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The Impact of Ag Nanoparticles and CdTe Quantum Dots on Expression and Function of Receptors Involved in Amyloid-β
Katarzyna Sikorska1, Iwona Grądzka1, Iwona Wasyk1
1Centre for Radiobiology and Biological Dosimetry, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, Poland.
Abstract:
Microglial cells clear the brain of pathogens and harmful debris, including amyloid-β (Aβ) deposits that are formed during Alzheimer's disease (AD). We studied the expression of Msr1, Ager and Cd36 receptors involved in Aβ uptake and expression of Cd33 protein, which is considered a risk factor in AD. The effect of silver nanoparticles (AgNPs) and cadmium telluride quantum dots (CdTeQDs) on the expression of the above receptors and Aβ uptake by microglial cells was investigated. Absorption of Aβ and NPs was confirmed by confocal microscopy. AgNPs, but not CdTeQDs, caused a decrease in Aβ accumulation. By using a specific inhibitor-polyinosinic acid-we demonstrated that Aβ and AgNPs compete for scavenger receptors. Real-time PCR showed up-regulation of Cd33 and Cd36 gene expression after treatment with CdTeQDs for 24 h. Analysis of the abundance of the receptors on the cell surface revealed that AgNP treatment significantly reduced the presence of Msr1, Cd33, Ager and Cd36 receptors (6 and 24 h), whereas CdTeQDs increased the levels of Msr1 and Cd36 (24 h). To summarize, we showed that AgNP uptake competes with Aβ uptake by microglial cells and consequently can impair the removal of the aggregates. In turn, CdTeQD treatment led to the accumulation of proinflammatory Cd36 protein on the cell surface.
Insights
Silver nanoparticles (AgNPs) hinder amyloid-β (Aβ) clearance by microglial cells by competing for scavenger receptors. Cadmium telluride quantum dots (CdTeQDs) increase Aβ risk factors, potentially worsening Alzheimer's disease (AD) pathology.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Microglial cells are crucial for brain homeostasis, clearing amyloid-β (Aβ) deposits implicated in Alzheimer's disease (AD).
- Receptors like Msr1, Ager, and Cd36 mediate Aβ uptake, while Cd33 is an AD risk factor. Understanding their regulation is key to AD pathogenesis.
Purpose of the Study:
- To investigate the impact of silver nanoparticles (AgNPs) and cadmium telluride quantum dots (CdTeQDs) on microglial Aβ uptake.
- To examine the effects of AgNPs and CdTeQDs on the expression of key Aβ uptake receptors (Msr1, Ager, Cd36) and the AD risk factor Cd33.
Main Methods:
- Microglial cells were treated with AgNPs and CdTeQDs.
- Aβ uptake and nanoparticle absorption were assessed using confocal microscopy.
- Gene expression (Msr1, Ager, Cd36, Cd33) was analyzed via real-time PCR, and receptor abundance on the cell surface was quantified.
Main Results:
- AgNPs, unlike CdTeQDs, reduced Aβ accumulation, indicating competition for scavenger receptors.
- CdTeQDs significantly upregulated Cd33 and Cd36 gene expression after 24 hours.
- AgNP treatment decreased cell surface Msr1, Cd33, Ager, and Cd36 levels, while CdTeQDs increased Msr1 and Cd36 at 24 hours.
Conclusions:
- AgNP uptake competes with Aβ uptake by microglial cells, potentially impairing Aβ aggregate removal and exacerbating AD pathology.
- CdTeQD treatment results in the accumulation of pro-inflammatory Cd36 on the microglial cell surface, suggesting a role in neuroinflammation associated with AD.
