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Endoplasmic reticulum, Bcl-2 and Ca2+ handling in apoptosis
D Ferrari1, P Pinton, G Szabadkai
1Department of Experimental Medicine, Section of General Pathology, Telethon Center for Cell Imaging, Interdisciplinary Center for the Study of Inflammation, University of Ferrara, Via Borsari 46, I-44100, Ferrara, Italy.
Cell Calcium
|January 25, 2003
Summary
Calcium signaling is crucial in apoptosis. The anti-apoptotic protein Bcl-2 impacts endoplasmic reticulum calcium (Ca2+) handling, reducing cell sensitivity to apoptotic stimuli and suggesting calcium homeostasis as a therapeutic target.
Area of Science:
- Cellular biology
- Molecular mechanisms of cell death
- Calcium signaling in apoptosis
Background:
- Extracellular signals are decoded into apoptotic cell death through complex signaling pathways.
- Calcium ions (Ca2+) play a significant role in this process.
- Alterations in calcium homeostasis are linked to apoptotic and necrotic cell death.
Purpose of the Study:
- To summarize the role of calcium homeostasis in apoptosis.
- To detail new findings on the direct effect of Bcl-2 on endoplasmic reticulum (ER) Ca2+ handling.
- To investigate how Bcl-2 influences ER Ca2+ store filling and cellular sensitivity to apoptotic stimuli.
Main Methods:
- Review of existing evidence on calcium homeostasis and apoptosis.
- Detailed analysis of recent data on Bcl-2's interaction with ER Ca2+.
- Assessment of the impact of Bcl-2-mediated Ca2+ signaling alterations on apoptotic sensitivity.
Main Results:
- Bcl-2 directly affects endoplasmic reticulum (ER) Ca2+ handling.
- Bcl-2 reduces the filling state of the ER Ca2+ store.
- This alteration in Ca2+ signaling makes cells less sensitive to apoptotic stimuli.
Conclusions:
- Bcl-2's modulation of ER Ca2+ homeostasis is a key mechanism in its anti-apoptotic function.
- Altered calcium signaling by Bcl-2 confers resistance to apoptosis.
- Calcium homeostasis represents a potential pharmacological target for treating pathological apoptosis.