AJP - Renal AJP: Lung Cellular and Molecular Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol (December 9, 2003). doi:10.1152/ajprenal.00284.2003
This Article
Right arrow Full Text (PDF)
Right arrow Supplemental Video
Right arrow All Versions of this Article:
286/4/F784    most recent
00284.2003v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (16)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smets, I.
Right arrow Articles by Steels, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smets, I.
Right arrow Articles by Steels, P.
Submitted on August 13, 2003
Accepted on November 30, 2003

Ca2+ uptake in depolarized mitochondria is mediated via the reversed action of the mitochondrial Na+/Ca2+ exchanger in metabolically inhibited MDCK cells

Ilse Smets1*, Adrian Caplanusi1, Sanda Despa1, Zsolt Molnar1, Mihai Radu1, Martin vandeVen1, Marcel Ameloot1, and Paul Steels1

1 Department of Physiology, Limburgs Universitair Centrum/transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, Diepenbeek, Belgium

* To whom correspondence should be addressed. E-mail: ilse.smets{at}luc.ac.be.

In ischemic or hypoxic tissues elevated calcium levels have emerged as one of the main damaging agents amongst other Ca2+-independent mechanisms of cellular injury. Since 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 the 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 of cellular ATP levels and a rapid increase of 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% from 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 CGP37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in [Ca2+]i was seen during MI, while 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 reversed mode.




This article has been cited by other articles:


Home page
 CirculationHome page
G. Michels, I. F. Khan, J. Endres-Becker, D. Rottlaender, S. Herzig, A. Ruhparwar, T. Wahlers, and U. C. Hoppe
Regulation of the Human Cardiac Mitochondrial Ca2+ Uptake by 2 Different Voltage-Gated Ca2+ Channels
Circulation, May 12, 2009; 119(18): 2435 - 2443.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S. A. Kempson, J. M. Edwards, A. Osborn, and M. Sturek
Acute inhibition of the betaine transporter by ATP and adenosine in renal MDCK cells
Am J Physiol Renal Physiol, July 1, 2008; 295(1): F108 - F117.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
B. Kim and S. Matsuoka
Cytoplasmic Na+-dependent modulation of mitochondrial Ca2+ via electrogenic mitochondrial Na+-Ca2+ exchange
J. Physiol., March 15, 2008; 586(6): 1683 - 1697.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
A. Caplanusi, A. J. Fuller, R. A. Gonzalez-Villalobos, T. G. Hammond, and L. G. Navar
Metabolic inhibition-induced transient Ca2+ increase depends on mitochondria in a human proximal renal cell line
Am J Physiol Renal Physiol, August 1, 2007; 293(2): F533 - F540.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
A. K. Ahrabi, S. Terryn, G. Valenti, N. Caron, C. Serradeil-Le Gal, D. Raufaste, S. Nielsen, S. Horie, J.-M. Verbavatz, and O. Devuyst
PKD1 Haploinsufficiency Causes a Syndrome of Inappropriate Antidiuresis in Mice
J. Am. Soc. Nephrol., June 1, 2007; 18(6): 1740 - 1753.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S. A. Kempson, J. M. Edwards, and M. Sturek
Inhibition of the renal betaine transporter by calcium ions
Am J Physiol Renal Physiol, August 1, 2006; 291(2): F305 - F313.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
S. Baron, A. Caplanusi, M. van de Ven, M. Radu, S. Despa, I. Lambrichts, M. Ameloot, P. Steels, and I. Smets
Role of Mitochondrial Na+ Concentration, Measured by CoroNa Red, in the Protection of Metabolically Inhibited MDCK Cells
J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3490 - 3497.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.