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The loss of Mcl‐1 expression in human polymorphonuclear leukocytes promotes apoptosis
Author(s) -
Leuenroth Stephanie J.,
Grutkoski Patricia S.,
Ayala Alfred,
Simms H. Hank
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.1.158
Subject(s) - apoptosis , microbiology and biotechnology , biology , laminin , cytoplasm , hypoxia (environmental) , immunology , extracellular matrix , biochemistry , chemistry , organic chemistry , oxygen
The regulation of polymorphonuclear leukoctye (PMN) apoptosis can influence the duration of the inflammatory response. We have previously shown that PMN apoptosis is delayed by matrix adhesion and hypoxia; however, the mechanisms responsible for this delay are not well understood. Mcl‐1, an antiapoptotic Bcl‐2 family member, is present in neutrophils; therefore, we sought to characterize its localization and function as it relates to PMN apoptosis. We found that Mcl‐1 localized to the nucleus and cytoplasm and that expression levels decreased as PMN were aged in culture. Reducing available Mcl‐1 through the use of antisense oligonucleotides demonstrated that Mcl‐1 is necessary to delay apoptosis during normal PMN aging and hypoxia but is not required for suppression of apoptosis by laminin adhesion. Our results demonstrate a distinct expression pattern of Mcl‐1 and that Mcl‐1 is crucial for the delay of apoptosis initiated by certain antiapoptotic factors.