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Molecular & Cellular Proteomics 5:1887-1898, 2006.
© 2006 by The American Society for Biochemistry and Molecular Biology, Inc.

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Other Diseases and Conditions

Novel Differential Neuroproteomics Analysis of Traumatic Brain Injury in Rats^*

Firas H. Kobeissy^,,¶,¶¶, Andrew K. Ottens^,,¶,||, Zhiqun Zhang, Ming Cheng Liu, Nancy D. Denslow^**, Jitendra R. Dave, Frank C. Tortella, Ronald L. Hayes^, and Kevin K. W. Wang^,,

From the Center for Neuroproteomics and Biomarkers Research, Department of Psychiatry and Center for Traumatic Brain Injury Studies, Department of Neuroscience, McKnight Brain Institute of the University of Florida and ^** Departments of Physiological Sciences and Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida 32611 and Department of Neuropharmacology and Molecular Biology, Division of Neurosciences, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910

Approximately two million traumatic brain injury (TBI) incidents occur annually in the United States, yet there are no specific therapeutic treatments. The absence of brain injury diagnostic endpoints was identified as a significant roadblock to TBI therapeutic development. To this end, our laboratory has studied mechanisms of cellular injury for biomarker discovery and possible therapeutic strategies. In this study, pooled naïve and injured cortical samples (48 h postinjury; rat controlled cortical impact model) were processed and analyzed using a differential neuroproteomics platform. Protein separation was performed using combined cation/anion exchange chromatography-PAGE. Differential proteins were then trypsinized and analyzed with reversed-phase LC-MSMS for protein identification and quantitative confirmation. The results included 59 differential protein components of which 21 decreased and 38 increased in abundance after TBI. Proteins with decreased abundance included collapsin response mediator protein 2 (CRMP-2), glyceraldehyde-3-phosphate dehydrogenase, microtubule-associated proteins MAP2A/2B, and hexokinase. Conversely C-reactive protein, transferrin, and breakdown products of CRMP-2, synaptotagmin, and II-spectrin were found to be elevated after TBI. Differential changes in the above mentioned proteins were confirmed by quantitative immunoblotting. Results from this work provide insight into mechanisms of traumatic brain injury and yield putative biochemical markers to potentially facilitate patient management by monitoring the severity, progression, and treatment of injury.

^|| To whom correspondence may be addressed: Dept. of Psychiatry, University of Florida, P. O. Box 100256, Gainesville, FL 32610-0256. Tel.: 352-392-8060; Fax: 352-392-2579; E-mail: aottens{at}mbi.ufl.edu

To whom correspondence may be addressed: Dept. of Psychiatry, University of Florida, P. O. Box 100256, Gainesville, FL 32610-0256. Tel.: 352-392-3681; Fax: 352-392-2579; E-mail: kwang{at}psychiatry.ufl.edu

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