Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/74892
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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorUgwu, FN-
dc.creatorYu, AP-
dc.creatorSin, TK-
dc.creatorTam, BT-
dc.creatorLai, CW-
dc.creatorWong, SC-
dc.creatorSiu, PM-
dc.date.accessioned2018-03-29T09:34:08Z-
dc.date.available2018-03-29T09:34:08Z-
dc.identifier.urihttp://hdl.handle.net/10397/74892-
dc.language.isoenen_US
dc.publisherFrontiers Media S.A.en_US
dc.rightsCopyright © 2017 Ugwu, Yu, Sin, Tam, Lai, Wong and Siu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_US
dc.rightsThe following publication Ugwu FN, Yu AP, Sin TK, Tam BT, Lai CW, Wong SC and Siu PM (2017) Protective Effect of Unacylated Ghrelin on Compression-Induced Skeletal Muscle Injury Mediated by SIRT1-Signaling. Front. Physiol. 8:962,1-13 is available at https://dx.doi.org/10.3389/fphys.2017.00962en_US
dc.subjectApoptosisen_US
dc.subjectEX527en_US
dc.subjectNecroptosisen_US
dc.subjectOxidative stressen_US
dc.subjectPressure soresen_US
dc.subjectUnacylated ghrelinen_US
dc.titleProtective effect of unacylated ghrelin on compression-induced skeletal muscle injury mediated by SIRT1-signalingen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1en_US
dc.identifier.epage13en_US
dc.identifier.volume8en_US
dc.identifier.doi10.3389/fphys.2017.00962en_US
dcterms.abstractUnacylated ghrelin, the predominant form of circulating ghrelin, protects myotubes from cell death, which is a known attribute of pressure ulcers. In this study, we investigated whether unacylated ghrelin protects skeletal muscle from pressure-induced deep tissue injury by abolishing necroptosis and apoptosis signaling and whether these effects were mediated by SIRT1 pathway. Fifteen adult Sprague Dawley rats were assigned to receive saline or unacylated ghrelin with or without EX527 (a SIRT1 inhibitor). Animals underwent two 6-h compression cycles with 100 mmHg static pressure applied over the mid-tibialis region of the right limb whereas the left uncompressed limb served as the intra-animal control. Muscle tissues underneath the compression region, and at the similar region of the opposite uncompressed limb, were collected for analysis. Unacylated ghrelin attenuated the compression-induced muscle pathohistological alterations including rounding contour of myofibers, extensive nucleus accumulation in the interstitial space, and increased interstitial space. Unacylated ghrelin abolished the increase in necroptosis proteins including RIP1 and RIP3 and attenuated the elevation of apoptotic proteins including p53, Bax, and AIF in the compressed muscle. Furthermore, unacylated ghrelin opposed the compression-induced phosphorylation and acetylation of p65 subunit of NF-kB. The anti-apoptotic effect of unacylated ghrelin was shown by a decrease in apoptotic DNA fragmentation and terminal dUTP nick-end labeling index in the compressed muscle. The protective effects of unacylated ghrelin vanished when co-treated with EX527. Our findings demonstrated that unacylated ghrelin protected skeletal muscle from compression-induced injury. The myoprotective effects of unacylated ghrelin on pressure-induced tissue injury were associated with SIRT1 signaling.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationFrontiers in physiology, 24 Nov. 2017, v. 8, 962, p. 1-13-
dcterms.isPartOfFrontiers in physiology-
dcterms.issued2017-11-24-
dc.identifier.scopus2-s2.0-85035020040-
dc.identifier.eissn1664-042Xen_US
dc.identifier.artn962en_US
dc.identifier.rosgroupid2017003862-
dc.description.ros2017-2018 > Academic research: refereed > Publication in refereed journalen_US
dc.description.validate201803 bcmaen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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