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Title of Journal: Apoptosis

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Abbravation: Apoptosis

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Springer US

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DOI

10.1002/nau.22299

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1573-675X

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Nanosecond pulsed electric fields modulate the exp

Authors: Larry E Estlack Caleb C Roth Gary L Thompson William A Lambert Bennett L Ibey
Publish Date: 2014/10/21
Volume: 19, Issue: 12, Pages: 1755-1768
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Abstract

In this publication we demonstrate that exposure of Jurkat and U937 cells to nanosecond pulsed electrical fields nsPEF can modulate the extrinsicmediated apoptotic pathway via the Fas/CD95 death receptor An inherent difference in survival between these two cell lines in response to 10 ns exposures has been previously reported Jurkat being more sensitive to nsPEF than U937 but the reason for this sensitivity difference remains unknown We found that exposure of each cell line to 100 10 ns pulses at 50 kV/cm caused a marked increase in expression of cFLIP extrinsic apoptosis inhibitor in U937 and FasL extrinsic apoptosis activator in Jurkat respectively Measurement of basal expression levels revealed an inherent difference between U937 cells having a higher expression of cFLIP and Jurkat cells having a higher expression of FasL From these data we hypothesize that the sensitivity difference between the cells to nsPEF exposure may be directly related to expression of extrinsic apoptotic regulators To validate this hypothesis we used siRNA to knockdown cFLAR coding for cFLIP protein expression in U937 and FasL expression in Jurkat and challenged them to 100 10 ns pulses at 150 kV/cm a typical lethal dose We observed that U937 survival was reduced nearly 60  in the knockdown population while Jurkat survival improved ~40  These findings support the hypothesis that cell survival following 10 ns pulse exposures depends on extrinsic apoptotic regulators Interestingly pretreatment of U937 with a 100pulse 50 kV/cm exposure to amplify cFLAR expression significantly reduced the lethality of a 150 kV/cm 100pulse exposure applied 24 h later From these data we conclude that the observed survival differences between cells exposed to 10 ns pulsed electric fields is due to inherent cell biochemistry rather than the biophysics of the exposure itself Understanding cell sensitivity to nsPEF may provide researchers/clinicians with a predicable way to control or avoid unintended cell death during nsPEF exposureThis research was supported by intramural funds from the Air Force Surgeon General’s Office Medical Research Program and the Air Force Office of Scientific Research LRIR 13RH08COR Mr Roth would like to thank the SMART Program grant N002440910081 OSDTE Office of Secretary DefenseTest and Evaluation DefenseWide/PE0601120D8Z National Defense Education Program NDEP/BA1 Basic Research

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  9. Atorvastatin inhibits the apoptosis of human umbilical vein endothelial cells induced by angiotensin II via the lysosomal-mitochondrial axis
  10. The c-Abl tyrosine kinase stabilizes Pitx1 in the apoptotic response to DNA damage
  11. Ouabain-induced apoptosis and Rho kinase: a novel caspase-2 cleavage site and fragment of Rock-2
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  19. Insulin inhibits myocardial ischemia-induced apoptosis and alleviates chronic adverse changes in post-ischemic cardiac structure and function
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