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,
Departments of
*
Pathology,
Medicine, and
Microbiology and Immunology, State University of New York Health Science Center, College of Medicine, Syracuse, NY 13210
Stimulation of the CD95/Fas/Apo-1 receptor leads to apoptosis
through activation of the caspase family of cysteine proteases and
disruption of the mitochondrial transmembrane potential
(
m). We show that, in Jurkat human T cells and
peripheral blood lymphocytes, Fas-induced apoptosis is preceded by 1)
an increase in reactive oxygen intermediates (ROI) and 2) an elevation
of m. These events are followed by externalization of
phosphatidylserine (PS), disruption of m, and cell
death. The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and
Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of
m, and cell death, suggesting that these events are
sequelae of caspase activation. By contrast, in the presence of caspase
inhibitors, ROI levels and m of Fas-stimulated cells
remained elevated. Because ROI levels and m are
regulated by the supply of reducing equivalents from the pentose
phosphate pathway (PPP), we studied the impact of transaldolase (TAL),
a key enzyme of the PPP, on Fas signaling. Overexpression of TAL
accelerated Fas-induced mitochondrial ROI production,
m elevation, activation of caspase-8 and caspase-3,
proteolysis of poly(A)DP-ribose polymerase, and PS externalization.
Additionally, suppression of TAL diminished these activities.
Therefore, by controlling the balance between mitochondrial ROI
production and metabolic supply of reducing equivalents through the
PPP, TAL regulates susceptibility to Fas-induced apoptosis. Early
increases in ROI levels and m as well as the dominant
effect of TAL expression on activation of caspase-8/Fas-associated
death domain-like IL-1ß-converting enzyme, the most upstream member
of the caspase cascade, suggest a pivotal role for redox signaling at
the initiation of Fas-mediated apoptosis.
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A. Perl, E. Colombo, E. Samoilova, M. C. Butler, and K. Banki Human Transaldolase-associated Repetitive Elements Are Transcribed by RNA Polymerase III J. Biol. Chem., March 15, 2000; 275(10): 7261 - 7272. [Abstract] [Full Text] [PDF]
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A. R. Khaled, D. A. Reynolds, H. A. Young, C. B. Thompson, K. Muegge, and S. K. Durum Interleukin-3 Withdrawal Induces an Early Increase in Mitochondrial Membrane Potential Unrelated to the Bcl-2 Family. ROLES OF INTRACELLULAR pH, ADP TRANSPORT, AND F0F1-ATPase J. Biol. Chem., February 23, 2001; 276(9): 6453 - 6462. [Abstract] [Full Text] [PDF]
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A. Almeida, J. Almeida, J. P. Bolanos, and S. Moncada Different responses of astrocytes and neurons to nitric oxide: The role of glycolytically generated ATP in astrocyte protection PNAS, December 18, 2001; 98(26): 15294 - 15299. [Abstract] [Full Text] [PDF]
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