scholarly journals Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs)

Cells ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 136-162 ◽  
Author(s):  
Stephen Beebe ◽  
Nova Sain ◽  
Wei Ren
2018 ◽  
Vol 101 (3) ◽  
pp. 38-48 ◽  
Author(s):  
RYUYA ADACHI ◽  
SHOTA HATAYAMA ◽  
NOBUAKI OHNISHI ◽  
SUNAO KATSUKI ◽  
TOSHIAKI WADA ◽  
...  

2017 ◽  
Vol 137 (6) ◽  
pp. 320-327
Author(s):  
Ryuta Andachi ◽  
Shota Hatayama ◽  
Nobuaki Ohnishi ◽  
Sunao Katsuki ◽  
Toshiaki Wada ◽  
...  

2009 ◽  
Vol 8 (4) ◽  
pp. 289-306 ◽  
Author(s):  
Axel T. Esser ◽  
Kyle C. Smith ◽  
T. R. Gowrishankar ◽  
James C. Weaver

Local and drug-free solid tumor ablation by large nanosecond pulsed electric fields leads to supra-electroporation of all cellular membranes and has been observed to trigger nonthermal cell death by apoptosis. To establish pore-based effects as the underlying mechanism inducing apoptosis, we use a multicellular system model (spatial scale 100 μm) that has irregularly shaped liver cells and a multiscale liver tissue model (spatial scale 200 mm). Pore histograms for the multicellular model demonstrate the presence of only nanometer-sized pores due to nanosecond electric field pulses. The number of pores in the plasma membrane is such that the average tissue conductance during nanosecond electric field pulses is even higher than for longer irreversible electroporation pulses. It is shown, however, that these nanometer-sized pores, although numerous, only significantly change the permeability of the cellular membranes to small ions, but not to larger molecules. Tumor ablation by nanosecond pulsed electric fields causes small to moderate temperature increases. Thus, the underlying mechanism(s) that trigger cell death by apoptosis must be non-thermal electrical interactions, presumably leading to different ionic and molecular transport than for much longer irreversible electroporation pulses.


Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2034 ◽  
Author(s):  
Alessandra Rossi ◽  
Olga N. Pakhomova ◽  
Peter A. Mollica ◽  
Maura Casciola ◽  
Uma Mangalanathan ◽  
...  

Depending on the initiating stimulus, cancer cell death can be immunogenic or non-immunogenic. Inducers of immunogenic cell death (ICD) rely on endoplasmic reticulum (ER) stress for the trafficking of danger signals such as calreticulin (CRT) and ATP. We found that nanosecond pulsed electric fields (nsPEF), an emerging new modality for tumor ablation, cause the activation of the ER-resident stress sensor PERK in both CT-26 colon carcinoma and EL-4 lymphoma cells. PERK activation correlates with sustained CRT exposure on the cell plasma membrane and apoptosis induction in both nsPEF-treated cell lines. Our results show that, in CT-26 cells, the activity of caspase-3/7 was increased fourteen-fold as compared with four-fold in EL-4 cells. Moreover, while nsPEF treatments induced the release of the ICD hallmark HMGB1 in both cell lines, extracellular ATP was detected only in CT-26. Finally, in vaccination assays, CT-26 cells treated with nsPEF or doxorubicin equally impaired the growth of tumors at challenge sites eliciting a protective anticancer immune response in 78% and 80% of the animals, respectively. As compared to CT-26, both nsPEF- and mitoxantrone-treated EL-4 cells had a less pronounced effect and protected 50% and 20% of the animals, respectively. These results support our conclusion that nsPEF induce ER stress, accompanied by bona fide ICD.


2021 ◽  
Vol 142 ◽  
pp. 107942
Author(s):  
Hongmei Liu ◽  
Yajun Zhao ◽  
Chenguo Yao ◽  
Eva M. Schmelz ◽  
Rafael V. Davalos

2021 ◽  
Vol 120 (3) ◽  
pp. 223a
Author(s):  
Flavia Mazzarda ◽  
Esin B. Sozer ◽  
Julia L. Pittaluga ◽  
Claudia Muratori ◽  
P. Thomas Vernier

Sign in / Sign up

Export Citation Format

Share Document