Changes of Creatine Kinase Gene Expression in Rat Heart Post-Myocardial Infarction

Creatine kinase (CK) plays a crucial role in cardiac energy transduction. During chronic cardiac stress conditions leading to hypertrophy and/or heart failure, the profile of CK isoenzyme activities changes towards a fetal pattern with increases of BB- and MB-CK and decreases of MM-CK and mito-CK. C...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 1998-04, Vol.30 (4), p.803-810
Main Authors: Neubauer, Stefan, Frank, Monika, Hu, Kai, Remkes, Helga, Laser, Anne, Horn, Michael, Ertl, Georg, Lohse, Martin J.
Format: Article
Language:English
Subjects:
Animals
Blood Pressure
Creatine Kinase - genetics
Creatine Kinase - metabolism
Creatine kinase activity
Creatine kinase gene expression
End-diastolic pressure
Energy metabolism
Gene Expression Regulation, Enzymologic
Heart - physiopathology
Heart failure
Isoenzymes
Male
Myocardial Infarction - enzymology
Myocardial Infarction - genetics
Myocardial Infarction - physiopathology
Myocardium - enzymology
Myocardium - metabolism
Post-MI rat model
Rats
Rats, Wistar
RNA, Messenger
Ventricular Dysfunction, Left - physiopathology
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Summary:Creatine kinase (CK) plays a crucial role in cardiac energy transduction. During chronic cardiac stress conditions leading to hypertrophy and/or heart failure, the profile of CK isoenzyme activities changes towards a fetal pattern with increases of BB- and MB-CK and decreases of MM-CK and mito-CK. Changes of myocardial CK gene expression are only indirectly reflected by measurements of CK activities. The purpose of this work was, therefore, to determine myocardial expression of B-, M- and sarcomeric mito-CK genes in an animal model of heart failure where hemodynamic alterations and CK system changes are well defined, that is, in the rat heart post-myocardial infarction. Intact residual left ventricular myocardium was harvested 2 months following infarction (MI;n=7) or sham operation (sham;n=6) afterin vivoleft-ventricular end-diastolic pressure (LVEDP) was recorded. Total CK activity was measured spectrophotometrically, CK isoenzyme distribution with agarose gel electrophoresis. Steady state mRNA levels coding for B-, M- and mito-CK genes were measured with quantitative PCR and were normalized for GAPDH expression. Total CK activity tended to be reduced in MI (5.51±0.62 IU/mg protein) compared to sham (6.77±0.24;P=0.55). CK isoenzyme distribution showed an increase of fetal BB- +MB-CK (MI 22.0±3.1%, sham 15.1±1.0%;P
ISSN:0022-2828
1095-8584
DOI:10.1006/jmcc.1998.0645