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Serum amyloid A induces WISH cell apoptosis
Seong-Ho Jo1, Jeanho Yun, Jong-Min Kim
1Medical Research Center for Cancer Molecular Therapy, College of Medicine, Dong-A University, Busan 602714, Korea.
Acta Pharmacologica Sinica
|December 23, 2006
Summary
Serum amyloid A (SAA) induces apoptosis in human amniotic WISH cells via a PTX-insensitive pathway. This study identifies SAA as a novel apoptosis inducer, highlighting its role in cell regulation.
Area of Science:
- Cell Biology
- Immunology
- Molecular Biology
Background:
- Serum amyloid A (SAA) is a key acute-phase reactant in mammals.
- The role of SAA in cellular apoptosis requires further investigation.
Purpose of the Study:
- To investigate the effect of SAA on apoptosis in human amniotic WISH cells.
- To elucidate the underlying molecular mechanisms of SAA-induced apoptosis.
Main Methods:
- Formyl peptide receptor-like 1 (FPRL1) expression was assessed via RT-PCR and ligand binding assays.
- Cell proliferation was measured using thymidine incorporation assays.
- Protein phosphorylation and caspase-3 activity were analyzed by Western blot.
Main Results:
- SAA significantly inhibited thymidine incorporation, indicating reduced proliferation in WISH cells.
- SAA induced nuclear condensation and caspase-3 activation, confirming apoptosis.
- The apoptosis-inducing effect of SAA was mediated through a pertussis toxin (PTX)-insensitive pathway involving mitogen-activated protein kinases (MAPKs).
Conclusions:
- SAA acts as a novel inducer of apoptosis in human amniotic WISH cells.
- The mechanism involves a PTX-insensitive signaling pathway, distinct from classical G-protein signaling.
- MAPK activation is crucial for SAA-mediated apoptosis.
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