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J. Biol. Chem., Vol. 277, Issue 43, 40775-40781, October 25, 2002
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From the Human neutrophil granulocytes die rapidly, and
their survival is contingent upon rescue from programmed cell death by
signals from the environment. Here we report that a novel signal
for delaying neutrophil apoptosis is the classic acute phase
reactant, C-reactive protein (CRP). However, this anti-apoptotic
activity is expressed only when the cyclic pentameric structure of CRP
is lost, resulting in formation of modified or monomeric CRP (mCRP),
which may be formed in inflamed tissues. By contrast, native pentameric
CRP and CRP peptides 77-82, 174-185, and 201-206 failed to affect neutrophil apoptosis. The apoptosis delaying action of mCRP was markedly attenuated by an antibody against the low affinity IgG immune
complex receptor (CD16) but not by an anti-CD32 antibody. mCRP evoked a
transient concurrent activation of the extracellular signal-regulated
kinase (ERK) and phosphatidylinositol 3-kinase/Akt signaling pathways,
leading to inhibition of caspase-3 and consequently to delaying
apoptosis. Consistently, pharmacological inhibition of either ERK or
Akt reversed the anti-apoptotic action of mCRP; however, they did not
produce additive inhibition. Thus, mCRP, but not pentameric CRP or
peptides derived from CRP, promotes neutrophil survival and may
therefore contribute to amplification of the inflammatory response.
Loss of Pentameric Symmetry of C-reactive Protein Is Associated
with Delayed Apoptosis of Human Neutrophils*
§,§,,
, and**
Research Center, Maisonneuve-Rosemont
Hospital and Department of Medicine, University of Montréal,
Montréal, Québec H1T 2M4, Canada, ¶ the Centre de
Recherche, Centre Hospitalier de l'Université de
Montréal-Hôtel Dieu, University of Montréal,
Québec H2W 1T8, Canada, and NextEra Therapeutics,
Vernon Hills, Illinois 60061
*
This study was supported by Grant MOP-12573 from the
Canadian Institutes of Health Research (to J. G. F.).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.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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