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Protein turnover in skeletal muscle of tumour-bearing transgenic mice overexpressing the soluble TNF receptor-1
|Published in||Cancer Letters. 1998, vol. 130, no. 1-2, p. 19-27|
|Abstract||The implantation of the Lewis lung carcinoma (a fast-growing mouse tumour that induces cachexia) to both wild-type and transgenic mice for the soluble TNF receptor type I protein (sTNF-R1) resulted in a considerable loss of carcass weight in both groups. However, while in the wild-type mice there was a loss of both fat and muscle, in the transgenic mice muscle waste was not affected to the same extent as in the wild-type group. Muscle waste in wild-type mice was accompanied by an increase in the fractional rate of protein degradation, while no changes were observed in protein synthesis. The result was a decreased rate of protein accumulation which accounted for the muscle weight loss observed as a result of the tumour burden. In contrast, transgenic mice did not have such low rates of protein accumulation after tumour implantation. The increase in protein degradation in the tumour-bearing transgenic mice was accompanied by a similar increase in protein synthesis which compensated for the loss of muscle protein by degradation. Both tumour-bearing groups showed an enhanced expression of ubiquitin and proteasome C8 subunit genes, all of them related to the activation of the ATP-dependent proteolytic system in skeletal muscle. It is suggested that TNF may, in part, be responsible for the loss of protein in skeletal muscle of tumour-bearing mice.|
|Keywords||Animals — Antigens, CD/*metabolism — Body Weight — Cachexia/etiology — Carcinoma, Lewis Lung/*metabolism/pathology — Mice — Mice, Inbred C57BL — Mice, Transgenic — Muscle Proteins/*metabolism — Muscle, Skeletal/*metabolism/pathology — Receptors, Tumor Necrosis Factor/*metabolism — Receptors, Tumor Necrosis Factor, Type I|