Open Access

Activation of the intrinsic and extrinsic pathways in high pressure-induced apoptosis of murine erythroleukemia cells

  • Takeo Yamaguchi1Email author,
  • Kenji Hashiguchi1,
  • Satoshi Katsuki1,
  • Wakako Iwamoto1,
  • Shoichiro Tsuruhara1 and
  • Shigeyuki Terada1
Cellular & Molecular Biology LettersAn International Journal200713:34

https://doi.org/10.2478/s11658-007-0034-x

Received: 26 February 2007

Accepted: 22 June 2007

Published: 19 October 2007

Abstract

We previously demonstrated that caspase-3, an executioner of apoptosis, is activated in the pressure-induced apoptosis of murine erythroleukemia (MEL) cells (at 100 MPa). Here, we examined the pathway of caspase-3 activation using peptide substrates and caspase inhibitors. Using the substrates of caspases-8 and -9, it was found that both are activated in cells under high pressure. The production of nuclei with sub-G1 DNA content in 100 MPa-treated MEL cells was suppressed by inhibitors of caspases-8 and -9, and pan-caspase. In 100 MPa-treated cells, pan-caspase inhibitor partially prevented the cytochrome c release from the mitochondria and the breakdown of mitochondrial membrane potential. These results suggest that the intrinsic and extrinsic pathways are activated in apoptotic signaling during the high pressure-induced death of MEL cells.

Key words

Apoptosis Caspases Cytochrome c Flow cytometry Membrane potential High pressure

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