• Login
    View Item 
    •   Home
    • UA Faculty Research
    • UA Faculty Publications
    • View Item
    •   Home
    • UA Faculty Research
    • UA Faculty Publications
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of UA Campus RepositoryCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournalThis CollectionTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournal

    My Account

    LoginRegister

    About

    AboutUA Faculty PublicationsUA DissertationsUA Master's ThesesUA Honors ThesesUA PressUA YearbooksUA CatalogsUA Libraries

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Neuronal Conditional Knockout of Collapsin Response Mediator Protein 2 Ameliorates Disease Severity in a Mouse Model of Multiple Sclerosis

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    1759091419892090.pdf
    Size:
    1.828Mb
    Format:
    PDF
    Description:
    Final Published Version
    Download
    Author
    Moutal, Aubin
    Kalinin, Sergey
    Kowal, Kathy
    Marangoni, Natalia
    Dupree, Jeffrey
    Lin, Shao Xia
    Lis, Kinga
    Lisi, Lucia
    Hensley, Kenneth
    Khanna, Rajesh
    Feinstein, Douglas L
    Show allShow less
    Affiliation
    Univ Arizona
    Issue Date
    2019-12-03
    Keywords
    CRMP2
    EAE
    LKE
    multiple sclerosis
    spinal cord
    upper motor neurons
    
    Metadata
    Show full item record
    Publisher
    SAGE PUBLICATIONS LTD
    Citation
    Moutal, A., Kalinin, S., Kowal, K., Marangoni, N., Dupree, J., Lin, S. X., … Feinstein, D. L. (2019). Neuronal Conditional Knockout of Collapsin Response Mediator Protein 2 Ameliorates Disease Severity in a Mouse Model of Multiple Sclerosis. ASN Neuro, 11, 175909141989209. https://doi.org/10.1177/1759091419892090 ‌
    Journal
    ASN NEURO
    Rights
    Copyright © The Author(s) 2019. Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons AttributionNonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/enus/nam/open-access-at-sage).
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    We previously showed that treatment with lanthionine ketimine ethyl ester (LKE) reduced disease severity and axonal damage in an experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis and increased neuronal maturation and survival in vitro. A major target of LKE is collapsin response mediator protein 2 (CRMP2), suggesting this protein may mediate LKE actions. We now show that conditional knockout of CRMP2 from neurons using a CamK2a promoter to drive Cre recombinase expression reduces disease severity in the myelin oligodendrocyte glycoprotein (MOG)35–55 EAE model, associated with decreased spinal cord axonal damage, and less glial activation in the cerebellum, but not the spinal cord. Immunohistochemical staining and quantitative polymerase chain reaction show CRMP2 depletion from descending motor neurons in the motor cortex, but not from spinal cord neurons, suggesting that the benefits of CRMP2 depletion on EAE may stem from effects on upper motor neurons. In addition, mice in which CRMP2 S522 phosphorylation was prevented by substitution for an alanine residue also showed reduced EAE severity. These results show that modification of CRMP2 expression and phosphorylation can influence the course of EAE and suggests that treatment with CRMP2 modulators such as LKE act in part by reducing CRMP2 S522 phosphorylation.
    Note
    Open access journal
    ISSN
    1759-0914
    PubMed ID
    31795726
    DOI
    10.1177/1759091419892090
    Version
    Final published version
    Sponsors
    National Multiple Sclerosis Society [RG-1501-02654]; US Department of Veteran Affairs [14S-RCS-003]; United States Department of Health & Human Services National Institutes of Health (NIH) - USA [1R01NS098772, 1R01DA042852]
    ae974a485f413a2113503eed53cd6c53
    10.1177/1759091419892090
    Scopus Count
    Collections
    UA Faculty Publications

    entitlement

    Related articles

    • Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation.
    • Authors: Petratos S, Ozturk E, Azari MF, Kenny R, Lee JY, Magee KA, Harvey AR, McDonald C, Taghian K, Moussa L, Mun Aui P, Siatskas C, Litwak S, Fehlings MG, Strittmatter SM, Bernard CC
    • Issue date: 2012 Jun
    • Astrogliosis in EAE spinal cord: derivation from radial glia, and relationships to oligodendroglia.
    • Authors: Bannerman P, Hahn A, Soulika A, Gallo V, Pleasure D
    • Issue date: 2007 Jan 1
    • Lanthionine ketimine ester provides benefit in a mouse model of multiple sclerosis.
    • Authors: Dupree JL, Polak PE, Hensley K, Pelligrino D, Feinstein DL
    • Issue date: 2015 Jul
    • MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.
    • Authors: Mao P, Manczak M, Shirendeb UP, Reddy PH
    • Issue date: 2013 Dec
    • Changes in spinal cord stiffness in the course of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis.
    • Authors: Pyka-Fościak G, Zemła J, Lis GJ, Litwin JA, Lekka M
    • Issue date: 2020 Feb 15
    The University of Arizona Libraries | 1510 E. University Blvd. | Tucson, AZ 85721-0055
    Tel 520-621-6442 | repository@u.library.arizona.edu
    DSpace software copyright © 2002-2017  DuraSpace
    Quick Guide | Contact Us | Send Feedback
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.