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Brown University School of Medicine and Rhode Island Hospital,
* Division of Surgical Research, and
Center for Surgical Research, Providence, Rhode Island
Correspondence: Dr. H. Hank Simms, MD, Rhode Island Hospital, 593 Eddy Street, Department of Surgery, APC 110, Providence, RI 02903. E-mail: hank_simms{at}brown.edu
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.
Key Words: neutrophil • hypoxia • laminin
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