Neuroprotection against traumatic brain injury by a peptide derived from the collapsin response mediator protein 2 (CRMP2)

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dc.contributor.authorBrittain, Joel M.
dc.contributor.authorChen, Liang
dc.contributor.authorWilson, Sarah M.
dc.contributor.authorBrustovetsky, Tatiana
dc.contributor.authorGao, Xiang
dc.contributor.authorAshpole, Nicole M.
dc.contributor.authorMolosh, Andrei I.
dc.contributor.authorYou, Haitao
dc.contributor.authorHudmon, Andy
dc.contributor.authorShekhar, Anantha S.
dc.contributor.authorWhite, Fletcher A.
dc.contributor.authorZamponi, Gerald W.
dc.contributor.authorBrustovetsky, Nickolay N.
dc.contributor.authorChen, Jinhui
dc.contributor.authorKhanna, Rajesh
dc.date.accessioned2018-06-06T15:07:06Z
dc.date.available2018-06-06T15:07:06Z
dc.date.issued2011-08-09
dc.description.abstractNeurological disabilities following traumatic brain injury (TBI) may be due to excitotoxic neuronal loss. The excitotoxic loss of neurons following TBI occurs largely due to hyperactivation of N-methyl-d-aspartate receptors (NMDARs), leading to toxic levels of intracellular Ca(2+). The axon guidance and outgrowth protein collapsin response mediator protein 2 (CRMP2) has been linked to NMDAR trafficking and may be involved in neuronal survival following excitotoxicity. Lentivirus-mediated CRMP2 knockdown or treatment with a CRMP2 peptide fused to HIV TAT protein (TAT-CBD3) blocked neuronal death following glutamate exposure probably via blunting toxicity from delayed calcium deregulation. Application of TAT-CBD3 attenuated postsynaptic NMDAR-mediated currents in cortical slices. In exploring modulation of NMDARs by TAT-CBD3, we found that TAT-CBD3 induced NR2B internalization in dendritic spines without altering somal NR2B surface expression. Furthermore, TAT-CBD3 reduced NMDA-mediated Ca(2+) influx and currents in cultured neurons. Systemic administration of TAT-CBD3 following a controlled cortical impact model of TBI decreased hippocampal neuronal death. These findings support TAT-CBD3 as a novel neuroprotective agent that may increase neuronal survival following injury by reducing surface expression of dendritic NR2B receptors.en_US
dc.identifier.citationBrittain, J. M., Chen, L., Wilson, S. M., Brustovetsky, T., Gao, X., Ashpole, N. M., … Khanna, R. (2011). Neuroprotection against traumatic brain Injury by a peptide derived from the Collapsin Response Mediator Protein 2 (CRMP2). Journal of Biological Chemistry, 286(43), 37778–37792. https://doi.org/10.1074/jbc.M111.255455en_US
dc.identifier.doihttp://dx.doi.org/10.1074/jbc.M111.255455en_US
dc.identifier.urihttp://hdl.handle.net/1880/106723
dc.identifier.urihttps://doi.org/10.11575/PRISM/43823
dc.language.isoenen_US
dc.publisherThe American Society for Biochemistry and Molecular Biology, Inc.en_US
dc.publisher.departmentPhysiology & Pharmacologyen_US
dc.publisher.facultyCumming School of Medicineen_US
dc.publisher.institutionUniversity of Calgaryen_US
dc.publisher.policyhttp://www.jbc.org/site/misc/edpolicy.xhtml#pipen_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.titleNeuroprotection against traumatic brain injury by a peptide derived from the collapsin response mediator protein 2 (CRMP2)en_US
dc.typejournal articleen_US
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