Data · dataset · 2016
Lysosomal iron liberation is responsible for the vulnerability of brain microglial cells to iron oxide nanoparticles: comparison with neurons and astrocytes
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Iron oxide nanoparticles (IONPs) are used for various biomedical and neurobiological applications.
Description
Thus, detailed knowledge on the accumulation and toxic potential of IONPs for the different types of brain cells is highly warranted. Literature data suggest that microglial cells are more vulnerable towards IONP exposure than other types of brain cells.
To investigate the mechanisms involved in IONP-induced microglial toxicity, we applied fluorescent dimercaptosuccinate-coated IONPs to primary cultures of microglial cells. Exposure to IONPs for 6 h caused a strong concentration-dependent increase in the microglial iron content which was accompanied by a substantial generation of reactive oxygen species (ROS) and by cell toxicity. In contrast, hardly any ROS staining and no loss in cell viability were observed for cultured primary astrocytes and neurons although these cultures accumulated similar specific amounts of IONPs than microglia.
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Co-localization studies with lysotracker revealed that after 6 h of incubation in microglial cells, but not in astrocytes and neurons, most IONP fluorescence was localized in lysosomes. ROS formation and toxicity in IONP-treated microglial cultures were prevented by neutralizing lysosomal pH by the application of NH 4 Cl or Bafilomycin A1 and by the presence of the iron chelator 2,2′-bipyridyl. These data demonstrate that rapid iron liberation from IONPs at acidic pH and iron-catalyzed ROS generation are involved in the IONP-induced toxicity of microglia and suggest that the relative resistance of astrocytes and neurons against acute IONP toxicity is a consequence of a slow mobilization of iron from IONPs in the lysosomal degradation pathway.
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Where it is published
- Repository landing page tandf.figshare.com/articles/journal_contribution/Lysosomal_iron_liberation_is_res… ↗
landing page · from DataCite
- DOI doi.org/10.6084/m9.figshare.1568167 ↗
DOI / persistent id · from DataCite
Documentation and papers
- Creative Commons Attribution 4.0 International creativecommons.org/licenses/by/4.0/legalcode ↗
license · from DataCite
- IsSupplementTo 10.3109/17435390.2015.1071445 doi.org/10.3109/17435390.2015.1071445 ↗
publication · from DataCite
Catalogue records · 2
- DataCite API api.datacite.org/dois/10.6084/m9.figshare.1568167 ↗
metadata API · from DataCite
- DataCite Commons commons.datacite.org/doi.org/10.6084/m9.figshare.1568167 ↗
catalogue entry · from DataCite
Topics
- Stated by source
- Biological sciences · Clinical medicine · Health sciences
- From keywords
- Biochemistry and cell biology · Cancer · Genetics · Immunology · Medicine & Health
Provenance · 1 source records, 13 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| DataCite | 10.6084/m9.figshare.1568167 | 13 d ago | JSON v1 |
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|---|---|---|---|
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| concepts[disease].local:disease:cancer | mapping · DataCite | vocabulary-mapper@1.0.0 | keywords['Cancer'] |
| concepts[field].fos:biological-sciences | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].fos:clinical-medicine | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].fos:health-sciences | source · DataCite | connector:datacite@1.0.0 | |
| concepts[field].local:field:medicine-health | mapping · DataCite | vocabulary-mapper@1.0.0 | keywords['Medicine'] |
| created_date | source · DataCite | connector:datacite@1.0.0 | |
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| title | source · DataCite | connector:datacite@1.0.0 | /data/attributes/titles/0/title |
| updated_date | source · DataCite | connector:datacite@1.0.0 |