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Blood, Vol. 92 No. 12 (December 15), 1998:
pp. 4545-4553
RAPID COMMUNICATION
Blood Cells With Reduced Mitochondrial Membrane Potential and
Cytosolic Cytochrome C Can Survive and Maintain Clonogenicity Given
Appropriate Signals to Suppress Apoptosis
Quan Chen,
Naoshi Takeyama,
Ged Brady,
Alastair J.M. Watson, and
Caroline Dive
From the School of Biological Sciences and the Department of
Medicine, Victoria University of Manchester, Manchester, UK.
Reduction of mitochondrial membrane potential ( m) and
release of cytochrome c from mitochondria appear to be key events
during apoptosis. Apoptosis was induced in IC.DP premast cells by the withdrawal of interleukin-3 (IL-3). m decreased by 12 hours and cytochrome c was detected in the cytosol at 18 hours. Despite these changes in the mitochondria after 18 hours of IL-3 deprivation, clonogenicity was unaffected when IL-3 was replenished at 18 hours. Activation of v-Abl tyrosine kinase (v-Abl TK) in IC.DP cells before
IL-3 depletion led to increased levels of Bcl-XL, prevented reduction of m and the release of mitochondrial
cytochrome c, and suppressed apoptosis. Activation of v-Abl TK 18 hours
after withdrawal of IL-3 when  10% of the cells had died restored
m in the remaining cells. More than 40% of cells thus
rescued by v-Abl TK between 18 and 42 hours could subsequently form
colonies in the presence of IL-3. These data suggest that reduction in m precedes loss of mitochondrial cytochrome c in IC.DP
cells; that v-Abl TK activation, probably via upregulation of
Bcl-XL, prevents loss of m and blocks the
release of cytochrome c from mitochondria; and that neither of these
mitochondrial events is sufficient for commitment to apoptosis.
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