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dc.contributor.authorSong, Hailongeng
dc.contributor.authorChen, Meieng
dc.contributor.authorChen, Cheneng
dc.contributor.authorCui, Jiankuneng
dc.contributor.authorJohnson, Catherineeng
dc.contributor.authorCheng, Jianlineng
dc.contributor.authorWang, Xiaowaneng
dc.contributor.authorSwerdlow, Russell H.eng
dc.contributor.authorDePalma, Ralpheng
dc.contributor.authorXia, Weimingeng
dc.contributor.authorGu, Zezongeng
dc.contributor.meetingnameHealth Sciences Research Day (2018 : University of Missouri)eng
dc.date.issued2018eng
dc.description.abstractService members during military actions or combat training are frequently exposed to primary blasts by weaponry. Most studies have investigated moderate or severe brain injuries from blasts generating overpressures over 100-kPa, while understanding the pathophysiology of low-intensity blast (LIB)-induced mild traumatic brain injury (mTBI) leading to neurological deficits remains elusive. Our recent studies, using an open-field LIB-induced mTBI mouse model with an peak overpressure at 46.6-kPa, demonstrated behavioral impairments and brain nanoscale damages, notably mitochondrial and axonal ultrastructural changes. In this study, we used tandem mass tagged (TMT) quantitative proteomics and bioinformatics analysis to seek insights into the molecular mechanisms underlying ultrastructural pathology. Changes in global- and phospho-proteomes were determined at 3 and 24 hours, 7 and 30 days post injury (DPI), and to investigate the biochemical and molecular correlates of mitochondrial dysfunction. Results showed striking dynamic changes in a total of 2216 global and 459 phosphorylated proteins at vary time points after blast. Disruption of key canonical pathways included evidence of mitochondrial dysfunction, oxidative stress, axonal/cytoskeletal/synaptic dysregulation, and neurodegeneration. Bioinformatic analysis identified blast induced trends in networks related to cellular growth/development/movement/assembly and cell-to-cell signaling interactions. With observations of proteomic changes, we found LIB-induced oxidative stress associated with mitochondrial dysfunction mainly at 7 and 30 DPI. These dysfunctions included impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated respiration-relevant enzyme activities. Insights on the early pahtogenesis of primary LIB-induced brain damage provide a template for further characterization of its chronic effects, identification of potential biomarkers and targets for intervention.eng
dc.description.statementofresponsibilityHailong song (1), Mei Chen (6), Chen Chen (2), Jiankun Cui (1,7), Catherine Johnson (3), Jianlin Cheng (2), Xiaowan Wang (4), Russell H. Swerdlow (4), Ralph DePalma (5), Weiming Xia (6), Zezong Gu (1,7) ; 1. Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine; 2. Department of Computer Sciences, University of Missouri; 3. Department of Mining and Nuclear Engineering, Missouri University of Science and Technology; 4. Department of Neurology, University of Kansas Medical Center; 5. Office of Research and Development, Department of Veterans Affairs; 6. Bedford VA Medical Center; 7. Truman VA Hospital Research Serviceeng
dc.format.extent1 postereng
dc.identifier.urihttps://hdl.handle.net/10355/66595
dc.languageEnglisheng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Health Sciences Research Dayeng
dc.rightsOpenAccess.eng
dc.rights.licenseThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.eng
dc.titleProteomic analysis and biochemical correlates of mitochondrial dysfunction following low-intensity primary blast exposureeng
dc.typePostereng


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