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

Authors
  • Yamaguchi, Takeo
  • Hashiguchi, Kenji
  • Katsuki, Satoshi
  • Iwamoto, Wakako
  • Tsuruhara, Shoichiro
  • Terada, Shigeyuki
Type
Published Article
Journal
Cellular & Molecular Biology Letters
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jan 01, 2008
Volume
13
Issue
1
Pages
49–57
Identifiers
PMID: 17952376
Source
Medline
License
Unknown

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.

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