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ORIGINAL ARTICLE
Year : 2011  |  Volume : 2  |  Issue : 2  |  Page : 110-114

Habitual short sleep duration and circulating endothelial progenitor cells


1 Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado Boulder, Colorado, USA
2 Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado Boulder; Department of Medicine, University of Colorado at Denver, Aurora and Denver Health Medical Center, Denver, CO, USA
3 Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado Boulder; Department of Medicine, University of Colorado at Denver, Aurora, USA

Correspondence Address:
Christopher A DeSouza
Integrative Vascular Biology Laboratory, Department of Integrative Physiology,354 UCB, University of Colorado, Boulder, CO 80309
USA
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DOI: 10.4103/0975-3583.83039

PMID: 21814415

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Chronic short sleep duration has been linked to endothelial dysfunction and increased risk of cardiovascular disease. Circulating endothelial progenitor cells (EPCs) are vital to endogenous vascular repair processes and cardiovascular health. We tested the hypothesis that habitual short sleep duration is associated with impairment in EPC number and function. Cells with phenotypic EPC characteristics were isolated from 37 healthy, sedentary adults: 20 with normal sleep duration (13M/7F; age: 59±1 years; sleep duration: 7.7±0.1 h/night) and 17 with short sleep duration (9M/8F; 56±2 years; 6.0±0.2 h/night). EPC number was assessed by flow cytometric analysis of the percentage of peripheral blood mononuclear cells negative for CD45 and positive for CD34, VEGFR-2, and CD133 antigens. EPC colony-forming capacity was determined by colony-forming unit (CFU) assay; migration by Boyden chamber; and intracellular caspase-3 concentrations by immunoassay. There were no significant differences between groups in EPC number (0.001±0.0004 vs. 0.001±0.0003 %), colony-forming capacity (6.1±1.5 vs. 5.4±1.7 CFUs), or migration to VEGF (1410.1±151.2 vs. 1334.3±111.1 AU). Furthermore, there were no group differences in basal and staurosporine-stimulated intracellular concentrations of active caspase-3 (0.3±0.03 vs. 0.5±0.1 ng/mL; and 2.9±0.4 vs. 2.7±0.3 ng/mL), a marker of apoptotic susceptibility. Taken together, these data indicate that short sleep duration is not associated with EPC dysfunction in healthy adults. Numerical and functional impairment in circulating EPCs may not contribute to the increased cardiovascular risk with habitual short sleep duration.


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