Title of article :
Cardiac Hypertrophy Alters Expression of Na+,K+-ATPase Subunit Isoforms at mRNA and Protein Levels in Rat Myocardium
Author/Authors :
Carol-Beth S. Book، نويسنده , , Russell L. Moore، نويسنده , , Anne Semanchik، نويسنده , , Yuk-Chow Ng، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1994
Pages :
10
From page :
591
To page :
600
Abstract :
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 α1 isoform remained unchanged at both mRNA and protein levels, whereas the relative abundances of both α2-mRNA and -protein decreased, to 0.63 and 0.54, respectively, of controls. In addition, the abundance of β1-mRNA remained unchanged, whereas β1-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 pre-translational as well as translational/post-translational mechanisms may be involved.
Keywords :
Isoforms , Renovascular hypertension , Northern blotting , Cardiac hypertrophy , immunoblotting , Na+ , K+-ATPase
Journal title :
Journal of Molecular and Cellular Cardiology
Serial Year :
1994
Journal title :
Journal of Molecular and Cellular Cardiology
Record number :
525123
Link To Document :
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