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

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.
AuthorsSatomi Kita, Ayako Furuta, Yukio Takano, Takahiro Iwamoto
JournalAnnals 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
PMID17446489 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate
  • Endothelin-1
  • Thiourea
  • Oxygen
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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