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dc.contributor.author
Huang, Jeffrey K.
dc.contributor.author
Ferrari, Carina Cintia
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dc.contributor.author
Monteiro De Castro, Glaucia
dc.contributor.author
Lafont, David
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Zhao, Chao
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Zaratin, Paola
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Pouly, Sandrine
dc.contributor.author
Greco, Beatrice
dc.contributor.author
Franklin, Robin J.M.
dc.date.available
2023-05-11T13:07:12Z
dc.date.issued
2012-11
dc.identifier.citation
Huang, Jeffrey K.; Ferrari, Carina Cintia; Monteiro De Castro, Glaucia; Lafont, David; Zhao, Chao; et al.; Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z; Elsevier; American Journal Of Pathology; 181; 5; 11-2012; 1518-1523
dc.identifier.issn
0002-9440
dc.identifier.uri
http://hdl.handle.net/11336/197139
dc.description.abstract
Protein tyrosine phosphatase receptor type Z (Ptprz) is widely expressed in the mammalian central nervous system and has been suggested to regulate oligodendrocyte survival and differentiation. We investigated the role of Ptprz in oligodendrocyte remyelination after acute, toxin-induced demyelination in Ptprz null mice. We found neither obvious impairment in the recruitment of oligodendrocyte precursor cells, astrocytes, or reactive microglia/macrophage to lesions nor a failure for oligodendrocyte precursor cells to differentiate and remyelinate axons at the lesions. However, we observed an unexpected increase in the number of dystrophic axons by 3 days after demyelination, followed by prominent Wallerian degeneration by 21 days in the Ptprz-deficient mice. Moreover, quantitative gait analysis revealed a deficit of locomotor behavior in the mutant mice, suggesting increased vulnerability to axonal injury. We propose that Ptprz is necessary to maintain central nervous system axonal integrity in a demyelinating environment and may be an important target of axonal protection in inflammatory demyelinating diseases, such as multiple sclerosis and periventricular leukomalacia.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
DEMYELINATION
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RPTPZ
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AXONAL LOSS
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REMYELINATION
dc.subject.classification
Neurociencias
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2023-05-10T15:50:52Z
dc.journal.volume
181
dc.journal.number
5
dc.journal.pagination
1518-1523
dc.journal.pais
Países Bajos
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dc.journal.ciudad
Amsterdam
dc.description.fil
Fil: Huang, Jeffrey K.. University of Cambridge; Estados Unidos
dc.description.fil
Fil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Cambridge; Estados Unidos
dc.description.fil
Fil: Monteiro De Castro, Glaucia. University of Cambridge; Estados Unidos. Universidade Federal de Sao Paulo; Brasil
dc.description.fil
Fil: Lafont, David. Merck Serono International; Suiza
dc.description.fil
Fil: Zhao, Chao. University of Cambridge; Estados Unidos
dc.description.fil
Fil: Zaratin, Paola. Merck Serono International; Suiza
dc.description.fil
Fil: Pouly, Sandrine. Merck Serono International; Suiza
dc.description.fil
Fil: Greco, Beatrice. Merck Serono International; Suiza
dc.description.fil
Fil: Franklin, Robin J.M.. University of Cambridge; Estados Unidos
dc.journal.title
American Journal Of Pathology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0002944012005767
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1016/j.ajpath.2012.07.011
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