Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs)
Pulse power technology using nanosecond pulsed electric fields (nsPEFs) offers a new stimulus to modulate cell functions or induce cell death for cancer cell ablation. New data and a literature review demonstrate fundamental and basic cellular mechanisms when nsPEFs interact with cellular targets. N...
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| Format: | Article |
| Language: | English |
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MDPI AG
2013-03-01
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| Series: | Cells |
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| Online Access: | http://www.mdpi.com/2073-4409/2/1/136 |
| _version_ | 1797725754907164672 |
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| author | Nova M. Sain Stephen J. Beebe Wei Ren |
| author_facet | Nova M. Sain Stephen J. Beebe Wei Ren |
| author_sort | Nova M. Sain |
| collection | DOAJ |
| description | Pulse power technology using nanosecond pulsed electric fields (nsPEFs) offers a new stimulus to modulate cell functions or induce cell death for cancer cell ablation. New data and a literature review demonstrate fundamental and basic cellular mechanisms when nsPEFs interact with cellular targets. NsPEFs supra-electroporate cells creating large numbers of nanopores in all cell membranes. While nsPEFs have multiple cellular targets, these studies show that nsPEF-induced dissipation of ΔΨm closely parallels deterioration in cell viability. Increases in intracellular Ca2+ alone were not sufficient for cell death; however, cell death depended of the presence of Ca2+. When both events occur, cell death ensues. Further, direct evidence supports the hypothesis that pulse rise-fall times or high frequency components of nsPEFs are important for decreasing ΔΨm and cell viability. Evidence indicates in Jurkat cells that cytochrome c release from mitochondria is caspase-independent indicating an absence of extrinsic apoptosis and that cell death can be caspase-dependent and –independent. The Ca2+ dependence of nsPEF-induced dissipation of ΔΨm suggests that nanoporation of inner mitochondria membranes is less likely and effects on a Ca2+-dependent protein(s) or the membrane in which it is embedded are more likely a target for nsPEF-induced cell death. The mitochondria permeability transition pore (mPTP) complex is a likely candidate. Data demonstrate that nsPEFs can bypass cancer mutations that evade apoptosis through mechanisms at either the DISC or the apoptosome. |
| first_indexed | 2024-03-12T10:35:50Z |
| format | Article |
| id | doaj.art-a5c541ae1f894beaa6f136b403dec8a7 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-12T10:35:50Z |
| publishDate | 2013-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-a5c541ae1f894beaa6f136b403dec8a72023-09-02T08:47:43ZengMDPI AGCells2073-44092013-03-012113616210.3390/cells2010136Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs)Nova M. SainStephen J. BeebeWei RenPulse power technology using nanosecond pulsed electric fields (nsPEFs) offers a new stimulus to modulate cell functions or induce cell death for cancer cell ablation. New data and a literature review demonstrate fundamental and basic cellular mechanisms when nsPEFs interact with cellular targets. NsPEFs supra-electroporate cells creating large numbers of nanopores in all cell membranes. While nsPEFs have multiple cellular targets, these studies show that nsPEF-induced dissipation of ΔΨm closely parallels deterioration in cell viability. Increases in intracellular Ca2+ alone were not sufficient for cell death; however, cell death depended of the presence of Ca2+. When both events occur, cell death ensues. Further, direct evidence supports the hypothesis that pulse rise-fall times or high frequency components of nsPEFs are important for decreasing ΔΨm and cell viability. Evidence indicates in Jurkat cells that cytochrome c release from mitochondria is caspase-independent indicating an absence of extrinsic apoptosis and that cell death can be caspase-dependent and –independent. The Ca2+ dependence of nsPEF-induced dissipation of ΔΨm suggests that nanoporation of inner mitochondria membranes is less likely and effects on a Ca2+-dependent protein(s) or the membrane in which it is embedded are more likely a target for nsPEF-induced cell death. The mitochondria permeability transition pore (mPTP) complex is a likely candidate. Data demonstrate that nsPEFs can bypass cancer mutations that evade apoptosis through mechanisms at either the DISC or the apoptosome.http://www.mdpi.com/2073-4409/2/1/136apoptosiscaspase-dependentcaspase-independentJurkat clonesAPAF-1FADDN1-S1 hepatocellular carcinoma cellsCa2+ mobilizationmitochondria membrane potentialmitochondria permeability transition porecytochrome celectroporationnanopores 3-10 |
| spellingShingle | Nova M. Sain Stephen J. Beebe Wei Ren Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) Cells apoptosis caspase-dependent caspase-independent Jurkat clones APAF-1 FADD N1-S1 hepatocellular carcinoma cells Ca2+ mobilization mitochondria membrane potential mitochondria permeability transition pore cytochrome c electroporation nanopores 3-10 |
| title | Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) |
| title_full | Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) |
| title_fullStr | Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) |
| title_full_unstemmed | Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) |
| title_short | Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs) |
| title_sort | induction of cell death mechanisms and apoptosis by nanosecond pulsed electric fields nspefs |
| topic | apoptosis caspase-dependent caspase-independent Jurkat clones APAF-1 FADD N1-S1 hepatocellular carcinoma cells Ca2+ mobilization mitochondria membrane potential mitochondria permeability transition pore cytochrome c electroporation nanopores 3-10 |
| url | http://www.mdpi.com/2073-4409/2/1/136 |
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