Abstract
BackgroundThe molecular mechanism initiating deep pressure ulcer remains to be elucidated. The present study tested the hypothesis that the ubiquitin proteasome system is involved in the signalling mechanism in pressure-induced deep tissue injury.MethodsAdult Sprague Dawley rats were subjected to an experimental compression model to induce deep tissue injury. The tibialis region of the right hind limb was subjected to 100 mmHg of static pressure for six hours on each of two consecutive days. The compression pressure was continuously monitored by a three-axial force transducer within the compression indentor. The left hind limb served as the intra-animal control. Muscle tissues underneath the compressed region were collected and used for analyses.ResultsOur results demonstrated that the activity of 20S proteasome and the protein abundance of ubiquitin and MAFbx/atrogin-1 were elevated in conjunction with pathohistological changes in the compressed muscle, as compared to control muscle. The administration of the proteasome inhibitor MG132 was found to be effective in ameliorating the development of pathological histology in compressed muscle. Furthermore, 20S proteasome activity and protein content of ubiquitin and MAFbx/atrogin-1 showed no apparent increase in the MG132-treated muscle following compression.ConclusionOur data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury.
Highlights
The molecular mechanism initiating deep pressure ulcer remains to be elucidated
Compression induced muscle pathohistology and increase in MAFbx/atrogin-1 protein expression Preliminary experiments were conducted in rats which had not been treated with DMSO or MG132 to demonstrate the potential involvement of the ubiquitin proteasome system in compression-induced muscle pathology
The nature of myopathy in pressureinduced deep tissue injury is different from the dystrophindeficiency disorders, the present findings indicated that the inflammationassociated myopathic histology as induced by sustained compression can be alleviated by MG132 treatment
Summary
The molecular mechanism initiating deep pressure ulcer remains to be elucidated. The present study tested the hypothesis that the ubiquitin proteasome system is involved in the signalling mechanism in pressureinduced deep tissue injury. Pressure ulcer represents a considerable clinical problem. A pressure ulcer is defined as localized damage to the skin and the underlying tissues in response to moderate but sustained mechanical compression [2]. Pressure ulcers are generally categorized into superficial or deep pressure ulcers. These are distinctly differentiated based on their developmental processes. A superficial ulcer is confined to the skin layer, and can be diagnosed visually at an early stage. A deep ulcer originates in the underlying tissues overlying
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