Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/5116
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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorSiu, PM-
dc.creatorTeng, BT-
dc.creatorPei, XM-
dc.creatorTam, EWC-
dc.date.accessioned2014-12-11T08:28:03Z-
dc.date.available2014-12-11T08:28:03Z-
dc.identifier.urihttp://hdl.handle.net/10397/5116-
dc.language.isoenen_US
dc.publisherBioMed Centralen_US
dc.rights© 2011 Siu et al; licensee BioMed Central Ltd. 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.en_US
dc.subjectUlcersen_US
dc.subjectMuscles -- diseasesen_US
dc.subjectMedicine, Preventiveen_US
dc.subjectUbiquitinen_US
dc.subjectProteinsen_US
dc.titleProteasome inhibition alleviates prolonged moderate compression-induced muscle pathologyen_US
dc.typeJournal/Magazine Articleen_US
dc.description.otherinformationAuthor name used in this publication: Bee T Tengen_US
dc.description.otherinformationAuthor name used in this publication: Eric W Tamen_US
dc.identifier.spage1-
dc.identifier.epage14-
dc.identifier.volume12-
dc.identifier.issue1-
dc.identifier.doi10.1186/1471-2474-12-58-
dcterms.abstractBackground: 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.-
dcterms.abstractMethods: 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.-
dcterms.abstractResults: 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.-
dcterms.abstractConclusion: Our data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationBMC musculoskeletal disorders, 7 Mar. 2011, v. 12, 58, p. 1-14-
dcterms.isPartOfBMC musculoskeletal disorders-
dcterms.issued2011-03-07-
dc.identifier.isiWOS:000288383400001-
dc.identifier.scopus2-s2.0-79952334660-
dc.identifier.pmid21385343-
dc.identifier.eissn1471-2474-
dc.identifier.rosgroupidr52662-
dc.description.ros2010-2011 > Academic research: refereed > Publication in refereed journal-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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