Rheumatology and Rehabilitation, 1975, 14, 237
THE STIMULATION OF PROTEIN SYNTHESIS IN HUMAN FIBROBLASTS BY THERAPEUTIC ULTRASOUND* BY W. HARVEY 1 , MARY DYSON 2 , J. B. POND 3 AND R. GRAHAME 1 ^Guy's Arthritis Research Unit, !'Anatomy Department, Guy's Hospital Medical School and 3Physics Department, Kingston Polytechnic
there is considerable evidence that therapeutic ultrasound can stimulate tissue repair, little is known of the mechanisms by which this stimulation occurs. Shortly after injury the fibroblast population of damaged tissue increases, and the protein synthesized by these cells forms much of the replacement tissue. Stimulation could result entirely from improvement in the local environment of the fibroblasts, being mediated by other cell types such as blood cells, or direct stimulation of the fibroblasts could also occur. The aim of this investigation was to use tissue techniques to discover if ultrasound could stimulate protein synthesis in fibroblasts directly. ALTHOUGH
RESULTS Treatment of the cells with continuous plane-wave ultrasound at 3 MHz and at intensities of 0.5-2.0 W.cm~2 was followed by a significant increase in protein synthesis compared with the paired controls. No such increase was found in cells which had been pretreated with cortisol. More membrane-associated changes were found in ultrasonically treated cells than in the control groups except where the cells* had been pretreated with cortisol. CONCLUSIONS The results suggest that therapeutic levels of ultrasound can stimulate protein synthesis in fibroblasts directly, without the mediation of other cell types. Membraneassociated changes induced by ultrasound may be involved in the stimulatory mechanism. GENERAL DISCUSSION (ABRIDGED) A suggestion was made that the increase in protein found in the medium might be simply due to cellular 'leakiness' rather than to an increase in synthesis. The presenter felt that this was a perfectly valid concept, but it was certainly not the whole story and there was in addition definite evidence of an increase in protein production. 'Abstract of paper read at the Annual Meeting of the British Association for Rheumatology and Rehabilitation, London, April 1975. A fuller account of this work will be published in the Proceedings of the II European Congress of Ultrasonics held in Munich, May 1975, to be published by Excerpta Medica, Amsterdam. 237
Downloaded from http://rheumatology.oxfordjournals.org/ at Russian Archive on December 30, 2013
METHOD Human fibroblasts were grown as monolayers in isolation from other cell types. After trypsinization, paired cell suspensions were treated simultaneously, one being insonated with therapeutic ultrasound, while the other was mock-insonated. Some cells were first treated with cortisol, a membrane-stabilizing agent. Aliquots of the treated cells were grown for four days in monolayer culture when the rate of protein synthesis was estimated by 3H-proline incorporation. Samples of the cells were also examined by electron microscopy.
THE STIMULATION OF PROTEIN SYNTHESIS IN HUMAN FIBROBLASTS BY THERAPEUTIC ULTRASOUND* BY W. HARVEY 1 , MARY DYSON 2 , J. B. POND 3 AND R. GRAHAME 1 ^Guy's Arthritis Research Unit, !'Anatomy Department, Guy's Hospital Medical School and 3Physics Department, Kingston Polytechnic
there is considerable evidence that therapeutic ultrasound can stimulate tissue repair, little is known of the mechanisms by which this stimulation occurs. Shortly after injury the fibroblast population of damaged tissue increases, and the protein synthesized by these cells forms much of the replacement tissue. Stimulation could result entirely from improvement in the local environment of the fibroblasts, being mediated by other cell types such as blood cells, or direct stimulation of the fibroblasts could also occur. The aim of this investigation was to use tissue techniques to discover if ultrasound could stimulate protein synthesis in fibroblasts directly. ALTHOUGH
RESULTS Treatment of the cells with continuous plane-wave ultrasound at 3 MHz and at intensities of 0.5-2.0 W.cm~2 was followed by a significant increase in protein synthesis compared with the paired controls. No such increase was found in cells which had been pretreated with cortisol. More membrane-associated changes were found in ultrasonically treated cells than in the control groups except where the cells* had been pretreated with cortisol. CONCLUSIONS The results suggest that therapeutic levels of ultrasound can stimulate protein synthesis in fibroblasts directly, without the mediation of other cell types. Membraneassociated changes induced by ultrasound may be involved in the stimulatory mechanism. GENERAL DISCUSSION (ABRIDGED) A suggestion was made that the increase in protein found in the medium might be simply due to cellular 'leakiness' rather than to an increase in synthesis. The presenter felt that this was a perfectly valid concept, but it was certainly not the whole story and there was in addition definite evidence of an increase in protein production. 'Abstract of paper read at the Annual Meeting of the British Association for Rheumatology and Rehabilitation, London, April 1975. A fuller account of this work will be published in the Proceedings of the II European Congress of Ultrasonics held in Munich, May 1975, to be published by Excerpta Medica, Amsterdam. 237
Downloaded from http://rheumatology.oxfordjournals.org/ at Russian Archive on December 30, 2013
METHOD Human fibroblasts were grown as monolayers in isolation from other cell types. After trypsinization, paired cell suspensions were treated simultaneously, one being insonated with therapeutic ultrasound, while the other was mock-insonated. Some cells were first treated with cortisol, a membrane-stabilizing agent. Aliquots of the treated cells were grown for four days in monolayer culture when the rate of protein synthesis was estimated by 3H-proline incorporation. Samples of the cells were also examined by electron microscopy.
