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Cardiovascular Research 2007 73(3):549-559; doi:10.1016/j.cardiores.2006.11.031
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Copyright © 2006, European Society of Cardiology

Cardioprotective effects of cerium oxide nanoparticles in a transgenic murine model of cardiomyopathy

Jianli Niu, Asim Azfer, Linda M. Rogers, Xihai Wang and Pappachan E. Kolattukudy*

Biomolecular Science Center, Burnett College of Biomedical Science, University of Central Florida, Orlando, FL 32816, USA

* Corresponding author. Biomolecular Science Center, Burnett College of Biomedical Science Center, University of Central Florida, Bldg. 20, Rm. 136, Orlando, FL 32826-2364, USA. Tel.: +1 407 823 1206; fax: +1 407 823 0956. Email address: pk{at}mail.ucf.edu

Objective: Cerium oxide (CeO2) nanoparticles have been shown to protect cells in culture from lethal stress, but no protection in vivo has been reported. Cardiac-specific expression of monocyte chemoattractant protein (MCP)-1 in mice causes ischemic cardiomyopathy associated with activation of endoplasmic reticulum (ER) stress. The aim of this study was to assess the effects of CeO2 nanoparticles on cardiac function and remodeling as well as ER stress response in this murine model of cardiomyopathy.

Methods: MCP-1 transgenic mice (MCP mice) and wild-type controls were administered intravenously 15 nmol of CeO2 nanoparticles or vehicle only twice a week for 2 weeks. Cardiac function, myocardial histology, nitrotyrosine formation, expression of cytokines, and ER stress-associated genes were evaluated.

Results: Treatment with CeO2 nanoparticles markedly inhibited progressive left ventricular dysfunction and dilatation in MCP mice and caused a significant decrease in serum levels of MCP-1, C-reactive protein, and total nitrated proteins. The infiltration of monocytes/macrophages, accumulation of 3-nitrotyrosine, apoptotic cell death, and expression of proinflammatory cytokines, tumor necrosis factor (TNF)-{alpha}, interleukin (IL)-1β, and IL-6 in the myocardium were markedly inhibited by CeO2 nanoparticles. Expression of the key ER stress-associated genes, including glucose-regulated protein 78 (Grp78), protein disulfide isomerase (PDI), and heat shock proteins (HSP25, HSP40, HSP70), were also suppressed by CeO2 nanoparticles.

Conclusions: CeO2 nanoparticles protect against the progression of cardiac dysfunction and remodeling by attenuation of myocardial oxidative stress, ER stress, and inflammatory processes probably through their autoregenerative antioxidant properties.

KEYWORDS MCP-1; Cardiomyopathy; ER stress; CeO2 nanoparticles; Transgenic animal model

Time for primary review 23 days


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