description:Sleep supports lifelong brain health and cognition. Sleep loss in early life can drive lasting changes in adult behavior, indicating sleep plays a distinct but poorly understood role supporting brain development. We systematically examined the molecular and behavioral adaptations and synaptic consequences of acute sleep deprivation (SD) in developing and adult mice. Developing mice lack robust adaptations to SD, exacerbating cognitive deficits. Synapse proteome and phosphoproteome analysis revealed profound vulnerability to SD in developing mice, including immediate impacts on synaptogenesis and key aspects of brain development. With maturation, a unified biochemical effect of sleep on synapses emerges, together with robust adaptations and resilience to SD. Our findings show sleep plays a distinct role in early life supporting synapse development, transitioning to homeostatic functions with maturation.
2024-10-08 | PXD047381 | Pride