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Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

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Nanoparticle-mediated decrease of lamin B1 pools promotes a TRF protein-based adaptive response in cultured cells.

Jennifer Mytych¹, Karolina Pacyk¹, Monika Pepek¹

¹Department of Genetics, University of Rzeszow, Rejtana 16C, 35-959 Rzeszow, Poland.

|April 20, 2015

Summary

This summary is machine-generated.

Nanoparticles induce oxidative stress, activating pathways that maintain telomere length. This adaptive response differs in cancer cells versus fibroblasts, suggesting nanoparticles promote telomere-focused cellular adaptation.

Keywords:

Adaptive response Lamin B1 Nanoparticles Oxidative stress TRF proteins Telomere length

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Area of Science:

Biomedical Engineering
Molecular Biology
Nanotechnology

Background:

Nanoparticle applications in diagnostics and therapeutics are expanding.
The molecular mechanisms underlying nanoparticle interactions in biological systems are not fully understood.
Oxidative stress and cellular signaling pathways are key areas of investigation.

Purpose of the Study:

To elucidate the molecular mechanisms of nanoparticle-induced cellular responses.
To investigate the role of oxidative stress and the NF-κB pathway in nanoparticle interactions.
To determine how these responses affect telomere maintenance and cellular fate.

Main Methods:

Exposure of cells (cancer cells and fibroblasts) to various nanoparticles (silica, silver, diamond).
Analysis of molecular markers including oxidative stress, NF-κB pathway activation, lamin B1 levels, and telomeric repeat binding factor (TRF) expression.
Assessment of p53 and p21 signaling pathways and observation of stress-induced premature senescence.

Main Results:

Nanoparticles induced oxidative stress and activated the NF-κB pathway, leading to lamin B1 depletion.
This resulted in increased telomeric repeat binding factor (TRF) expression and telomere length maintenance.
In cancer cells, the TRF response was independent of the p53 pathway, while in fibroblasts, active p53/p21 signaling led to senescence.

Conclusions:

Nanoparticles trigger a conserved cellular adaptive response centered on telomere maintenance.
The cellular outcome (senescence vs. telomere maintenance) depends on the p53/p21 signaling status.
These findings provide crucial insights into nanoparticle-cell interactions at the molecular level.