Abstract |
Because of its key role in proteosynthesis, the total content of elongation factor-2 (EF-2) and the distribution of six main EF-2 variants were investigated after Pseudomonas Exotoxin A catalyzed [37P]ADP-ribosylation using 1D-PAGE and isoelectric focusing (IEF) in a rat model of hemodynamic overload with variable degrees of cardiac hypertrophy: Chronic NO-synthase inhibition by L-NAME ( N-omega-nitro-L-arginine-methyl-ester; 0.75 mg/ml drinking water) induced arterial hypertension without hypertrophy but myocardial apoptosis; additional treatment with IGF-1 (osmotic micropumps) did not modify hypertension but reduced apoptosis allowing moderate hypertrophy of the left ventricles. Total EF-2 did not significantly increase in rats with hemodynamic overload with or without IGF-1 supplementation. A positive correlation was found between an acidic EF-2 variant and apoptosis (p = 0.01). Hypertrophy under additional IGF-1 was combined with a shift of the EF-2 variants to basic subtypes (p < 0.01). This finding may be indicative of the trophic potency of IGF-1.
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Authors | Doris Jäger, Ursula Müller-Werdan, Klaus Pönicke, Jürgen Holtz, Karl Werdan, Sylvana P Müller |
Journal | Molecular and cellular biochemistry
(Mol Cell Biochem)
Vol. 229
Issue 1-2
Pg. 25-34
(Jan 2002)
ISSN: 0300-8177 [Print] Netherlands |
PMID | 11936844
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Enzyme Inhibitors
- Peptide Elongation Factor 2
- Insulin-Like Growth Factor I
- Nitric Oxide Synthase
- NG-Nitroarginine Methyl Ester
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Topics |
- Animals
- Apoptosis
- Body Weight
- Cardiomegaly
(metabolism)
- DNA Fragmentation
- Disease Models, Animal
- Enzyme Inhibitors
(pharmacology)
- Genetic Variation
- Heart
(drug effects)
- Hemodynamics
- Hypertension
(metabolism)
- Insulin-Like Growth Factor I
(pharmacology)
- Male
- Myocardium
(metabolism)
- NG-Nitroarginine Methyl Ester
(pharmacology)
- Nitric Oxide Synthase
(antagonists & inhibitors)
- Peptide Elongation Factor 2
(genetics, metabolism)
- Rats
- Rats, Wistar
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