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This Article Full Text Full Text (PDF) All Versions of this Article: 285/3/H1055    most recent 00865.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Elmoselhi, A. B. Articles by Dhalla, N. S. Search for Related Content PubMed PubMed Citation Articles by Elmoselhi, A. B. Articles by Dhalla, N. S.

Preconditioning attenuates ischemia-reperfusion-induced remodeling of Na⁺-K⁺-ATPase in hearts

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada

Submitted 2 October 2002 ; accepted in final form 15 May 2003

The aim of this study was to determine whether changes in protein content and/or gene expression of Na⁺-K⁺-ATPase subunits underlie its decreased enzyme activity during ischemia and reperfusion. We measured protein and mRNA subunit levels in isolated rat hearts subjected to 30 min of ischemia and 30 min of reperfusion (I/R). The effect of ischemic preconditioning (IP), induced by three cycles of ischemia and reperfusion (10 min each), was also assessed on the molecular changes in Na⁺-K⁺-ATPase subunit composition due to I/R. I/R reduced the protein levels of the ₂-, ₃-, ₁-, and ₂-isoforms by 71%, 85%, 27%, and 65%, respectively, whereas the ₁-isoform was decreased by <15%. A similar reduction in mRNA levels also occurred for the isoforms of Na⁺-K⁺-ATPase. IP attenuated the reduction in protein levels of Na⁺-K⁺-ATPase ₂-, ₃-, and ₂-isoforms induced by I/R, without affecting the ₁- and ₁-isoforms. Furthermore, IP prevented the reduction in mRNA levels of Na⁺-K⁺-ATPase ₂-, ₃-, and ₁-isoforms following I/R. Similar alterations in protein contents and mRNA levels for the Na⁺/Ca²⁺ exchanger were seen due to I/R as well as IP. These findings indicate that remodeling of Na⁺-K⁺-ATPase may occur because of I/R injury, and this may partly explain the reduction in enzyme activity in ischemic heart disease. Furthermore, IP may produce beneficial effects by attenuating the remodeling of Na⁺-K⁺-ATPase and changes in Na⁺/Ca²⁺ exchanger in hearts after I/R.

ischemic preconditioning; myocardium; Na⁺-K⁺-ATPase gene expression; Na⁺/Ca²⁺ exchanger

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