Research Paper Volume 9, Issue 3 pp 778—789
Microvesicles from the plasma of elderly subjects and from senescent endothelial cells promote vascular calcification
- 1 Departamento de Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud, Universidad de Alcalá, Alcalá de Henares, Madrid, Spain
- 2 Departamento de Biomedicina y Biotecnología, Facultad de Biología, Química y Ciencias Ambientales, Universidad de Alcalá. Alcalá de Henares, Madrid, Spain
- 3 Unidad de Anestesia, Hospital Universitario Reina Sofía/Universidad de Córdoba, Córdoba, Andalucía, Spain
- 4 Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC)/Hospital Universitario Reina Sofía/Universidad de Córdoba, Córdoba, Andalucía, Spain
- 5 Departamento de Química Orgánica, Universidad de Córdoba, Edificio Marie Curie (C-3), Carretera Nacional IV-A, Km 396, E14014, Córdoba, Andalucía, Spain
- 6 Departamento de Fisiología Animal (II), Facultad de Biología, Universidad Complutense de Madrid, Madrid, Spain
- 7 Institute of Investigation, Hospital 12 de Octubre, Madrid, Spain
- 8 These authors contributed equally to this paper
- 9 These senior authors contributed equally to this paper
Received: September 7, 2016 Accepted: February 26, 2017 Published: March 8, 2017
https://doi.org/10.18632/aging.101191How to Cite
Abstract
Vascular calcification is commonly seen in elderly people, though it can also appear in middle-aged subjects affected by premature vascular aging. The aim of this work is to test the involvement of microvesicles (MVs) produced by senescent endothelial cells (EC) and from plasma of elderly people in vascular calcification. The present work shows that MVs produced by senescent cultured ECs, plus those found in the plasma of elderly subjects, promote calcification in vascular smooth muscle cells. Only MVs from senescent ECs, and from elderly subjects' plasma, induced calcification. This ability correlated with these types of MVs' carriage of: a) increased quantities of annexins (which might act as nucleation sites for calcification), b) increased quantities of bone-morphogenic protein, and c) larger Ca contents. The MVs of senescent, cultured ECs, and those present in the plasma of elderly subjects, promote vascular calcification. The present results provide mechanistic insights into the observed increase in vascular calcification-related diseases in the elderly, and in younger patients with premature vascular aging, paving the way towards novel therapeutic strategies.