The Role of Na+/Ca2+ Exchanger in Endothelin-1-aggravated Hypoxia/Reoxygenation-induced Injury in Renal Epithelial Cells.
From: Department of Pharmacology, School of Medicine, Fukuoka University, Fukuoka 814-0180, Japan.
Annals of the New York Academy of Sciences
- Publish Date: Mar 2007
- ISSN: 0077-8923
- Volume: 1099
- Issue:
- Pages: 473-7
- Medium: Print
- Language: English
- Citation (JAMA): Kita Satomi, Furuta Ayako, Takano Yukio, et al. The Role of Na+/Ca2+ Exchanger in Endothelin-1-aggravated Hypoxia/Reoxygenation-induced Injury in Renal Epithelial Cells.. Ann. N. Y. Acad. Sci. Mar 2007;1099:473-7
Abstract
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.
Mesh Headings (Keywords): Animals, Anoxia, Endothelin-1, Epithelial Cells, Kidney, LLC-PK1 Cells, Oxygen, Swine, Thiourea
Check for Full Text / PubMed Unique Identifier (PMID): 17446489
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