Journal
CELL CALCIUM
Volume 47, Issue 5, Pages 433-440Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2010.03.004
Keywords
Mitochondrial Ca2+ uptake; Store-operated Ca2+ entry; ER; Ca2+ release; UCP2/3; Uncoupling proteins
Categories
Funding
- Austrian Science Funds (FWF) [P20181-B05, F3010-B05, P21857-818, P20181-B5]
- Austrian ministry of science and research
- Austrian Science Fund (FWF) [P 21857] Funding Source: researchfish
- Austrian Science Fund (FWF) [P20181, P21857] Funding Source: Austrian Science Fund (FWF)
Ask authors/readers for more resources
The transmission of Ca2+ 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 Ca2+ uniport (MCU). In the present study we investigate the contribution of UCP2/3 to mitochondrial accumulation of Ca2+ either exclusively released from the ER or entering the cell via the store-operated Ca2+ entry (SOCE) pathway. Using siRNA we demonstrate that constitutively expressed UCP2/3 are essentially involved in mitochondrial sequestration of intracellularly released Ca2+ but not of that entering the cells via SOCE. However, overexpression of UCP2/3 yielded elevated mitochondrial Ca2+ uptake from both sources, though it was more pronounced in case of entering Ca2+, indicating that the expression levels of UCP2/3 are crucial for the capacity of mitochondria to sequester entering Ca2+. Our data point to distinct UCP2/3-dependent and UCP2/3-independent modes of mitochondrial Ca2+ sequestration, which may meet the various demands necessary for an adequate organelle Ca2+ loading from different Ca2+ sources in intact cells. (C) 2010 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available