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Bcl-2 Decreases the Free Ca2+Concentration within the Endoplasmic Reticulum
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Journal Article
Bcl-2 Decreases the Free Ca2+Concentration within the Endoplasmic Reticulum
2000
Overview
The antiapoptotic protein Bcl-2 localizes not only to mitochondria but also to the endoplasmic reticulum (ER). However, the function of Bcl-2 at the level of the ER is poorly understood. In this study, we have investigated the effects of Bcl-2 expression on Ca2+storage and release by the ER. The expression of Bcl-2 decreased the amount of Ca2+that could be released from intracellular stores, regardless of the mode of store depletion, the cell type, or the species from which Bcl-2 was derived. Bcl-2 also decreased cellular Ca2+store content in the presence of mitochondrial inhibitors, suggesting that its effects were not mediated through mitochondrial Ca2+uptake. Direct measurements with ER-targeted Ca2+-sensitive fluorescent \"cameleon\" proteins revealed that Bcl-2 decreased the free Ca2+concentration within the lumen of the ER, [Ca2+]ER. Analysis of the kinetics of Ca2+store depletion in response to the Ca2+-ATPase inhibitor thapsigargin revealed that Bcl-2 increased the permeability of the ER membrane. These results suggest that Bcl-2 decreases the free Ca2+concentration within the ER lumen by increasing the Ca2+permeability of the ER membrane. The increased ER Ca2+permeability conferred by Bcl-2 would be compatible with an ion channel function of Bcl-2 at the level of the ER membrane.
Publisher
National Academy of Sciences of the United States of America,National Acad Sciences,National Academy of Sciences,The National Academy of Sciences
