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Am J Physiol Renal Physiol 286: F784-F794, 2004. First published December 9, 2003; doi:10.1152/ajprenal.00284.2003
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Ca2+ uptake in mitochondria occurs via the reverse action of the Na+/Ca2+ exchanger in metabolically inhibited MDCK cells

Ilse Smets, Adrian Caplanusi,* Sanda Despa,* Zsolt Molnar, Mihai Radu, Martin vandeVen, Marcel Ameloot, and Paul Steels

Department of Physiology, Limburgs Universitair Centrum/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium

Submitted 13 August 2003 ; accepted in final form 30 November 2003

In ischemic or hypoxic tissues, elevated Ca2+ levels have emerged as one of the main damaging agents among other Ca2+-independent mechanisms of cellular injury. Because mitochondria, besides the endoplasmic reticulum, play a key role in the maintainance of cellular Ca2+ homeostasis, alterations in the mitochondrial Ca2+ content ([Ca2+]m) were monitored in addition to changes in cytosolic Ca2+ concentration ([Ca2+]i) during metabolic inhibition (MI) in renal epithelial Madin-Darby canine kidney (MDCK) cells. [Ca2+]i and [Ca2+]m were monitored via, respectively, fura 2 and rhod 2 measurements. MI induced an increase in [Ca2+]i reaching 631 ± 78 nM in ~20 min, followed by a decrease to 118 ± 9 nM in the next ~25 min. A pronounced drop in cellular ATP levels and a rapid increase in intracellular Na+ concentrations in the first 20 min of MI excluded Ca2+ efflux in the second phase via plasma membrane ATPases or Na+/Ca2+ exchangers (NCE). Mitochondrial rhod 2 intensities increased to 434 ± 46% of the control value during MI, indicating that mitochondria sequester Ca2+ during MI. The mitochondrial potential ({Delta}{Psi}m) was lost in 20 min of MI, excluding mitochondrial Ca2+ uptake via the {Delta}{Psi}m-dependent mitochondrial Ca2+ uniporter after 20 min of MI. Under Na+-free conditions, or when CGP-37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in [Ca2+]i was seen during MI, whereas the MI-induced increase in mitochondrial rhod 2 fluorescence was strongly reduced. To our knowledge, this study is the first to report that in metabolically inhibited renal epithelial cells mitochondria take up Ca2+ via the NCE acting in the reverse mode.

renal epithelial cells; intramitochondrial calcium; rhod 2; CGP-37157


Address for reprint requests and other correspondence: I. Smets, MBW-Dept. of Physiology, Limburgs Universitair Centrum/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, Universitaire Campus Gebouw D, B-3590 Diepenbeek, Belgium (E-mail: ilse.smets{at}luc.ac.be).




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