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J Biol Chem, Vol. 275, Issue 20, 15343-15349, May 19, 2000
From the Apoptotic cell death, characterized by chromatin
condensation, nuclear fragmentation, cell membrane blebbing, and
apoptotic body formation, is also accompanied by typical mitochondrial
changes. The latter includes enhanced membrane permeability, fall in
mitochondrial membrane potential (
Gelsolin Inhibits Apoptosis by Blocking Mitochondrial Membrane
Potential Loss and Cytochrome c Release*
,,,,¶
Division of Cancer Gene Regulation,
Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7,
Kita-Ku, Sapporo 060-0815 and the § Department of Medical
Genetics, Biomedical Research Center, Osaka University School of
Medicine, Osaka 565-0871, Japan
m) and
release of cytochrome c into the cytosol. Gelsolin, an
actin regulatory protein, has been shown to inhibit apoptosis, but when
cleaved by caspase-3, a fragment that is implicated as an effector of
apoptosis is generated. The mechanism by which the full-length form of
gelsolin inhibits apoptosis is unclear. Here we show that the
overexpression of gelsolin inhibits the loss of m and
cytochrome c release from mitochondria resulting in the
lack of activation of caspase-3, -8, and -9 in Jurkat cells treated
with staurosporine, thapsigargin, and protoporphyrin IX. These effects
were corroborated in vitro using recombinant gelsolin protein on isolated rat mitochondria stimulated with Ca2+,
atractyloside, or Bax. This protective function of gelsolin, which was
not due to simple Ca2+ sequestration, was inhibited by
polyphosphoinositide binding. In addition we confirmed that gelsolin,
besides its localization in the cytosol, is also present in the
mitochondrial fraction of cells. Gelsolin thus acts on an early step in
the apoptotic signaling at the level of mitochondria.
*
This work was supported in part by Grants-in-Aid for
Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan, the Tokyo Biochemical Research Foundation, and the
Novartis Foundation for the Promotion of Science, Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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