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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

ABSTRACT: Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases.

SUBMITTER: Aho V

PROVIDER: S-EPMC4840329 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

Aho Vilma V Ollila Hanna M HM Kronholm Erkki E Bondia-Pons Isabel I Soininen Pasi P Kangas Antti J AJ Hilvo Mika M Seppälä Ilkka I Kettunen Johannes J Oikonen Mervi M Raitoharju Emma E Hyötyläinen Tuulia T Kähönen Mika M Viikari Jorma S A JS Härmä Mikko M Sallinen Mikael M Olkkonen Vesa M VM Alenius Harri H Jauhiainen Matti M Paunio Tiina T Lehtimäki Terho T Salomaa Veikko V Orešič Matej M Raitakari Olli T OT Ala-Korpela Mika M Porkka-Heiskanen Tarja T

Scientific reports 20160422

Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and seru ...[more]

PMID: 27102866

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Project description:Background and aimsObstructive sleep apnea (OSA) is characterized by intermittent airway obstruction and systemic hypoxia during sleep, which can contribute to an increase in reactive oxygen species, vascular remodeling, vasoconstriction and ultimately cardiovascular disease. Continuous positive airway pressure (CPAP) is a clinical therapy that maintains airway patency and mitigates several symptoms of OSA. However, it is currently unknown whether CPAP therapy also reduces the overall inflammatory potential in the circulation; to address this in an unbiased manner, we applied a novel endothelial biosensor approach, the serum cumulative inflammatory potential (SCIP) assay.MethodsWe studied healthy controls (n = 7), OSA subjects receiving no treatment, (OSA controls) (n = 7) and OSA subjects receiving CPAP for 3 months (n = 8). Serum was obtained from OSA subjects before and after CPAP or no treatment. A battery of quantitative and functional assays was performed to assess the serum inflammatory potential, in terms of endothelial responses. For the SCIP assay, human coronary artery endothelial cells (hCAECs) were incubated with 5% serum in media from individual subjects for 4 h. qPCR was performed to assess endothelial inflammatory transcript (ICAM-1, VCAM-1, IL-8, P-selectin, CCL5, and CXCL12) responses to serum. Additionally, transendothelial resistance was measured in serum-incubated hCAECs following leukocyte challenge.ResultshCAECs exhibited significant increases in VCAM-1, ICAM-1, IL-8 and P-selectin mRNA when incubated with serum from OSA patients compared to serum from healthy control subjects. Furthermore, compared to no treatment, serum from CPAP-treated individuals was less potent at inducing inflammatory gene expression in the SCIP assay. Similarly, in a leukocyte adhesion assay, naïve cells treated with serum from patients who received CPAP exhibited improved endothelial barrier function than cells treated with OSA control serum.ConclusionsOSA results in greater serum inflammatory potential, thereby driving endothelial activation and dysfunction.

Dataset Information

Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

Publications

Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

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