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A decrease in remodeling accounts for the accumulation of arachidonic acid in murine mast cells undergoing apoptosis
A N Fonteh1, T LaPorte, D Swan
1Department of Internal Medicine, Pulmonary and Critical Care Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27154, USA. afonteh@wfubmc.edu
The Journal of Biological Chemistry
|October 7, 2000
Summary
During apoptosis, free arachidonic acid (AA) levels increase in mast cells. This accumulation is due to reduced AA remodeling from phosphatidylcholine to phosphatidylethanolamine, not altered synthesis or degradation.
Area of Science:
- Cell Biology
- Immunology
- Biochemistry
Background:
- Mast cells play crucial roles in immune responses.
- Apoptosis is a regulated process of cell death.
- Arachidonic acid (AA) is a key fatty acid involved in cellular signaling.
Purpose of the Study:
- To investigate arachidonic acid (AA) metabolism in murine bone marrow-derived mast cells (BMMC) undergoing apoptosis.
- To determine the mechanisms behind AA accumulation during cytokine-depleted apoptosis.
Main Methods:
- Induction of apoptosis in BMMC via cytokine depletion.
- Quantification of AA and other lipids using chromatographic techniques.
- Assay of enzyme activities involved in AA metabolism (e.g., phospholipase A2, lipoxygenase, cyclooxygenase, CoA-dependent transferase, CoA-independent transacylase).
Main Results:
- AA levels correlated with the percentage of apoptotic BMMC.
- No significant changes in AA mobilization enzymes (e.g., cytosolic phospholipase A2, 5-lipoxygenase, cyclooxygenase).
- Decreased capacity for AA remodeling from phosphatidylcholine (PC) to phosphatidylethanolamine (PE) was observed, linked to reduced microsomal CoA-independent transacylase activity.
Conclusions:
- Free AA accumulation during BMMC apoptosis is primarily mediated by impaired AA remodeling.
- The study identifies a specific lipid remodeling defect as a key factor in AA dynamics during apoptosis.