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Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
Published on: September 7, 2012
The mitochondrial membrane potential and Ca2+ oscillations in smooth muscle
Susan Chalmers1, John G McCarron
1Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, John Arbuthnott Building, 27 Taylor Street, Glasgow, G4 0NR, UK.
Journal of Cell Science
|December 13, 2007
Summary
Mitochondria do not change membrane potential during normal calcium signaling in smooth muscle cells. However, during sustained calcium oscillations or oxidative stress, individual mitochondria can depolarize, impacting cellular energy production.
Area of Science:
- Cellular Physiology
- Mitochondrial Biology
- Calcium Signaling
Background:
- Mitochondrial calcium (Ca2+) uptake influences cytosolic Ca2+ levels and mitochondrial membrane potential (ΔΨm), potentially affecting ATP production.
- Understanding how physiological Ca2+ signaling impacts cellular energy is crucial for cell function.
Purpose of the Study:
- To investigate the effect of physiological Ca2+ signaling on mitochondrial membrane potential (ΔΨm) in smooth muscle cells.
- To determine if Ca2+ oscillations alter mitochondrial energy production.
Main Methods:
- Voltage-clamped single smooth muscle cells were used to examine ΔΨm during Ca2+ oscillations.
- Mitochondrial Ca2+ accumulation was inhibited to assess its impact on Ca2+ release and restoration.
- ΔΨm was monitored using a sensitive dye (TMRE) and observed under various conditions, including fluorescence excitation and oxidative stress.
Main Results:
- Inhibition of mitochondrial Ca2+ uptake affected inositol trisphosphate-evoked Ca2+ release and slowed cytosolic Ca2+ restoration.
- No significant ΔΨm changes were observed during single or repetitive Ca2+ oscillations induced by physiological stimuli.
- Spontaneous, persistent Ca2+ oscillations led to stochastic ΔΨm depolarizations in individual mitochondria, independent of Ca2+ oscillations.
- These depolarizations were mimicked by increased dye/light exposure and inhibited by antioxidants and cyclosporin A (CsA).
Conclusions:
- Individual mitochondria can depolarize during sustained Ca2+ oscillations or oxidative stress in smooth muscle cells.
- Mitochondrial membrane potential (ΔΨm) remains stable during transient Ca2+ events evoked by Ca2+ influx or store release.
- Mitochondria do not appear to limit ATP production during normal physiological Ca2+ signaling in these cells.
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