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Accelerated Axonal Loss Following Acute CNS Demyelination in Mice Lacking Protein Tyrosine Phosphatase Receptor Type Z

Authors :
Sandrine Pouly
Jeffrey K. Huang
Chao Zhao
Beatrice Greco
David Lafont
Glaucia Monteiro de Castro
Robin J.M. Franklin
Carina C. Ferrari
Paola Zaratin
Source :
The American Journal of Pathology. 181:1518-1523
Publication Year :
2012
Publisher :
Elsevier BV, 2012.

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.

Details

ISSN :
00029440
Volume :
181
Database :
OpenAIRE
Journal :
The American Journal of Pathology
Accession number :
edsair.doi.dedup.....91ef9df066cf1efca554fd9b802c8dc4