Dysfunction of mitochondrial respiratory chain complex I in human failing myocardium is not due to disturbed mitochondrial gene expression
Robert J. Scheubel, MD* ,*,
Mike Tostlebe, MS,
Andreas Simm, PhD*,
Susanne Rohrbach, MD,
Roland Prondzinsky, MD ,
Frank N. Gellerich, PhD ,
Rolf-Edgar Silber, MD* and
Juergen Holtz, MD
* Cardio-Thoracic Surgery, Halle/Saale, Germany
Cardiology, Halle/Saale, Germany
Neurology , Halle/Saale, Germany
Institute of Pathophysiology, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany
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Figure 1 Enzymatic activity of electron transport chain complexes I (A), II + III (B), III (C), and IV (D) normalized to citrate synthase activity (CS) in human left ventricular myocardium of terminally failing hearts (n = 43) and donor hearts (n = 10). Data are given as mean ± SEM. ***p < 0.001.
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Figure 2 (A) Reverse transcriptase-polymerase chain reaction analysis of messenger ribonucleic acid (mRNA) expression of mitochondrially encoded subunits of respiratory chain complexes (C-I, C-III, C-IV) in human failing left ventricular myocardium given as percent of donor values. Data were obtained by densitometric quantification of the negatives of gel-images and are given as mean ± SEM. (B) Representative Northern blot analysis of mitochondrially encoded ND1 mRNA and nuclear encoded 18S ribosomal ribonucleic acid (rRNA) in left ventricular myocardium of donors and terminally failing patients.
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Figure 3 Comparison of enzymatic activity of electron transport chain complexes I (A), II + III (B), III (C), and IV (D) normalized to citrate synthase activity (CS) in human left ventricular myocardium from terminal heart failure patients receiving beta-blocker therapy (ß-bl. pos., n = 25) before explantation and patients without this therapy (ß-bl. neg., n = 18). Data are given as mean ± SEM. *p < 0.05.
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