Reassessing the effects of continuous positive airway pressure (CPAP) on arterial stiffness and peripheral blood derived CD34+ progenitor cells in subjects with sleep apnea

Abstract

Background Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular diseases (CVD) and vascular health. Peripheral blood-derived CD34+ progenitor cells have been used as biomarker for CVD risk and may play a similar role in OSA and CVD risk assessment. Although there are some controversial results in the literature, OSA patients may have a reduction in the number and function of CD34+ cells. The damages promoted by OSA in CD34+ cells may lead to an increase in endothelial oxidative stress and endothelial inflammation which may lead to a reduced endothelial repair capacity. In this study, we explored the effect of continuous positive airway pressure (CPAP) on peripheral blood-derived CD34+ cells and arterial stiffness (another predictor of endothelial health and CVD risk) in OSA patients. Methods and results Nine overweight and obese subjects without prediabetes or diabetes were recruited. Eight out of nine subjects had moderate to severe degree of OSA. CD34+ cells were isolated from peripheral blood. Number and function of these cells were monitored before and after 3 months of treatment with CPAP. No significant changes were observed in the number of CD34+ cells, CFU-Hill’s colony formation unit (CFU) count or migratory response to the chemotactic factor SDF-1a after CPAP use. However, CXCR4 mRNA expression significantly increased by 2.2-fold indicating that CPAP may have a positive effect on SDF1a receptor (CXCR4), thereby improving migration of CD34+ cells mediated by SDF1a after the 3 month period. Interestingly, in clinical arena our results showed a reduction of pulse wave velocity (an established parameter of arterial stiffness) following CPAP therapy. Conclusions Our findings suggest that 3-month CPAP intervention does not show statistical significant increase in CD34+ cell number and function, in mostly moderate to severe OSA subjects; however, it did demonstrate a positive trend. CPAP therapy, did help improve arterial stiffness parameter. Electronic supplementary material The online version of this article (10.1186/s13287-019-1251-8) contains supplementary material, which is available to authorized users.

Sudden infant death syndrome: Melatonin, serotonin, and CD34 factor as possible diagnostic markers and prophylactic targets

“…It is known that an assembly of CD34 molecules in tissue is a marker of active proliferation of endothelial cells, stimulating angiogenesis in ischemia and reperfusion under conditions of hypoxic damage [53][54][55][56]. On the contrary, decreased expression of CD34 is observed in cases of expressed oxidative stress and endothelial inflammation, thus evidencing the absence of reparation processes [57]. Similar disturbances are observed in fetuses whose intrauterine development proceeded under conditions of chronic hypoxia and lacking maternal melatonin [58].…”

No impact of acute hyperglycaemia on arterial stiffness in the early and late follicular phases of the menstrual cycle in young females

“…Acute changes in arterial stiffness occur with a change in blood pressure and tone (Zieman, Melenovsky, & Kass, ), whereas chronic changes in stiffness occur with remodelling of the vascular wall, secondary to changes in gene expression triggered by repeated molecular and mechanical signals (Domingues et al., ; Kahlberg et al., ; Lucitti, Visconti, Novak, & Keller, ; Ribeiro Júnior et al., ; Zieman et al., ). Chronically increased stiffness, particularly of the central arteries, is related to increased risk of cardiovascular disease (van Sloten et al., ; Vlachopoulos, Aznaouridis, & Stefanadis, ).…”

Advances in the study of OSA and diabetic foot

“…In addition, in patients with moderate and severe OSA, the atherosclerotic plaque was larger than that in the control group [ 35 ]. In OSA patients treated with continuous positive airway pressure (CPAP), arterial stiffness can be improved [ 36 , 37 ].…”

“…Reactive oxygen species can cause different degrees of endothelial cell damage, and then affect its normal physiological function [ 32 ]. And decreased mobilization of endothelial progenitor cells (ERC) and EPC apoptosis, resulting in the reduction of circulating EPCs, resulting in the reduction of endothelial cell repair ability, which leads to the delay of wound healing [ 36 ].…”