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Updated: Oct 5, 2025
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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
Published on: April 1, 2011
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Mitochondria modulate ameloblast Ca2+ signaling
Veronica Costiniti1, Guilherme H S Bomfim1, Maria Neginskaya1
1Department of Molecular Pathobiology, New York University College of Dentistry, New York, New York, USA.
Summary
Mitochondria handle calcium differently in enamel-forming cells during maturation. Increased mitochondrial calcium uptake via the mitochondrial calcium uniporter (MCU) occurs during maturation, especially when calcium influx is stimulated by store-operated calcium entry (SOCE).
Area of Science:
- Biomineralization
- Cell Physiology
- Mitochondrial Function
Background:
- Mitochondria play a poorly understood role in enamel formation, a highly mineralized tissue.
- Ameloblast cells, responsible for enamel production, undergo distinct secretory and maturation stages crucial for mineralization.
- Understanding ameloblast physiology, particularly calcium (Ca2+) signaling, is key to comprehending enamel mineralization.
Purpose of the Study:
- To investigate the functional characteristics of mitochondria in rat primary secretory and maturation-stage ameloblasts.
- To elucidate the specific role of mitochondria in Ca2+ signaling during enamel development.
- To determine the contribution of mitochondrial Ca2+ uptake and extrusion mechanisms in different ameloblast stages.
Main Methods:
- Quantified mitochondrial Ca2+ storage using trifluoromethoxy carbonylcyanide phenylhydrazone stimulation.
- Assessed mitochondrial Ca2+ uptake and extrusion via Na+-Li+-Ca2+ exchanger using adenosine triphosphate and rhod2AM.
- Investigated the role of the mitochondrial Ca2+ uniporter (MCU) in cytosolic Ca2+ buffering by stimulating store-operated Ca2+ entry (SOCE) and using the MCU inhibitor Ru265 in LS8 cells and primary ameloblasts.
Main Results:
- Mitochondrial Ca2+ storage was similar between secretory and maturation ameloblasts.
- Mitochondrial Ca2+ extrusion via the Na+-Li+-Ca2+ exchanger was more pronounced in maturation-stage ameloblasts.
- Stimulation of SOCE led to significantly higher mitochondrial Ca2+ uptake in maturation ameloblasts, which was inhibited by Ru265, indicating MCU involvement.
Conclusions:
- Mitochondria exhibit enhanced Ca2+ handling capabilities in maturation-stage ameloblasts, particularly when Ca2+ influx is stimulated via SOCE.
- The mitochondrial Ca2+ uniporter (MCU) plays a role in Ca2+ buffering during enamel maturation.
- SOCE and mitochondrial Ca2+ uptake are complementary processes essential for biological mineralization in ameloblasts.
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