Cargando…

Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology

BACKGROUND: 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 pressure-induced deep tissue injury. METHODS: Adult Sprague Dawley rats were subjected...

Descripción completa

Detalles Bibliográficos
Autores principales: Siu, Parco M, Teng, Bee T, Pei, Xiao M, Tam, Eric W
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058073/
https://www.ncbi.nlm.nih.gov/pubmed/21385343
http://dx.doi.org/10.1186/1471-2474-12-58
_version_ 1782200338134073344
author Siu, Parco M
Teng, Bee T
Pei, Xiao M
Tam, Eric W
author_facet Siu, Parco M
Teng, Bee T
Pei, Xiao M
Tam, Eric W
author_sort Siu, Parco M
collection PubMed
description BACKGROUND: 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 pressure-induced deep tissue injury. METHODS: Adult 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. RESULTS: Our 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. CONCLUSION: Our data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury.
format Text
id pubmed-3058073
institution National Center for Biotechnology Information
language English
publishDate 2011
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-30580732011-03-16 Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology Siu, Parco M Teng, Bee T Pei, Xiao M Tam, Eric W BMC Musculoskelet Disord Research Article BACKGROUND: 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 pressure-induced deep tissue injury. METHODS: Adult 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. RESULTS: Our 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. CONCLUSION: Our data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury. BioMed Central 2011-03-07 /pmc/articles/PMC3058073/ /pubmed/21385343 http://dx.doi.org/10.1186/1471-2474-12-58 Text en Copyright ©2011 Siu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Siu, Parco M
Teng, Bee T
Pei, Xiao M
Tam, Eric W
Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title_full Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title_fullStr Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title_full_unstemmed Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title_short Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
title_sort proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058073/
https://www.ncbi.nlm.nih.gov/pubmed/21385343
http://dx.doi.org/10.1186/1471-2474-12-58
work_keys_str_mv AT siuparcom proteasomeinhibitionalleviatesprolongedmoderatecompressioninducedmusclepathology
AT tengbeet proteasomeinhibitionalleviatesprolongedmoderatecompressioninducedmusclepathology
AT peixiaom proteasomeinhibitionalleviatesprolongedmoderatecompressioninducedmusclepathology
AT tamericw proteasomeinhibitionalleviatesprolongedmoderatecompressioninducedmusclepathology