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

Pandey, Anshuman; Oliver, Ryan; Kar, Sasmita

doi:10.3390/clockssleep2040033

Cited by 7 publications

(6 citation statements)

References 192 publications

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“…The ZNF184 encodes a Kruppel C2H2-type zinc-finger protein family member, which participates in gene expression regulation. One study found that REM sleep deprivation in rats induced significant ZNF184 down-regulation in the brain [ 46 ]. The effects of this mutation on other features of PD are unknown.…”

Section: Discussionmentioning

confidence: 99%

The Genetic Basis of Probable REM Sleep Behavior Disorder in Parkinson’s Disease

Perez-Lloret,

Chevalier,

Bordet

et al. 2023

Brain Sciences

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Patients with Parkinson’s Disease (PD) experience REM sleep behavior disorder (RBD) more frequently than healthy controls. RBD is associated with torpid disease evolution. To test the hypothesis that differential genetic signatures might contribute to the torpid disease evolution in PD patients with RBD we compared the rate of genetic mutations in PD patients with or without probable RBD. Patients with a clinical diagnosis of PD in the Parkinson’s Progression Markers Initiative (PPMI) database entered the study. We excluded those with missing data, dementia, psychiatric conditions, or a diagnosis change over the first five years from the initial PD diagnosis. Probable RBD (pRBD) was confirmed by a REM Sleep Behavior Disorder Screening Questionnaire score > 5 points. Logistic regression and Machine Learning (ML) algorithms were used to relate Single Nucleotide Polymorphism (SNPs) in PD-related genes with pRBD. We included 330 PD patients fulfilling all inclusion and exclusion criteria. The final logistic multivariate model revealed that the following SNPs increased the risk of pRBD: GBA_N370S_rs76763715 (OR, 95% CI: 3.38, 1.45–7.93), SNCA_A53T_rs104893877 (8.21, 2.26–36.34), ANK2. CAMK2D_rs78738012 (2.12, 1.08–4.10), and ZNF184_rs9468199 (1.89, 1.08–3.33). Conversely, SNP COQ7. SYT17_rs11343 reduced pRBD risk (0.36, 0.15–0.78). The ML algorithms led to similar results. The predictive models were highly specific (95–99%) but lacked sensitivity (9–39%). We found a distinctive genetic signature for pRBD in PD. The high specificity and low sensitivity of the predictive models suggest that genetic mutations are necessary but not sufficient to develop pRBD in PD. Additional investigations are needed.

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Section: Discussionmentioning

confidence: 99%

The Genetic Basis of Probable REM Sleep Behavior Disorder in Parkinson’s Disease

Perez-Lloret,

Chevalier,

Bordet

et al. 2023

Brain Sciences

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“…Although previous reports have shown a close relation between sleep and sleep deprivation and ER stress and UPR [ 43 , 44 , 45 ], most of the basic research has been done in brain regions such as the hypothalamus and cerebral cortex. Pandey et al [ 20 ] evaluated gene transcript expression in the brain and liver of rats treated with 9 days of REM sleep deprivation. In their report, 652 genes were altered in brain and 426 genes were affected in the liver, but only 23 genes had changes in common (10 opposite, 13 in the same directions) across the brain and liver tissue.…”

Section: Discussionmentioning

confidence: 99%

“…These findings suggest that biological molecular changes induced by sleep and sleep deprivation may be consistent between the central and peripheral regions, while others may not. Indeed, Pandey et al [ 20 ] concluded that the brain functions related to synaptic potentiation, learning and memory, oxidative stress, and circadian rhythms were more vulnerable to REM sleep deprivation. On the other hand, REM sleep loss strongly affected protein synthesis, stress balance, and detoxification in the liver.…”

Section: Discussionmentioning

confidence: 99%

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Recovery Sleep Immediately after Prolonged Sleep Deprivation Stimulates the Transcription of Integrated Stress Response-Related Genes in the Liver of Male Rats

et al. 2022

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Sleep loss induces performance impairment and fatigue. The reactivation of human herpesvirus-6, which is related to the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), is one candidate for use as an objective biomarker of fatigue. Phosphorylated eIF2α is a key regulator in integrated stress response (ISR), an intracellular stress response system. However, the relation between sleep/sleep loss and ISR is unclear. The purpose of the current study was to evaluate the effect of prolonged sleep deprivation and recovery sleep on ISR-related gene expression in rat liver. Eight-week-old male Sprague–Dawley rats were subjected to a 96-hour sleep deprivation using a flowerpot technique. The rats were sacrificed, and the liver was collected immediately or 6 or 72 h after the end of the sleep deprivation. RT-qPCR was used to analyze the expression levels of ISR-related gene transcripts in the rat liver. The transcript levels of the Atf3, Ddit3, Hmox-1, and Ppp15a1r genes were markedly increased early in the recovery sleep period after the termination of sleep deprivation. These results indicate that both activation and inactivation of ISRs in the rat liver occur simultaneously in the early phase of recovery sleep.

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“…A study revealed that, in the cortex and hypothalamus of sleep-deprived mice, 2499 genes changed their expression due to sleep deprivation [27]. Similar variations were observed in the rat liver, where 426 genes were modified [28]. On the other hand, analysis of the blood transcriptome is a reference tool with which to relate gene expression with other systems in the organism [29].…”

Section: Sleep As a Modulator Of Circadian Rhythmsmentioning

confidence: 95%

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

Moreno-Cortés,

Meza-Alvarado,

García-Mena

et al. 2024

Nutrients

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The desynchronization of physiological and behavioral mechanisms influences the gut microbiota and eating behavior in mammals, as shown in both rodents and humans, leading to the development of pathologies such as Type 2 diabetes (T2D), obesity, and metabolic syndrome. Recent studies propose resynchronization as a key input controlling metabolic cycles and contributing to reducing the risk of suffering some chronic diseases such as diabetes, obesity, or metabolic syndrome. In this analytical review, we present an overview of how desynchronization and its implications for the gut microbiome make people vulnerable to intestinal dysbiosis and consequent chronic diseases. In particular, we explore the eubiosis–dysbiosis phenomenon and, finally, propose some topics aimed at addressing chronotherapy as a key strategy in the prevention of chronic diseases.

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

Cited by 7 publications

References 192 publications

The Genetic Basis of Probable REM Sleep Behavior Disorder in Parkinson’s Disease

The Genetic Basis of Probable REM Sleep Behavior Disorder in Parkinson’s Disease

Recovery Sleep Immediately after Prolonged Sleep Deprivation Stimulates the Transcription of Integrated Stress Response-Related Genes in the Liver of Male Rats

Chronodisruption and Gut Microbiota: Triggering Glycemic Imbalance in People with Type 2 Diabetes

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