Cardiac hypertrophy alters expression of Na+,K(+)-ATPase subunit isoforms at mRNA and protein levels in rat myocardium.
In myocardium from different rat models of cardiac hypertrophy, expression of Na+,K(+)-ATPase isoforms has been shown to be altered at the mRNA level. However, it has not been determined whether these alterations translate into changes at the protein level. This distinction is important because post-transcriptional events have been shown to regulate isoform expression. In the present study, relative abundances of the Na+,K(+)-ATPase isoforms were examined in hypertrophied left ventricles of renovascular hypertensive rats at both the protein and mRNA levels, using immunoblotting and dot blot hybridization, respectively. Stenosis of the left renal artery elicited an increase in systolic blood pressure, cardiac hypertrophy, and a shift in expression of the myosin heavy chain isoforms. In hypertrophied left ventricles, expression of the alpha 1 isoform remained unchanged at both mRNA and protein levels, whereas the relative abundances of both alpha 2-mRNA and -protein decreased, to 0.63 and 0.54, respectively, of controls. In addition, the abundance of beta 1-mRNA remained unchanged, whereas beta 1-protein decreased to 0.67 of controls. These results suggest that in hypertrophied myocardium of renovascular hypertensive rats Na+,K(+)-ATPase isoform expression is altered at both the protein and mRNA levels, and that pretranslational as well as translational/post-translational mechanisms may be involved.
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Department of Pharmacology, College of Medicine, Pennsylvania State University, Hershey 17033.
Moore
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Semanchik
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D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D015152:Blotting, Northern; D004195:Disease Models, Animal; D004591:Electrophoresis, Polyacrylamide Gel; D015971:Gene Expression Regulation, Enzymologic; D006321:Heart / Q000502:physiology; D006973:Hypertension / Q000150:complications / Q000201:enzymology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000201:enzymology / Q000209:etiology / Q000235:genetics*; D007527:Isoenzymes / Q000032:analysis* / Q000235:genetics*; D008297:Male; D009206:Myocardium / Q000737:chemistry* / Q000201:enzymology*; D014176:Protein Biosynthesis; D011499:Protein Processing, Post-Translational; D012333:RNA, Messenger / Q000032:analysis* / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis* / Q000235:genetics*
D007527:Isoenzymes; D012333:RNA, Messenger; D000254:Sodium-Potassium-Exchanging ATPase