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dc.contributor.authorSwier, Vicki J
dc.contributor.authorWhite, Katherine A
dc.contributor.authorMeyerholz, David K
dc.contributor.authorChefdeville, Aude
dc.contributor.authorKhanna, Rajesh
dc.contributor.authorSieren, Jessica C
dc.contributor.authorQuelle, Dawn E
dc.contributor.authorWeimer, Jill M
dc.date.accessioned2020-11-09T23:50:46Z
dc.date.available2020-11-09T23:50:46Z
dc.date.issued2020-02-19
dc.identifier.citationSwier, V. J., White, K. A., Meyerholz, D. K., Chefdeville, A., Khanna, R., Sieren, J. C., ... & Weimer, J. M. (2020). Validating indicators of CNS disorders in a swine model of neurological disease. PloS one, 15(2), e0228222.en_US
dc.identifier.issn1932-6203
dc.identifier.pmid32074109
dc.identifier.doi10.1371/journal.pone.0228222
dc.identifier.urihttp://hdl.handle.net/10150/648181
dc.description.abstractGenetically modified swine disease models are becoming increasingly important for studying molecular, physiological and pathological characteristics of human disorders. Given the limited history of these model systems, there remains a great need for proven molecular reagents in swine tissue. Here, to provide a resource for neurological models of disease, we validated antibodies by immunohistochemistry for use in examining central nervous system (CNS) markers in a recently developed miniswine model of neurofibromatosis type 1 (NF1). NF1 is an autosomal dominant tumor predisposition disorder stemming from mutations in NF1, a gene that encodes the Ras-GTPase activating protein neurofibromin. Patients classically present with benign neurofibromas throughout their bodies and can also present with neurological associated symptoms such as chronic pain, cognitive impairment, and behavioral abnormalities. As validated antibodies for immunohistochemistry applications are particularly difficult to find for swine models of neurological disease, we present immunostaining validation of antibodies implicated in glial inflammation (CD68), oligodendrocyte development (NG2, O4 and Olig2), and neuron differentiation and neurotransmission (doublecortin, GAD67, and tyrosine hydroxylase) by examining cellular localization and brain region specificity. Additionally, we confirm the utility of anti-GFAP, anti-Iba1, and anti-MBP antibodies, previously validated in swine, by testing their immunoreactivity across multiple brain regions in mutant NF1 samples. These immunostaining protocols for CNS markers provide a useful resource to the scientific community, furthering the utility of genetically modified miniswine for translational and clinical applications.en_US
dc.language.isoenen_US
dc.publisherPUBLIC LIBRARY SCIENCEen_US
dc.rights© 2020 Swier et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleValidating indicators of CNS disorders in a swine model of neurological diseaseen_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Coll Med, Dept Pharmacolen_US
dc.contributor.departmentUniv Arizona, Coll Med, Grad Interdisciplinary Program Neuroscien_US
dc.identifier.journalPLOS ONEen_US
dc.description.noteOpen access journalen_US
dc.description.collectioninformationThis 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.en_US
dc.eprint.versionFinal published versionen_US
dc.source.journaltitlePloS one
dc.source.volume15
dc.source.issue2
dc.source.beginpagee0228222
dc.source.endpage
refterms.dateFOA2020-11-09T23:50:47Z
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States


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© 2020 Swier et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.
Except where otherwise noted, this item's license is described as © 2020 Swier et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.