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Updated: Jun 13, 2026

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
Published on: April 27, 2018
The contribution of UCP2 and UCP3 to mitochondrial Ca(2+) uptake is differentially determined by the source of
Markus Waldeck-Weiermair1, Roland Malli, Shamim Naghdi
1Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Medical University Graz, Austria.
Abstract:
The transmission of Ca(2+) signals to mitochondria is an important phenomenon in cell signaling. We have recently reported that the novel uncoupling proteins UCP2 and UCP3 (UCP2/3) are fundamental for mitochondrial Ca(2+) uniport (MCU). In the present study we investigate the contribution of UCP2/3 to mitochondrial accumulation of Ca(2+) either exclusively released from the ER or entering the cell via the store-operated Ca(2+) entry (SOCE) pathway. Using siRNA we demonstrate that constitutively expressed UCP2/3 are essentially involved in mitochondrial sequestration of intracellularly released Ca(2+) but not of that entering the cells via SOCE. However, overexpression of UCP2/3 yielded elevated mitochondrial Ca(2+) uptake from both sources, though it was more pronounced in case of entering Ca(2+), indicating that the expression levels of UCP2/3 are crucial for the capacity of mitochondria to sequester entering Ca(2+). Our data point to distinct UCP2/3-dependent and UCP2/3-independent modes of mitochondrial Ca(2+) sequestration, which may meet the various demands necessary for an adequate organelle Ca(2+) loading from different Ca(2+) sources in intact cells.
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