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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 2492858, 8 pages
http://dx.doi.org/10.1155/2016/2492858
Research Article

The Impact of Lipoprotein-Associated Oxidative Stress on Cell-Specific Microvesicle Release in Patients with Familial Hypercholesterolemia

1Danish PhD School of Molecular Metabolism, University of Southern Denmark, 5000 Odense, Denmark
2Department of Clinical Biochemistry, Aalborg University Hospital, 9000 Aalborg, Denmark
3Department of Medicine and Cardiology A, Aarhus University Hospital, 8000 Aarhus, Denmark
4Department of Radiology, Aarhus University Hospital, 8000 Aarhus, Denmark
5Department of Cardiology, Aalborg University Hospital, 9000 Aalborg, Denmark
6Department of Endocrinology M, University of Southern Denmark, 5000 Odense, Denmark
7Department of Clinical Medicine, Faculty of Medicine, Aalborg University, 9000 Aalborg, Denmark

Received 5 October 2015; Accepted 31 December 2015

Academic Editor: Domenico D’Arca

Copyright © 2016 M. H. Nielsen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. Microvesicles (MVs) are small cell-derived particles shed upon activation. Familial hypercholesterolemia (FH) particularly when associated with Achilles tendon xanthomas (ATX) predisposes to atherosclerosis, possibly through oxLDL-C interaction with the CD36 receptor. To investigate the hypothesis that MVs derived from cells involved in atherosclerosis are increased in FH and that CD36 expressing MVs (CD36+ MVs) may be markers of oxLDL-C-induced cell activation, cell-specific MVs were measured in FH patients with and without ATX and their association with atherogenic lipid profile was studied. Approach and Results. Thirty FH patients with and without ATX and twenty-three controls were included. Plasma concentrations of MVs and CD36+ MVs derived from platelets (PMVs), erythrocytes (ErytMVs), monocytes (MMVs), and endothelial cells (EMVs), as well as tissue factor-positive cells (TF+ MVs), were measured by flow cytometry. Total MVs, MMVs, EMVs, ErytMVs, and TF+ MVs were significantly increased in FH patients, compared to controls. CD36+ MVs derived from endothelial cells and monocytes were significantly higher in FH patients and oxLDL-C predicted all the investigated cell-specific CD36+ MVs in FH patients with ATX. Conclusions. MVs derived from cells involved in atherosclerosis were increased in FH and may contribute to elevated atherothrombosis risk. The increased cell-specific CD36+ MVs observed in FH may represent markers of oxLDL-C-induced cell activation.