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Myocardial hypertrophy in transgenic mice overexpressing the bovine growth hormone (bGH) gene.

Artikel i vetenskaplig tidskrift
Författare Michael Fu
Jan Törnell
W Schulze
Johan Hoebeke
Olle Isaksson
Jonas Sandstedt
Åke Hjalmarson
Publicerad i Journal of internal medicine
Volym 247
Nummer/häfte 5
Sidor 546-52
ISSN 0954-6820
Publiceringsår 2000
Publicerad vid Wallenberglaboratoriet
Institutionen för invärtesmedicin
Institutionen för invärtesmedicin, Avdelningen för kroppssammansättning och metabolism
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 546-52
Språk en
Länkar dx.doi.org/10.1046/j.1365-2796.2000...
Ämnesord Animals, Binding, Competitive, Cardiomegaly, genetics, metabolism, Cattle, Gene Expression, Growth Hormone, genetics, metabolism, Mice, Mice, Transgenic, Microscopy, Electron, Myocardium, ultrastructure, Radioimmunoassay, Receptors, Adrenergic, beta, analysis, Receptors, Muscarinic, analysis
Ämneskategorier Fysiologi

Sammanfattning

OBJECTIVES: The main purpose of the present study was to characterize cardiac muscle hypertrophy using both qualitative and quantitative microscopy in mice overexpressing the bovine growth hormone. RESULTS: Measurements of 30 fibres from each group revealed that fibre diameter in transgenic hearts was significantly larger than in control hearts. There was a significant decrease in interfibrillar space in transgenic hearts as compared with control hearts. The enlarged transgenic hearts displayed unchanged organelles such as normal myofibrils and mitochondria in a normal pattern, suggesting balanced growth. Myelin structures were occasionally observed between normal myofibrils. Moreover, myocardial beta-adrenergic receptors and muscarinic receptors in the hearts of transgenic mice overproducing GH were studied to see whether they are involved in the hypertrophic process. It was shown that the density of muscarinic receptors had decreased and the super-high affinity of muscarinic receptors was lost, without any significant changes in either the density or the affinity of beta-adrenergic receptors, as compared with controls. CONCLUSIONS: These results demonstrate that a GH excess was able to induce significant myocardial hypertrophy and that there was a downregulation of muscarinic receptors.

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