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

Autores
Huang, Jeffrey K.; Ferrari, Carina Cintia; Monteiro De Castro, Glaucia; Lafont, David; Zhao, Chao; Zaratin, Paola; Pouly, Sandrine; Greco, Beatrice; Franklin, Robin J.M.
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Fil: Huang, Jeffrey K.. University of Cambridge; Estados Unidos
Fil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Cambridge; Estados Unidos
Fil: Monteiro De Castro, Glaucia. University of Cambridge; Estados Unidos. Universidade Federal de Sao Paulo; Brasil
Fil: Lafont, David. Merck Serono International; Suiza
Fil: Zhao, Chao. University of Cambridge; Estados Unidos
Fil: Zaratin, Paola. Merck Serono International; Suiza
Fil: Pouly, Sandrine. Merck Serono International; Suiza
Fil: Greco, Beatrice. Merck Serono International; Suiza
Fil: Franklin, Robin J.M.. University of Cambridge; Estados Unidos
Materia
DEMYELINATION
RPTPZ
AXONAL LOSS
REMYELINATION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/197139
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/197139
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type ZHuang, Jeffrey K.Ferrari, Carina CintiaMonteiro De Castro, GlauciaLafont, DavidZhao, ChaoZaratin, PaolaPouly, SandrineGreco, BeatriceFranklin, Robin J.M.DEMYELINATIONRPTPZAXONAL LOSSREMYELINATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Protein 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.Fil: Huang, Jeffrey K.. University of Cambridge; Estados UnidosFil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Cambridge; Estados UnidosFil: Monteiro De Castro, Glaucia. University of Cambridge; Estados Unidos. Universidade Federal de Sao Paulo; BrasilFil: Lafont, David. Merck Serono International; SuizaFil: Zhao, Chao. University of Cambridge; Estados UnidosFil: Zaratin, Paola. Merck Serono International; SuizaFil: Pouly, Sandrine. Merck Serono International; SuizaFil: Greco, Beatrice. Merck Serono International; SuizaFil: Franklin, Robin J.M.. University of Cambridge; Estados UnidosElsevier2012-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/197139Huang, 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; 1518-15230002-9440CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0002944012005767info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2012.07.011info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:27Zoai:ri.conicet.gov.ar:11336/197139instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:44:27.626CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
title Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
spellingShingle Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
Huang, Jeffrey K.
DEMYELINATION
RPTPZ
AXONAL LOSS
REMYELINATION
title_short Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
title_full Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
title_fullStr Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
title_full_unstemmed Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
title_sort Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z
dc.creator.none.fl_str_mv Huang, Jeffrey K.
Ferrari, Carina Cintia
Monteiro De Castro, Glaucia
Lafont, David
Zhao, Chao
Zaratin, Paola
Pouly, Sandrine
Greco, Beatrice
Franklin, Robin J.M.
author Huang, Jeffrey K.
author_facet Huang, Jeffrey K.
Ferrari, Carina Cintia
Monteiro De Castro, Glaucia
Lafont, David
Zhao, Chao
Zaratin, Paola
Pouly, Sandrine
Greco, Beatrice
Franklin, Robin J.M.
author_role author
author2 Ferrari, Carina Cintia
Monteiro De Castro, Glaucia
Lafont, David
Zhao, Chao
Zaratin, Paola
Pouly, Sandrine
Greco, Beatrice
Franklin, Robin J.M.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv DEMYELINATION
RPTPZ
AXONAL LOSS
REMYELINATION
topic DEMYELINATION
RPTPZ
AXONAL LOSS
REMYELINATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Huang, Jeffrey K.. University of Cambridge; Estados Unidos
Fil: Ferrari, Carina Cintia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Cambridge; Estados Unidos
Fil: Monteiro De Castro, Glaucia. University of Cambridge; Estados Unidos. Universidade Federal de Sao Paulo; Brasil
Fil: Lafont, David. Merck Serono International; Suiza
Fil: Zhao, Chao. University of Cambridge; Estados Unidos
Fil: Zaratin, Paola. Merck Serono International; Suiza
Fil: Pouly, Sandrine. Merck Serono International; Suiza
Fil: Greco, Beatrice. Merck Serono International; Suiza
Fil: Franklin, Robin J.M.. University of Cambridge; Estados Unidos
description 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.
publishDate 2012
dc.date.none.fl_str_mv 2012-11
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/197139
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
0002-9440
CONICET Digital
CONICET
url http://hdl.handle.net/11336/197139
identifier_str_mv 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
0002-9440
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0002944012005767
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2012.07.011
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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