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.
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Authors | Satomi Kita, Ayako Furuta, Yukio Takano, Takahiro Iwamoto |
Journal | Annals of the New York Academy of Sciences
(Ann N Y Acad Sci)
Vol. 1099
Pg. 473-7
(Mar 2007)
ISSN: 0077-8923 [Print] United States |
PMID | 17446489
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- 2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate
- Endothelin-1
- Thiourea
- Oxygen
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Topics |
- Animals
- Endothelin-1
(physiology)
- Epithelial Cells
(pathology)
- Hypoxia
(physiopathology)
- Kidney
(pathology)
- LLC-PK1 Cells
- Oxygen
(metabolism)
- Swine
- Thiourea
(analogs & derivatives, pharmacology)
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