Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries

Proof of principle

Maria A K Schwartz, John C Lieske, Vivek Kumar, Gerard Farel-Baril, Virginia M Miller

Research output: Contribution to journalArticle

31 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)243-248
Number of pages6
JournalInternational Journal of Nanomedicine
Volume3
Issue number2
StatePublished - 2008

Fingerprint

Carotid Arteries
Nanoparticles
Blood Vessels
Rabbits
Wounds and Injuries
Kidney Calculi
Arteries
Tunica Intima
Endothelium
Hyperplasia
Animals
Tissue

Keywords

  • Arterial calcification
  • Endothelial injury
  • Intimal hyperplasia

ASJC Scopus subject areas

  • Biophysics
  • Bioengineering
  • Biomaterials
  • Organic Chemistry
  • Drug Discovery

Cite this

Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries : Proof of principle. / Schwartz, Maria A K; Lieske, John C; Kumar, Vivek; Farel-Baril, Gerard; Miller, Virginia M.

In: International Journal of Nanomedicine, Vol. 3, No. 2, 2008, p. 243-248.

Research output: Contribution to journalArticle

@article{77ece067a8e84655b44ad913471c8b95,
title = "Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries: Proof of principle",
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",
author = "Schwartz, {Maria A K} and Lieske, {John C} and Vivek Kumar and Gerard Farel-Baril and Miller, {Virginia M}",
year = "2008",
language = "English (US)",
volume = "3",
pages = "243--248",
journal = "International Journal of Nanomedicine",
issn = "1176-9114",
publisher = "Dove Medical Press Ltd.",
number = "2",

}

TY - JOUR

T1 - Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries

T2 - Proof of principle

AU - Schwartz, Maria A K

AU - Lieske, John C

AU - Kumar, Vivek

AU - Farel-Baril, Gerard

AU - Miller, Virginia M

PY - 2008

Y1 - 2008

N2 - 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.

AB - 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.

KW - Arterial calcification

KW - Endothelial injury

KW - Intimal hyperplasia

UR - http://www.scopus.com/inward/record.url?scp=61349112920&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=61349112920&partnerID=8YFLogxK

M3 - Article

VL - 3

SP - 243

EP - 248

JO - International Journal of Nanomedicine

JF - International Journal of Nanomedicine

SN - 1176-9114

IS - 2

ER -