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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

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
PubMed

Insights

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.

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