期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 99, 期 4, 页码 1165-1174出版社
WILEY
DOI: 10.1002/jcb.20985
关键词
ischemia; ATP; apoptosis; transplantation; calcium; mitochondria
资金
- NCI NIH HHS [T32 CA009592] Funding Source: Medline
- NIDDK NIH HHS [DK064669, DK59390] Funding Source: Medline
Ischemia-reperfusion injury remains a major clinical problem in liver transplantation. One contributing factor is mitochondrial calcium (mCa(2+)) overload, which triggers apoptosis; calcium also regulates mitochondrial respiration and adenosine 5-triphosphate (ATP) production. Recently, we reported the presence of purinergic P2Y(1)- and P2Y(2)-like receptor proteins in mitochondrial membranes. Herein, we present an evaluation of the functional characteristics of these receptors. In experiments with isolated mitochondria, specific P2Y(1) and P2Y(2) receptors ligands: 2-methylthio-adenosine 5'-diphosphate (2meSADP) and uridine 5'-triphosphate (UTP), respectively, were used, and mitochondrial calcium uptake was measured. 2meSADP and UTP had a maximum effect at concentrations in the range of the known P2Y, and P2Y2 receptors. The P2Y inhibitor phosphate-6-azophenyl -2',4'-disulfonate (PPADS) blocked the effects of both ligands. The phospholipase C (PLC) antagonist U73122 inhibited the effect of both ligands while its inactive analog U73343 had no effect. These data strongly support the hypothesis that mitochondrial Ca2+ uptake is regulated in part by adenine nucleotides via a P2Y-like receptor mechanism that involves mitochondrial PLC activation. J. Cell. Biochem.
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