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Induction of apoptosis in WEHI 231 cells by cationic liposomes
1School of Pharmacy, Tokyo University of Pharmacy and Life Science, Hachioji, Japan. aramaki@ps.toyaku.ac.jp
Insights
Cationic liposomes, but not neutral or anionic ones, were found to induce apoptosis, programmed cell death, in B cells. Reactive oxygen species play a key role in this liposome-induced B cell apoptosis.
Area of Science:
- Cell Biology
- Immunology
- Nanotechnology
Background:
- Liposomes are widely utilized as drug carriers and immunoadjuvants.
- Limited research exists on the cellular effects of liposomes upon interaction.
- Understanding liposome-cell interactions is crucial for optimizing therapeutic applications.
Purpose of the Study:
- To investigate the potential of liposomes to induce apoptosis in B cells.
- To determine if liposome charge influences apoptosis induction.
- To elucidate the mechanisms underlying liposome-mediated B cell apoptosis.
Main Methods:
- Treatment of mouse B cell lines (WEHI 231) and primary splenic B cells with various liposomes.
- Assessment of apoptosis using flow cytometry to measure DNA content and chromatin condensation.
- Analysis of DNA fragmentation via agarose gel electrophoresis and morphological examination.
Main Results:
- Cationic liposomes induced significant apoptosis in WEHI 231 cells, while neutral and anionic liposomes did not.
- A brief 30-minute incubation with cationic liposomes was sufficient to trigger apoptosis in 80% of cells.
- The apoptosis induced by stearylamine-containing cationic liposomes was mitigated by N-acetyl-cysteine, an oxidant scavenger.
Conclusions:
- Cationic liposomes effectively induce apoptosis in B cells.
- Reactive oxygen species generation is a critical factor in cationic liposome-induced apoptosis.
- Apoptosis is a likely contributor to the observed cytotoxicity of cationic liposomes.
Purpose:
Liposomes are of considerable interest as drug carriers and immunoadjuvants. However, few investigators have studied the changes exerted by liposomes in the cells with which they interact. The purpose of this study was to investigate whether liposomes induce apoptosis in B cells.
Methods:
The mouse immature B cell line WEHI 231 cells and mouse splenic B cells were treated with liposomes, and the induction of apoptosis was evaluated by monitoring changes in DNA content, DNA fragmentation and chromatin condensation by flow cytometry, agarose gel electrophoresis and by morphological investigation.
Results:
Cationic liposomes induced apoptosis in WEHI 231 cells, but neutral and anionic liposomes did not. A contact time of 30 min between WEHI 231 cells and cationic liposomes was sufficient to induce apoptosis, and 80% of the cells showed hypodiploid DNA content. Apoptosis induced by cationic liposomes composed of stearylamine was inhibited by addition of the oxidant scavenger, N-acetyl-cysteine.
Conclusions:
Cationic liposomes induced apoptosis in WEHI 231 cells, and the production of reactive oxygen species is important in the regulation of apoptosis induced by cationic liposomes. It is well known that cationic liposomes show cytotoxicity, and apoptosis may be one of the causes of this toxicity.