| First Author | Huang JK | Year | 2012 |
| Journal | Am J Pathol | Volume | 181 |
| Issue | 5 | Pages | 1518-23 |
| PubMed ID | 22940073 | Mgi Jnum | J:190023 |
| Mgi Id | MGI:5447859 | Doi | 10.1016/j.ajpath.2012.07.011 |
| Citation | Huang JK, et al. (2012) Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z. Am J Pathol 181(5):1518-23 |
| abstractText | 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. |
