Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z

dc.creatorHuang, Jeffrey K.
dc.creatorFerrari, Carina Cintia
dc.creatorMonteiro De Castro, Glaucia
dc.creatorLafont, David
dc.creatorZhao, Chao
dc.creatorZaratin, Paola
dc.creatorPouly, Sandrine
dc.creatorGreco, Beatrice
dc.creatorFranklin, Robin J.M.
dc.date2012-11
dc.date.accessioned2023-08-31T00:32:55Z
dc.date.available2023-08-31T00:32:55Z
dc.identifierhttp://hdl.handle.net/11336/197139
dc.identifierHuang, 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.identifier0002-9440
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8543547
dc.descriptionProtein 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.descriptionFil: Huang, Jeffrey K.. University of Cambridge; Estados Unidos
dc.descriptionFil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Cambridge; Estados Unidos
dc.descriptionFil: Monteiro De Castro, Glaucia. University of Cambridge; Estados Unidos. Universidade Federal de Sao Paulo; Brasil
dc.descriptionFil: Lafont, David. Merck Serono International; Suiza
dc.descriptionFil: Zhao, Chao. University of Cambridge; Estados Unidos
dc.descriptionFil: Zaratin, Paola. Merck Serono International; Suiza
dc.descriptionFil: Pouly, Sandrine. Merck Serono International; Suiza
dc.descriptionFil: Greco, Beatrice. Merck Serono International; Suiza
dc.descriptionFil: Franklin, Robin J.M.. University of Cambridge; Estados Unidos
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherElsevier
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0002944012005767
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2012.07.011
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subjectDEMYELINATION
dc.subjectRPTPZ
dc.subjectAXONAL LOSS
dc.subjectREMYELINATION
dc.subjecthttps://purl.org/becyt/ford/3.1
dc.subjecthttps://purl.org/becyt/ford/3
dc.titleAccelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:ar-repo/semantics/artículo
dc.typeinfo:eu-repo/semantics/publishedVersion


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