Short Sleep Duration and Endothelial Progenitor Cell Function

Abstract

Chronic short sleep duration is associated with increased cardiovascular (CV) morbidity. Mechanisms underlying this increased CV risk are not clear. Endothelial progenitor cells (EPCs) contribute to both reendothelialization and neovascularization. Numerical and functional impairment of EPCs has been linked to CV risk. Currently, there is no information regarding the influence of short sleep duration on EPC function. We tested the hypothesis that EPC function is impaired in adults who sleep less than 7 hrs/night (short sleep) compared with those who sleep 7 to 9 hrs/night (normal sleep). Cells with phenotypic EPC characteristics were isolated from 37 healthy, sedentary adults: 20 normal sleepers (13M/7F; age: 59±1 yr; sleep: 7.7±0.1 hrs/night) and 17 short sleepers (9M/8F; 56±2 yr; 6.0±0.2 hrs/night). There were no significant differences between groups in EPC number via FACS (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 in a Boyden chamber (1410.1±151.2 vs 1334.3±111.1 AU). Furthermore, 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) and cytochrome c (16.4±0.7 vs 14.5±1.4 ng/mL), markers of apoptotic susceptibility. Short sleep duration is not associated with EPC dysfunction in healthy adults.