The role of Na+/Ca2+ exchanger in endothelin-1-aggravated hypoxia/reoxygenation-induced injury in renal epithelial cells

被引：2
作者：
Kita, Satomi
Furuta, Ayako
Takano, Yukio
Iwamoto, Takahiro
机构：
[1] Fukuoka Univ, Sch Med, Dept Pharmacol, Jonan Ku, Fukuoka 8140180, Japan
[2] Fukuoka Univ, Fac Pharmaceut Sci, Dept Physiol & Pharmacol, Fukuoka 8140180, Japan
来源：
SODIUM-CALCIUM EXCHANGE AND THE PLASMA MEMBRANE CA2+-ATPASE IN CELL FUNCTION: FIFTH INTERNATIONAL CONFERENCE | 2007年 / 1099卷
关键词：
sodium-calcium exchange; endothelin-1; KB-R7943; hypoxia/reoxygenation; LLC-PK1; cell;
D O I：
10.1196/annals.1387.041
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We analyzed the role of the Na+/Ca2+ exchanger (NCX) in endothelin-1-aggravated hypoxia/reoxygenation-induced injury in renal epithelial LLC-PK1 cells. KB-R7943, a selective NCX inhibitor, suppressed hypoxia/reoxygenation-induced cell damage, whereas overexpression of NCX1 into cells enhanced it. Endothelin-1 significantly aggravated hypoxia/reoxygenation-induced injury in parental and NCX1-overexpressing LLC-PK1 cells. Such aggravation by endothelin-1 was not observed in cells overexpressing a deregulated NCX1 mutant, which displays no protein kinase C-dependent activation. These results suggest that Ca2+ overload via NCX plays a critical role in hypoxia/reoxygenation-induced renal tubular injury, and that endothelin-1 aggravates the cell damage through the activation of NCX.
引用
收藏
页码：473 / 477
页数：5
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