The role of mitochondrial dysfunction in regulation of store‐operated calcium channels in glioma C6 and human fibroblast cells

FEBS Letters

Waśniewska, Magdalena¹  Duszyński, Jerzy¹ 

[1] Department of Cellular Biochemistry, Nencki Institute of Experimental Biology, 3 Pasteur Street, 02 093 Warsaw, Poland

关键词: Store-operated calcium channel;    Calcium influx;    Uncoupler;    [Ca2+]c;    cytosolic calcium concentration;    SOCs;    store-operated calcium channels;    CCCP;    carbonyl cyanide m-chlorophenylhydrazone;    DMSO;    dimethylsulfoxide;   

DOI  :  10.1016/S0014-5793(00)01862-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The store-operated calcium influx into electrically non-excitable cells is greatly modified under the condition of deenergized mitochondria in situ. The rate of calcium influx into cells with empty intracellular calcium stores is greatly diminished when cells were pretreated with 2 μM carbonyl cyanide m-chlorophenylhydrazone (a mitochondrial uncoupler) or with 4 μM myxothiazol (an inhibitor of the respiratory chain). We demonstrate that this general phenomenon takes place in the case of transformed (glioma C6 and Ehrlich ascites tumor cells) as well as non-transformed (human fibroblasts) cells. We also demonstrate that the deenergization of mitochondria affects the cellular calcium influx rate and not the calcium pump on the plasma membrane.

【 授权许可】

Unknown