Power frequency magnetic fields induced reactive oxygen species-related autophagy in mouse embryonic fibroblasts
Yanfeng Chen1, Ling Hong1, Ying Zeng1
1Bioelectromagnetics Laboratory, School of Medicine, Zhejiang University, 866 Yuhangtang Road, Hangzhou, 310058, China.
Abstract:
Power frequency magnetic fields (PFMF) have been reported to affect several cellular functions, such as cell proliferation and apoptosis. In this study, we investigated the effects of PFMF on mouse embryonic fibroblasts (MEF) autophagy. After cells were exposed to 50 Hz PFMF at 2 mT for 0.5 h, 2 h, 6 h, 12 h, and 24 h, we observed a significant increase in autophagic markers at 6 h, including (i) higher microtubule-associated protein 1 light chain 3-II (LC3-II), (ii) the increased formation of GFP-LC3 puncta, and (iii) increased numbers of autophagic vacuoles under transmission electron microscope. Moreover, we provide convincing evidence using chloroquine (CQ) that the increase of autophagic markers was the result of enhanced autophagic flux and not the suppression of lysosomal function. In a search for molecular mechanisms underlying PFMF-mediated autophagy, we observe that the autophagic process involved reactive oxygen species (ROS) and was independent of the mammalian target of rapamycin (mTOR) signaling pathway.
Insights
Power frequency magnetic fields (PFMF) significantly increase autophagy in mouse embryonic fibroblasts (MEF) by enhancing autophagic flux. This process involves reactive oxygen species (ROS) and is independent of mTOR signaling.
Area of Science:
- Cell Biology
- Biophysics
Background:
- Power frequency magnetic fields (PFMF) are known to influence cellular functions.
- Autophagy is a critical cellular process involved in maintaining homeostasis.
Purpose of the Study:
- To investigate the impact of PFMF on autophagy in mouse embryonic fibroblasts (MEF).
Main Methods:
- Exposure of MEF cells to 50 Hz PFMF at 2 mT for varying durations.
- Assessment of autophagic markers, including LC3-II and GFP-LC3 puncta.
- Evaluation of autophagic flux using chloroquine (CQ).
- Analysis of the involvement of reactive oxygen species (ROS) and mTOR signaling.
Main Results:
- PFMF exposure led to a significant increase in autophagic markers at 6 hours.
- Increased microtubule-associated protein 1 light chain 3-II (LC3-II) and GFP-LC3 puncta formation were observed.
- Enhanced autophagic flux was confirmed, independent of lysosomal function suppression.
- The PFMF-induced autophagy involved reactive oxygen species (ROS) but not the mTOR signaling pathway.
Conclusions:
- PFMF exposure stimulates autophagy in MEF cells.
- The observed increase in autophagy is due to enhanced autophagic flux.
- Reactive oxygen species (ROS) play a role in PFMF-mediated autophagy, while mTOR signaling is not involved.
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