Human-derived nanoparticles and vascular response to injury in rabbit
carotid arteries: Proof of principle

Maria A K Schwartz1, John C Lieske2, Vivek Kumar2, Gerard Farell-
Baril2, Virginia M Miller1,3

1Departments of Physiology and Biomedical Engineering, Internal
Medicine; 2Division of Nephrology, and 3Surgery, Mayo Clinic College
of Medicine, Rochester, MN, USA

Abstract: Self-calcifying, self-replicating nanoparticles have been
isolated from calcified human tissues. However, it is unclear if these
nanoparticles participate in disease processes. Therefore, this study
was designed to preliminarily test the hypothesis that human-derived
nanoparticles are causal to arterial disease processes. One carotid
artery of 3 kg male rabbits was denuded of endothelium; the
contralateral artery remained unoperated as a control. Each rabbit was
injected intravenously with either saline, calcified, or decalcified
nanoparticles cultured from calcified human arteries or kidney stones.
After 35 days, both injured and control arteries were removed for
histological examination. Injured arteries from rabbits injected with
saline showed minimal, eccentric intimal hyperplasia. Injured arteries
from rabbits injected with calcified kidney stone- and arterial-
derived nanoparticles occluded, sometimes with canalization. The
calcified kidney stone-derived nanoparticles caused calcifications
within the occlusion. Responses to injury in rabbits injected with
decalcified kidney stone-derived nanoparticles were similar to those
observed in saline-injected animals. However, decalcified arterial-
derived nanoparticles produced intimal hyperplasia that varied from
moderate to occlusion with canalization and calcification. This study
offers the first evidence that there may be a causal relationship
between human-derived nanoparticles and response to injury including
calcification in arteries with damaged endothelium.

Keywords: arterial calcification, endothelial injury, intimal
hyperplasia

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