Myocardial hypertrophy in transgenic mice overexpressing the bovine growth hormone (bGH) gene
Version of Record online: 25 DEC 2001
Journal of Internal Medicine
Volume 247, Issue 5, pages 546–552, May 2000
How to Cite
Fu, M. L. X., Törnell, J., Schulze, W., Hoebeke, J., Isaksson, O. G. P., Sandstedt, J. and Hjalmarson, Å. (2000), Myocardial hypertrophy in transgenic mice overexpressing the bovine growth hormone (bGH) gene. Journal of Internal Medicine, 247: 546–552. doi: 10.1046/j.1365-2796.2000.00651.x
- Issue online: 25 DEC 2001
- Version of Record online: 25 DEC 2001
- Cited By
- growth hormone;
- transgenic mice
Abstract. Fu MLX, Törnell J, Schulze W, Hoebeke J, Isaksson OGP, Sandstedt J, Hjalmarson A (Sahlgrenska University Hospital and University of Göteborg, Göteborg, Sweden; Max-Delbrück-Centrum, Berlin, Germany; and IBMC, Strasbourg, France). Myocardial hypertrophy in transgenic mice overexpressing the bovine growth hormone (bGH) gene. J Intern Med 2000; 247: 546–552.
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 β-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 β-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.