期刊
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
卷 457, 期 4, 页码 941-954出版社
SPRINGER
DOI: 10.1007/s00424-008-0551-0
关键词
ATP; Ca2+ signal; Ca2+ uptake; Inositol 1,4,5-trisphosphate; Magnesium; Mitochondria
类别
资金
- Hungarian National Science Foundation [OTKA 049851, NK72661]
- Council for Medical Research [ETT 0007/2006]
- Spanish Ministerio de Educacion y Ciencia [BFU200760157]
Cytosolic Ca2+ signals are followed by mitochondrial Ca2+ uptake, which, in turn, modifies several biological processes. Mg2+ is known to inhibit Ca2+ uptake by isolated mitochondria, but its significance in intact cells has not been elucidated. In HEK293T cells, activation of purinergic receptors with extracellular ATP caused cytosolic Ca2+ signals associated with parallel changes in cytosolic [Mg2+]. Neither signals were affected by omitting bivalent cations from the extracellular medium. The effect of store-operated Ca2+ influx on cytosolic Mg2+ concentration ([Mg2+](c)) was negligible. Uncaged Ca2+ displaced Mg2+ from cytosolic binding sites, but for an equivalent Ca2+ signal, the change in [Mg2+] was significantly smaller than that measured after adding extracellular ATP. Inositol 1,4,5-trisphosphate mobilized Ca2+ and Mg2+ from internal stores in permeabilized cells. The increase of [Mg2+] in the range that occurred in ATP-stimulated cells inhibited mitochondrial Ca2+ uptake in permeabilized cells without affecting mitochondrial Ca2+ efflux. Therefore, the Mg2+ signal generated by Ca2+ mobilizing agonists may attenuate mitochondrial Ca2+ uptake.
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