Intense picosecond pulsed electric fields induce apoptosis through a             mitochondrial-mediated pathway in HeLa cells.
The application of pulsed electric fields (PEF) is emerging as a new technique             for tumor therapy. Picosecond pulsed electric fields (psPEF) can be transferred             to target deep tissue non-invasively and precisely, but the research of the biological             effects of psPEF on cells is limited. Electric theory predicts that intense psPEF             will target mitochondria and lead to changes in transmembrane potential, therefore,             it is hypothesized that it can induce mitochondrial-mediated apoptosis. HeLa cells             were exposed to psPEF in this study to investigate this hypothesis. MTT assay             demonstrated that intense psPEF significantly inhibited the proliferation of HeLa             cells in a dose-dependent manner. Typical characteristics of apoptosis in HeLa             cells were observed, using transmission electron microscopy. Loss of mitochondrial             transmembrane potential was explored using laser scanning confocal microscopy             with Rhodamine-123 (Rh123) staining. Furthermore, the mitochondrial apoptotic             events were also confirmed by western blot analysis for the release of cytochrome             C and apoptosis-inducing factor from mitochondria into the cytosol. In addition,             activation of caspase-3, caspase-9, upregulation of Bax, p53 and downregulation             of Bcl-2 were observed in HeLa cells also indicating apoptosis. Taken together,             these results demonstrate that intense psPEF induce cell apoptosis through a mitochondrial-mediated             pathway.
Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China.
Yuan-Yuan
YY
Hua
Xiao-Shu
XS
Wang
Yu
Y
Zhang
Chen-Guo
CG
Yao
Xi-Ming
XM
Zhang
Zheng-Ai
ZA
Xiong
D017209:Apoptosis; D051033:Apoptosis Inducing Factor / Q000378:metabolism; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D053453:Caspase 9 / Q000235:genetics / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D004560:Electricity; D006367:HeLa Cells; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000502:physiology; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D020112:Rhodamine 123 / Q000737:chemistry; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
D051033:Apoptosis Inducing Factor; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D020112:Rhodamine 123; D045304:Cytochromes c; D053148:Caspase 3; D053453:Caspase 9