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B determine cell fate?
Cellular Injury and Adaptation Laboratory,
* Departments of Surgery,
Anesthesiology, and Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA
2Correspondence: Department of Surgery, Campus Box 8109, 660 South Euclid Ave., St. Louis, MO, 63110, USA. E-mail: cobb{at}msnotes.wustl.edu
Cellular injury induces an adaptive response whether the insult is
physical (e.g., heat, radiation), chemical (e.g., reactive oxygen
species), infectious (e.g., bacteria), or inflammatory (e.g.,
lipopolysaccharide). Recent data indicate that the interactions of
these responses are not predictable and that sequence permutations can
have opposite effects on outcome after injury. Our overarching
hypothesis is that interactions among stress responses contribute to
the fate of cells, tissues, and organisms and that modulation of these
interactions can have important affects on both function and survival.
For example, whereas it is well known that a prior heat
shock stress can protect cells against inflammatory stress both
in vitro and in vivo, we and others have
shown that induction of a subsequent heat stress in
cells ‘primed’ by inflammation can precipitate cell death by
apoptosis. We call this seemingly paradoxical ability of heat shock to
induce cytoprotection and cytotoxicity the heat shock
paradox. The molecular mechanisms by which cells integrate
responses to these and other stresses are poorly understood. We present
data linking the heat shock paradox to the activity of the acute-phase
transcription factor nuclear factor kappa B (identifying an ‘NF-
B
paradox’) and hypothesize that the mechanism is linked to the
downstream effects of induction of NF-B’s endogenous inhibitor,
IB
, a putative heat shock protein.—DeMeester, S. L.,
Buchman, T. G., Cobb, J. P. The heat shock paradox: does
NF-B determine cell fate?
Key Words: injury • cell death • apoptosis • IB
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