Older adults had significantly higher concentrations of circulating apoptosis-derived endothelial microvesicles compared to young adults (306.1 vs 163.8 EMVs/µL, p=0.0016).
Cross-Sectional (n=36)
Aging is associated with an increase in circulating apoptosis-derived endothelial microvesicles, which correlates with increased arterial stiffness.
Tasa de eventos absoluta: 306.1% vs 163.8%
valor p: p=0.0016
Cardiovascular disease (CVD) risk increases with age. Underpinning age-related CVD risk is an increase in arterial stiffness and a decline in endothelial function. Microvesicles are released by many cells and participate in intracellular communication and have been found to play a role in disease. In response to apoptosis, endothelial cells release apoptosis-derived endothelial microvesicles (EMVs) that are CD31+/CD42b-. The purpose of this study was to assess the effects of age on circulating concentrations of large apoptosis-derived EMVs and their relation to arterial stiffness. We hypothesized that aging would be associated with an increase in the concentration of large apoptosis-derived EMVs and that EMV concentration would be associated with arterial stiffness. Venous blood samples were collected from thirty-six young (6M/6F, 25.8 ± 2.4 y/o), midlife (6M/6F, 48.9 ± 6.3 y/o) and older adults (5M/7F, 66.6 ± 5.2 y/o), who were free of chronic disease, had a SBP ≤ 140mmHg and DBP ≤ 90mmHg, and were non-obese (BMI ≤ 30 kg/m 2 ). Platelet-free plasma was incubated with fluorochrome-labeled CD31–APC and CD42b–PE antibodies. EMV concentration was determined via nanoscale flow cytometry (CytoFLEX LX). Size threshold was established by calibrator beads (Megamix-Plus FSC beads). CD31+/CD42b- events between 200 nm and 900 nm were considered large apoptosis-derived EMVs. Arterial stiffness was assessed using applanation tonometry (Sphygmocor CVMS) to determine carotid-femoral pulse wave velocity (cfPWV). Kruskal-Wallis testing found differences in concentrations of circulating CD31+/CD42b- EMVs across age groups (Young: 163.8 ± 55.0 EMVs/µL, Midlife: 204.1 ± 37.2 EMVs/µL, Older: 306.1 ± 129.3 EMVs/µL, p=0.0023). Post-hoc comparisons found higher concentrations of CD31+/CD42b- EMVs in older adults compared to young adults (p=0.0016). CD31+/CD42b- EMVs concentrations were positively associated with age (r2= 0.2505, p=0.0023). cfPWV was different across age groups (Young: 5.7 ± 0.5 m/s, Midlife: 6.2 ± 1.3 m/s, Older: 8.4 ± 2.0 m/s, p=0.0002). cfPWV was higher in older adults compared to young (p=0.0002) and midlife adults (p=0.0091). Concentrations of circulating CD31+/CD42b- EMVs were positively associated with cfPWV (r2 = 0.1607, p=0.0365). Overall, these data indicate an age-related increase in apoptosis-derived EMVs that is associated with an increase in arterial stiffness. EMVs may represent a novel biomarker and potential mediator of age-related increase in arterial stiffness and decline in vascular function, but this requires further study. This work was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health (2P20GM113125) This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Zercher et al. (Fri,) conducted a cross-sectional in Healthy adults (n=36). Older age vs. Young age was evaluated on Concentration of circulating CD31+/CD42b- EMVs (p=0.0016). Older adults had significantly higher concentrations of circulating apoptosis-derived endothelial microvesicles compared to young adults (306.1 vs 163.8 EMVs/µL, p=0.0016).