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The University of Liverpool, School of Biological Sciences, Life Sciences Building, Crown Street, Liverpool L69 7ZB, United Kingdom
Correspondence: Steven W. Edwards, University of Liverpool, School of Biological Sciences, Life Sciences Building, Crown Street, Liverpool L69 7ZB, United Kingdom. E-mail: sbir12{at}liv.ac.uk
The human neutrophil spontaneously undergoes apoptosis, but this type
of cell death can be delayed or accelerated by a wide variety of
agents. There are wide discrepancies in the literature regarding the
expression of the Bcl-2 family of proteins in human neutrophils. Here,
we show that A1, Mcl-1, Bcl-XL, and Bad are major
transcripts in human neutrophils and that levels of these transcripts
are cytokine regulated. However, no Bcl-XL protein was
detected in Western blots. Protein levels for the proapoptotic proteins
Bad, Bax, Bak, and Bik remained constant during culture, despite
changes in the levels of mRNA for these gene products. These
proapoptotic proteins were extremely stable, having very long
half-lives. In contrast, A1 and Mcl-1 transcripts were extremely
unstable (with 
3-h half-lives), and Mcl-1 protein was also subject
to rapid turnover. These results indicate that neutrophil survival is
regulated by the inducible expression of the short-lived Mcl-1 and
possibly the A1 gene products. In the absence of their continued
expression, these prosurvival gene products are rapidly turned over,
and then the activity of the stable death proteins predominates and
promotes apoptosis.
Key Words: A1 • Mcl-1 • Bcl-X • Bcl-2
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