CARDIAC-HYPERTROPHY ALTERS EXPRESSION OF NA+,K+-ATPASE SUBUNIT ISOFORMS AT MESSENGER-RNA AND PROTEIN-LEVELS IN RAT MYOCARDIUM

被引:49
作者
BOOK, CBS
MOORE, RL
SEMANCHIK, A
NG, YC
机构
[1] PENN STATE UNIV, MILTON S HERSHEY MED CTR, COLL MED, DEPT PHARMACOL, HERSHEY, PA 17033 USA
[2] PENN STATE UNIV, COLL MED, DEPT MED, HERSHEY, PA 17033 USA
[3] PENN STATE UNIV, COLL MED, DEPT CELLULAR & MOLEC PHYSIOL, HERSHEY, PA 17033 USA
关键词
IMMUNOBLOTTING; NORTHERN BLOTTING; ISOFORMS; NA+; K+-ATPASE; RENOVASCULAR HYPERTENSION; CARDIAC HYPERTROPHY;
D O I
10.1006/jmcc.1994.1071
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 pretranslational as well as translational/post-translational mechanisms may be involved. © 1993 Academic Press Limited.
引用
收藏
页码:591 / 600
页数:10
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