%0 Journal Article %1 Jame_1999_555 %A James, P. F. %A Grupp, I. L. %A Grupp, G. %A Woo, A. L. %A Askew, G. R. %A Croyle, M. L. %A Walsh, R. A. %A Lingrel, J. B. %D 1999 %J Mol. Cell %K /&/ ATPase, Animals; Calcium Calcium, Cells Contraction, Enzyme Failure, Fibers, Glycosides, Heart Heterozygote; Inhibitors, Isoenzymes, Messenger, Mice, Mice; Muscle Myocardial Myocardium, Ouabain, RNA, Signaling, Sodium-Potassium-Exchanging Stem Transgenic; Ventricles, antagonists cytology/enzymology; drug effects/physiology; enzymology; inhibitors/genetics/metabolism; metabolism; pharmacology; physiology; %N 5 %P 555--563 %T Identification of a specific role for the Na,K-ATPase alpha 2 isoform as a regulator of calcium in the heart. %V 3 %X It is well accepted that inhibition of the Na,K-ATPase in the heart, through effects on the Na/Ca exchanger, raises the intracellular Ca$^2+$ concentration and strengthens cardiac contraction. However, the contribution that individual isoforms make to this calcium regulatory role is unknown. Assessing the phenotypes of mouse hearts with genetically reduced levels of Na,K-ATPase alpha 1 or alpha 2 isoforms clearly demonstrates different functional roles for these isoforms in vivo. Heterozygous alpha 2 hearts are hypercontractile as a result of increased calcium transients during the contractile cycle. In contrast, heterozygous alpha 1 hearts are hypocontractile. The different functional roles of these two isoforms are further demonstrated since inhibition of the alpha 2 isoform with ouabain increases the contractility of heterozygous alpha 1 hearts. These results definitively illustrate a specific role for the alpha 2 Na,K-ATPase isoform in Ca$^2+$ signaling during cardiac contraction.

@article{Jame_1999_555, abstract = {It is well accepted that inhibition of the Na,K-ATPase in the heart, through effects on the Na/Ca exchanger, raises the intracellular {C}a$^{2+}$ concentration and strengthens cardiac contraction. However, the contribution that individual isoforms make to this calcium regulatory role is unknown. Assessing the phenotypes of mouse hearts with genetically reduced levels of Na,K-ATPase alpha 1 or alpha 2 isoforms clearly demonstrates different functional roles for these isoforms in vivo. Heterozygous alpha 2 hearts are hypercontractile as a result of increased calcium transients during the contractile cycle. In contrast, heterozygous alpha 1 hearts are hypocontractile. The different functional roles of these two isoforms are further demonstrated since inhibition of the alpha 2 isoform with ouabain increases the contractility of heterozygous alpha 1 hearts. These results definitively illustrate a specific role for the alpha 2 Na,K-ATPase isoform in {C}a$^{2+}$ signaling during cardiac contraction.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {James, P. F. and Grupp, I. L. and Grupp, G. and Woo, A. L. and Askew, G. R. and Croyle, M. L. and Walsh, R. A. and Lingrel, J. B.}, biburl = {https://www.bibsonomy.org/bibtex/2839097da34b082d1c019b88085da0a52/hake}, description = {The whole bibliography file I use.}, file = {Jame_1999_555.pdf:Jame_1999_555.pdf:PDF}, institution = {Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Ohio 45267, USA.}, interhash = {07c1b2a1d532346bd4d4bd5fb0ff7702}, intrahash = {839097da34b082d1c019b88085da0a52}, journal = {Mol. Cell}, keywords = {/&/ ATPase, Animals; Calcium Calcium, Cells Contraction, Enzyme Failure, Fibers, Glycosides, Heart Heterozygote; Inhibitors, Isoenzymes, Messenger, Mice, Mice; Muscle Myocardial Myocardium, Ouabain, RNA, Signaling, Sodium-Potassium-Exchanging Stem Transgenic; Ventricles, antagonists cytology/enzymology; drug effects/physiology; enzymology; inhibitors/genetics/metabolism; metabolism; pharmacology; physiology;}, month = May, number = 5, pages = {555--563}, pdf = {Jame_1999_555.pdf}, pii = {S1097-2765(00)80349-4}, pmid = {10360172}, timestamp = {2009-06-03T11:21:16.000+0200}, title = {Identification of a specific role for the Na,K-ATPase alpha 2 isoform as a regulator of calcium in the heart.}, volume = 3, year = 1999 }