| Cellular uptake mechanisms and toxicity of quantum dots in dendritic cells. | |
| | |
MedLine Citation:
|
PMID: 21793671 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Quantum dots (QDs) are nanoparticles with strong fluorescent emission and are novel tools used in biomedical applications, but the toxicity and mechanism of cellular uptake are poorly understood. QD655-COOH (negative charge, 18 nm) consist of a cadmium/selenide core and a zinc sulfide shell with a carboxylic acid coating with an emission wavelength of 655 nm. Materials & Methods: Peripheral blood mononuclear cells were isolated from porcine blood by gradient centrifugation, and monocytes, which are CD14 positive, were purified. Monocytes were differentiated into dendritic cells (DCs) with GM-CSF and IL-4. Results: Monocytes showed cellular uptake of QD655-COOH, while lymphocytes did not. Monocyte differentiation into DCs increased the cellular uptake by sixfold when dosed with 2 nM of QD655-COOH. Transmission electron microscopy depicted QD655-COOH in the cytoplasmic vacuoles of DCs. Twelve endocytic inhibitors demonstrated QD655-COOH endocytosis in DCs, which was recognized by clathrin and scavenger receptors and regulated by F-actin and phospholipase C. In addition, DC maturation with lipopolysaccharide (LPS) caused an increase in QD655-COOH uptake compared with DCs without LPS stimulation. Viability assays, including 96AQ, CCK-8, alamar blue and ApoTox, exhibited minimal toxicity in DCs dosed with QD655-COOH at 24 h. However, glutathione levels showed a significant decrease with 10 nM of QD655-COOH. Finally, QD655-COOH exposure was associated with a decrease in CD80/CD86 expression after LPS stimulation, suggesting suppression with DC maturation. Conclusion: These findings shed light on the mechanism of QD655-COOH uptake in DCs and that cellular uptake pathways are dependent on cell type and cell differentiation. |
| | |
Authors:
|
Leshuai W Zhang; Wolfgang Bäumer; Nancy A Monteiro-Riviere |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
|
Title: Nanomedicine (London, England) Volume: 6 ISSN: 1748-6963 ISO Abbreviation: Nanomedicine (Lond) Publication Date: 2011 Jul |
Date Detail:
|
Created Date: 2011-07-28 Completed Date: 2011-12-05 Revised Date: 2012-05-02 |
Medline Journal Info:
|
Nlm Unique ID: 101278111 Medline TA: Nanomedicine (Lond) Country: England |
Other Details:
|
Languages: eng Pagination: 777-91 Citation Subset: IM |
Affiliation:
|
Center for Chemical Toxicology Research & Pharmacokinetics, North Carolina State University, Raleigh, NC 27606, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Antigens, CD80 / immunology Antigens, CD86 / immunology Cell Differentiation Cell Survival Cells, Cultured Dendritic Cells / cytology*, immunology Endocytosis* Granulocyte-Macrophage Colony-Stimulating Factor / immunology Lipopolysaccharides / immunology Monocytes / cytology, immunology Quantum Dots* Swine |
| Grant Support | |
ID/Acronym/Agency:
|
R01 ES016138/ES/NIEHS NIH HHS; R01 ES016138-01/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Antigens, CD80; 0/Antigens, CD86; 0/Lipopolysaccharides; 83869-56-1/Granulocyte-Macrophage Colony-Stimulating Factor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Season of birth and morningness: comparison between the northern and southern hemispheres.
Next Document: Attenuation of the in vivo toxicity of biomaterials by polydopamine surface modification.