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Induction of apoptosis by nitric oxide in macrophages is independent of apoptotic volume decrease.
S Hortelano1, M Zeini, A Castrillo
1Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Universidad Complutense, 28040 Madrid, Spain.
Cell Death and Differentiation
|May 29, 2002
Summary
Apoptosis involves cell death changes. Mitochondrial membrane potential changes differ by cell type, and apoptotic volume decrease is not always required for this cell death process.
Area of Science:
- Cell Biology
- Biochemistry
- Immunology
Background:
- Apoptosis, or programmed cell death, is characterized by specific biochemical and morphological alterations.
- Key events include changes in mitochondrial inner membrane potential (DeltaPsi(m)), cytochrome c release, apoptotic volume decrease (AVD), and caspase activation.
Purpose of the Study:
- To investigate the sequence and cell-type dependency of apoptotic events.
- To determine the role of mitochondrial membrane potential changes and AVD in apoptosis induced by various agents.
Main Methods:
- RAW 264.7 (macrophages), HeLa, and Jurkat T cells were treated with apoptosis-inducing agents (NO, staurosporine, etoposide, camptothecin).
- Measurements included DeltaPsi(m), cytochrome c release, AVD, and caspase activation.
- The sequence of these events was analyzed.
Main Results:
- NO, staurosporine, etoposide, and camptothecin increased DeltaPsi(m) in macrophages but decreased it in HeLa and Jurkat cells.
- Apoptosis induced by NO in macrophages may occur without AVD.
- In RAW 264.7 cells, DeltaPsi(m) changes preceded AVD and caspase activation.
- AVD inhibition blocked apoptosis in HeLa and Jurkat cells, irrespective of the inducer.
Conclusions:
- Mitochondrial membrane potential changes during apoptosis are cell-type specific.
- Apoptotic volume decrease is dispensable for apoptosis in macrophages but essential in HeLa and Jurkat cells.