dc.contributor.author | Constantinou, Constantina | en |
dc.contributor.author | Apidianakis, Yiorgos | en |
dc.contributor.author | Psychogios, N. | en |
dc.contributor.author | Righi, V. | en |
dc.contributor.author | Mindrinos, M. N. | en |
dc.contributor.author | Khan, N. | en |
dc.contributor.author | Swartz, H. M. | en |
dc.contributor.author | Szeto, H. H. | en |
dc.contributor.author | Tompkins, R. G. | en |
dc.contributor.author | Rahme, L. G. | en |
dc.contributor.author | Aria Tzika, A. | en |
dc.creator | Constantinou, Constantina | en |
dc.creator | Apidianakis, Yiorgos | en |
dc.creator | Psychogios, N. | en |
dc.creator | Righi, V. | en |
dc.creator | Mindrinos, M. N. | en |
dc.creator | Khan, N. | en |
dc.creator | Swartz, H. M. | en |
dc.creator | Szeto, H. H. | en |
dc.creator | Tompkins, R. G. | en |
dc.creator | Rahme, L. G. | en |
dc.creator | Aria Tzika, A. | en |
dc.date.accessioned | 2019-11-04T12:50:24Z | |
dc.date.available | 2019-11-04T12:50:24Z | |
dc.date.issued | 2016 | |
dc.identifier.issn | 1107-3756 | |
dc.identifier.uri | http://gnosis.library.ucy.ac.cy/handle/7/53008 | |
dc.description.abstract | Trauma is the most common cause of mortality among individuals aged between 1 and 44 years and the third leading cause of mortality overall in the US. In this study, we examined the effects of trauma on the expression of genes in Drosophila melanogaster, a useful model for investigating genetics and physiology. After trauma was induced by a non-lethal needle puncture of the thorax, we observed the differential expression of genes encoding for mitochondrial uncoupling proteins, as well as those encoding for apoptosis-related and insulin signaling-related proteins, thus indicating muscle functional dysregulation. These results prompted us to examine the link between insulin signaling and mitochondrial dysfunction using in vivo nuclear magnetic resonance (NMR) with complementary electron paramagnetic resonance (EPR) spectroscopy. Trauma significantly increased insulin resistance biomarkers, and the NMR spectral profile of the aged flies with trauma-induced thoracic injury resembled that of insulin-resistant chico mutant flies. In addition, the mitochondrial redox status, as measured by EPR, was significantly altered following trauma, indicating mitochondrial uncoupling. A mitochondria-targeted compound, Szeto-Schiller (SS)-31 that promotes adenosine triphosphate (ATP) synthesis normalized the NMR spectral profile, as well as the mitochondrial redox status of the flies with trauma-induced thoracic injury, as assessed by EPR. Based on these findings, we propose a molecular mechanism responsible for trauma-related mortality and also propose that trauma sequelae in aging are linked to insulin signaling and mitochondrial dysfunction. Our findings further suggest that SS-31 attenuates trauma-associated pathological changes. | en |
dc.source | International journal of molecular medicine | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84954544853&doi=10.3892%2fijmm.2015.2426&partnerID=40&md5=601cc482f56420ee8ffef14462d1faf0 | |
dc.subject | human | en |
dc.subject | Humans | en |
dc.subject | aged | en |
dc.subject | controlled study | en |
dc.subject | priority journal | en |
dc.subject | Aging | en |
dc.subject | male | en |
dc.subject | unclassified drug | en |
dc.subject | complication | en |
dc.subject | nonhuman | en |
dc.subject | pathology | en |
dc.subject | signal transduction | en |
dc.subject | upregulation | en |
dc.subject | Article | en |
dc.subject | metabolism | en |
dc.subject | biological marker | en |
dc.subject | gene expression | en |
dc.subject | apoptosis | en |
dc.subject | Animals | en |
dc.subject | animal | en |
dc.subject | animal experiment | en |
dc.subject | animal model | en |
dc.subject | biosynthesis | en |
dc.subject | disease model | en |
dc.subject | genetics | en |
dc.subject | injury | en |
dc.subject | image analysis | en |
dc.subject | Oligopeptides | en |
dc.subject | Biomarkers | en |
dc.subject | Wounds and Injuries | en |
dc.subject | thorax injury | en |
dc.subject | medical school | en |
dc.subject | Magnetic Resonance Spectroscopy | en |
dc.subject | nuclear magnetic resonance spectroscopy | en |
dc.subject | electron spin resonance | en |
dc.subject | Electron paramagnetic resonance | en |
dc.subject | Nuclear magnetic resonance | en |
dc.subject | in vivo study | en |
dc.subject | Drosophila melanogaster | en |
dc.subject | Disease Models, Animal | en |
dc.subject | insulin receptor | en |
dc.subject | Ion Channels | en |
dc.subject | adenosine triphosphate | en |
dc.subject | apoptosis inducing factor | en |
dc.subject | arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide | en |
dc.subject | Drosophila forkhead box O protein | en |
dc.subject | Drosophila phosphatase and tensin homolog protein | en |
dc.subject | Electron Spin Resonance Spectroscopy | en |
dc.subject | enzyme synthesis | en |
dc.subject | genome analysis | en |
dc.subject | High-resolution magic angle spinning | en |
dc.subject | insulin resistance | en |
dc.subject | Insulin signaling | en |
dc.subject | ion channel | en |
dc.subject | Mitochondria | en |
dc.subject | mitochondrial protein | en |
dc.subject | Mitochondrial Proteins | en |
dc.subject | mitochondrial uncoupling protein 4 | en |
dc.subject | mitochondrion | en |
dc.subject | oligopeptide | en |
dc.subject | oxidative phosphorylation uncoupling | en |
dc.subject | Thoracic Injuries | en |
dc.subject | uncoupling protein 1 | en |
dc.title | In vivo high-resolution magic angle spinning magnetic and electron paramagnetic resonance spectroscopic analysis of mitochondria-targeted peptide in Drosophila melanogaster with trauma-induced thoracic injury | en |
dc.type | info:eu-repo/semantics/article | |
dc.identifier.doi | 10.3892/ijmm.2015.2426 | |
dc.description.volume | 37 | |
dc.description.startingpage | 299 | |
dc.description.endingpage | 308 | |
dc.author.faculty | Σχολή Θετικών και Εφαρμοσμένων Επιστημών / Faculty of Pure and Applied Sciences | |
dc.author.department | Τμήμα Βιολογικών Επιστημών / Department of Biological Sciences | |
dc.type.uhtype | Article | en |
dc.source.abbreviation | Int.J.Mol.Med. | en |
dc.contributor.orcid | Apidianakis, Yiorgos [0000-0002-7465-3560] | |
dc.gnosis.orcid | 0000-0002-7465-3560 | |