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Review
. 2013 Aug;33(8):1753-8.
doi: 10.1161/ATVBAHA.112.300128. Epub 2013 Jun 13.

Role of extracellular vesicles in de novo mineralization: an additional novel mechanism of cardiovascular calcification

Sophie E P New  1 , Elena Aikawa
Affiliations
Review

Role of extracellular vesicles in de novo mineralization: an additional novel mechanism of cardiovascular calcification

Sophie E P New et al. Arterioscler Thromb Vasc Biol. 2013 Aug.

Abstract

Extracellular vesicles are membrane micro/nanovesicles secreted by many cell types into the circulation and the extracellular milieu in physiological and pathological conditions. Evidence suggests that extracellular vesicles, known as matrix vesicles, play a role in the mineralization of skeletal tissue, but emerging ultrastructural and in vitro studies have demonstrated their contribution to cardiovascular calcification as well. Cells involved in the progression of cardiovascular calcification release active vesicles capable of nucleating hydroxyapatite on their membranes. This review discusses the role of extracellular vesicles in cardiovascular calcification and elaborates on this additional mechanism of calcification as an alternative pathway to the currently accepted mechanism of biomineralization via osteogenic differentiation.

Keywords: atherosclerosis; calcification; extracellular vesicles; inflammation; macrophages; rupture; valve disease.

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Figures

Figure 1
Figure 1
Mechanism of pathological matrix vesicle mineralization: A mineral imbalance leads to an influx of phosphate and calcium into the vesicle via appropriate channels – ALP generates inorganic phosphate in the extravesicular space. Nucleation of hydroxyapatite (HA) is facilitated by an annexin (Anx)-PS complex, enabling generation of microcalcification/calcification.
Figure 2
Figure 2
Ultrastructural images of a calcified human tissue: A, defined border of microcalcification; B, higher magnification shows extracellular vesicles (red arrowhead) within regions of microcalcification and nucleation of hydroxyapatite on the outer membrane of MV (red arrow). Inset image shows the nucleation of MV on the inner membrane.
See this image and copyright information in PMC

References

    1. Johnson RC, Leopold JA, Loscalzo J. Vascular calcification: pathobiological mechanisms and clinical implications. Circ Res. 2006;99:1044–1059. - PubMed
    1. Bobryshev YV, Killingsworth MC, Lord RS, Grabs AJ. Matrix vesicles in the fibrous cap of atherosclerotic plaque: possible contribution to plaque rupture. J Cell Mol Med. 2008;12:2073–2082. - PMC - PubMed
    1. Vengrenyuk Y, Carlier S, Xanthos S, Cardoso L, Ganatos P, Virmani R, Einav S, Gilchrist L, Weinbaum S. A hypothesis for vulnerable plaque rupture due to stress-induced debonding around cellular microcalcifications in thin fibrous caps. Proc Natl Acad Sci USA. 2006;103:14678–14683. - PMC - PubMed
    1. Vengrenyuk Y, Kaplan TJ, Cardoso L, Randolph GJ, Weinbaum S. Computational stress analysis of atherosclerotic plaques in ApoE knockout mice. Ann Biomed Eng. 2010;38:738–747. - PubMed
    1. Wenk JF. Numerical modeling of stress in stenotic arteries with microcalcifications: a parameter sensitivity study. J Biomech Eng. 2011;133:014503. - PubMed

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