Regulation of protein synthesis and degradation in adult ventricular cardiomyocytes.
For studies on the regulation of myocardial protein metabolism, isolated adult cardiomyocytes were introduced as an experimental model about a decade ago. When used shortly after isolation, this model represents a tool for studying the properties of normal and diseased myocardium on the cellular level. The influence of various peptide hormones, neurotransmitters, and mechanical stimulation on protein synthesis and degradation in isolated cardiomyocytes has been studied. It has been demonstrated, for example, that alpha 1-adrenoceptor stimulation increases protein synthesis in newly isolated cardiomyocytes, independently of any mechanical effects. Other potential growth stimuli require appropriate conditions to induce cellular responsiveness. Neuropeptide Y, for example, does not stimulate cellular protein synthesis in newly isolated cells, whereas it does so in cells that have been cultured for a week in the presence of serum. Mechanical stretch also represents a growth stimulant. It seems that its signal transduction involves an autocrine loop. Thus different mechanisms, by which exogenous influences can modify cellular protein synthesis and degradation, have been identified on the cellular level, with the use of isolated adult cardiomyocytes.
Schlüter
K D
KD
Physiologisches Institut, Justus-Liebig-Universität Giessen, Germany.
Millar
B C
BC
McDermott
B J
BJ
Piper
H M
HM
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000328:Adult; D006352:Heart Ventricles; D006728:Hormones / Q000494:pharmacology; D006801:Humans; D009124:Muscle Proteins / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000494:pharmacology; D010812:Physical Stimulation
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D006728:Hormones; D009124:Muscle Proteins; D018377:Neurotransmitter Agents