@article{KlettBonebergTrenzetal.2004,
  author    = {M. V. Klett and E-M Boneberg and K. Trenz and R. Knippers and H. Illges},
  title     = {Hydrostatic pressure induces apoptosis in the human leukaemic T-cell line Jurkat via the mitochondrial pathway},
  series   = {Scand J Immunol. (Scandinavian Journal of Immunology)},
  volume    = {60},
  number    = {4},
  publisher = {Blackwell Publishing},
  issn      = {0300-9475},
  doi       = {10.1111/j.0300-9475.2004.01496.x},
  pages     = {403 -- 411},
  year      = {2004},
  abstract  = {We investigated the effect of pressure levels ranging from 80 to 500 bar on the proliferative capacity and viability of Jurkat leukaemic T cells. Pressurization at 360 bar induced apoptotic cell death as shown by apoptotic morphology after Hoechst staining, DNA fragmentation in the TdT-mediated dUTP nick end labelling-assay and cleavage of several caspase substrates. Cell death could be prevented by the general caspase inhibitor zVAD-fmk. Breakdown of the mitochondrial membrane potential and the release of cytochrome c provided strong evidence for an involvement of the mitochondrial pathway, whereas a central role of the death receptor pathway was excluded because caspase-8 was not significantly activated. Pressure incubation led to calcium influx after 5 min, and we hypothesize that calcium influx could be the primary trigger for pressure-induced apoptosis.},
  language  = {en}
}