Effects of tumor necrosis factor alpha on skeletal muscle amino acid metabolism studied in-vivo.

Exogenously administered tumor necrosis factor-alpha (TNF-alpha) elicits several symptoms of generalized infections such as fever, increased sleep, and anorexia. The aim of the present work was to localize these effects of TNF-alpha to specific amino acid sequences of the parent molecule by characterizing the in vivo and in vitro activities of several synthetic TNF-alpha fragments. Intracerebroventricular injection of TNF-alpha elicited dose-dependent fevers and increases in non-rapid-eye-movement sleep (NREMS) in rabbits. Four fragments also promoted NREMS and five elicited monophasic fevers. All of the somnogenic fragments share the amino acid sequence 31-36. In rats, TNF-alpha and one of the fragments [TNF-alpha-(69-100)] suppressed 12-h food intake. Furthermore, TNF-alpha increased the expression of the intercellular adhesion molecule-1 and enhanced interferon-gamma-induced HLA-DR expression in human glioblastoma cell line. In contrast, none of the fragments possessed these in vitro activities. Our in vivo results support the concept that there are biologically active regions in the TNF-alpha molecule.

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In vivo Antitumor Activities of Tumor Necrosis Factor-Alpha

Molecular Basis of Lymphokine Action ◽

10.1007/978-1-4612-4598-8_21 ◽

1987 ◽

pp. 223-232 ◽

Cited By ~ 2

Author(s):

Michael A. Palladino

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Antitumor Activities ◽

Necrosis Factor Alpha ◽

Factor Alpha ◽

Necrosis Factor

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Treadmill exercise training could attenuate the upregulation of Interleukin-1 beta and tumor necrosis factor alpha in the skeletal muscle of mouse model of chronic/progressive Parkinson disease

Neurorehabilitation ◽

10.3233/nre-182492 ◽

2019 ◽

Vol 43 (4) ◽

pp. 501-507 ◽

Cited By ~ 1

Author(s):

Muhammed D. Al-Jarrah ◽

Nour S. Erekat

Keyword(s):

Skeletal Muscle ◽

Tumor Necrosis Factor ◽

Exercise Training ◽

Tumor Necrosis ◽

Treadmill Exercise ◽

Interleukin 1 ◽

Interleukin 1 Beta ◽

Necrosis Factor Alpha ◽

Factor Alpha ◽

Necrosis Factor

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Low-dose prostacyclin has potent capillary permeability-reducing effect in cat skeletal muscle in vivo

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.1.h200 ◽

1997 ◽

Vol 273 (1) ◽

pp. H200-H207 ◽

Cited By ~ 4

Author(s):

A. D. Moller ◽

P. O. Grande

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Vascular Tone ◽

Low Dose ◽

Capillary Permeability ◽

Necrosis Factor Alpha ◽

Factor Alpha ◽

Necrosis Factor

The dose-response effects of intravenous infusion of prostacyclin on capillary permeability (the capillary filtration coefficient technique), hydrostatic capillary pressure, transcapillary filtration, and vascular tone were analyzed in vivo on cat skeletal muscle from a normal and an increased permeability level. Increased permeability was accomplished by intra-arterial infusion of tumor necrosis factor-alpha or histamine. Permeability effects of bradykinin were also analyzed. Prostacyclin decreased capillary permeability by 8% at a dose of 0.1 ng.kg-1.min-1 and at most by 30% below control attained at 2 ng.kg-1.min-1, also with no effect on vascular tone and hydrostatic capillary pressure. The permeability increase by tumor necrosis factor-alpha and histamine (by 54 and 73%) was more than counteracted by the simultaneous infusion of prostacyclin at 2 ng.kg-1.min-1. The vasodilator effect of tumor necrosis factor-alpha was also restituted. Indomethacin (prostacyclin inhibitor)-induced increase in capillary permeability (25%) was more than restituted by prostacyclin at 2 ng.kg-1.min-1. Surprisingly, bradykinin decreased capillary permeability. We conclude that endogenous prostacyclin may be a physiological regulator of capillary permeability and that low-dose prostacyclin infusion may have clinical relevance in states of increased permeability.

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