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The expression of genes modulating programmed cell death in normal human polymorphonuclear neutrophils
S C Hsieh1, M H Huang, C Y Tsai
1Department of Medicine, Veterans General Hospital, Taipei, Taiwan, Republic of China.
Biochemical and Biophysical Research Communications
|April 28, 1997
Summary
Polymorphonuclear neutrophils (PMN) undergo apoptosis. Fas-FasL interactions promote PMN apoptosis, while low c-myc expression contributes to their short lifespan and apoptosis.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Normal human polymorphonuclear neutrophils (PMN) have a limited lifespan and undergo programmed cell death (apoptosis).
- Understanding the molecular mechanisms regulating PMN apoptosis is crucial for immune system regulation.
Purpose of the Study:
- To investigate the molecular basis of spontaneous polymorphonuclear neutrophil apoptosis.
- To determine the expression patterns of key apoptosis-related and survival-related genes in PMNs.
Main Methods:
- Gene expression analysis using flow cytometry, Western blot, and reverse transcription-assisted polymerase chain reaction (RT-PCR).
- Functional assays involving monoclonal antibodies against Fas and Fas-ligand (FasL).
Main Results:
- Fas and FasL were expressed on PMN surfaces, with FasL diminishing faster than Fas.
- p53 and bcl-2 were detected in the cytoplasm, while c-myc expression was negligible.
- Anti-Fas antibody enhanced PMN apoptosis, whereas anti-FasL antibody suppressed it.
Conclusions:
- Fas-FasL pathway activation is a key mechanism driving spontaneous PMN apoptosis.
- The absence of c-myc expression contributes to PMN non-proliferative nature and may enhance apoptosis.