Journal
NANOMEDICINE
Volume 7, Issue 5, Pages 705-717Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/NNM.11.148
Keywords
atherosclerosis; cytokine; degradation; iron; lysosomal; monocyte; nanoparticle
Funding
- Swedish Heart Lung Foundation
- research fund of Torsten och Ragnar Soderbergs
- research fund of Stroke
- research fund of Gamla Tjanarinnor
- Linkoping University Hospital
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Aim: To examine the physiological impact of superparamagnetic iron oxide nanoparticles (SPIONs) on cell function and its interaction with oxysterol laden cells. Materials & methods: Intracellular iron was determined by Prussian blue staining. Cellular ferritin, cathepsin L and ferroportin were analyzed by flow cytometry and fluorescence microscopy. Cytokine secretion was determined by ELISA and immunoblotting. Results: In U937 and THP 1 cells, we did not detect any loss of cell viability on SPION loading. Desferrioxamine prevents induction of both ferritin and cathepsin L by SPIONs. Inhibition of lysosomal cathepsins upregulates both endogenous- and SPION-induced ferritin. SPION loading induces membranous ferroportin and incites secretion of ferritin, TNF-alpha and IL-10. 7 beta-hydroxycholesterol exposure reduces SPION uptake by cells. Conclusion: SPION loading results in upregulation of lysosomal cathepsin, membranous ferroportin and ferritin degradation, which is associated with secretion of both pro- and anti-inflammatory cytokines. A reduced SPION uptake by oxysterol-laden cells may lead to a compromised MRI with elevated cathepsins and ferritin.
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