ArticleThe American journal of pathology2012
Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Clemastine Induces Oligodendrocyte Progenitor Pool Exhaustion and Senescence in the Context of Chronic Demyelination in a Rabbit Model.Annals of neurology · 2024Article
- Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish.American journal of physiology. Heart and circulatory physiology · 2022Article
- Harnessing the Benefits of Neuroinflammation: Generation of Macrophages/Microglia with Prominent Remyelinating Properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Role of RPTPβ/ζ in neuroinflammation and microglia-neuron communication.Scientific reports · 2020Article
- Aging-Exacerbated Acute Axon and Myelin Injury Is Associated with Microglia-Derived Reactive Oxygen Species and Is Alleviated by the Generic Medication Indapamide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Cell Densities in the Mouse Brain: A Systematic Review.Frontiers in neuroanatomy · 2018Article
- Neuronal expression of pathological tau accelerates oligodendrocyte progenitor cell differentiation.Glia · 2016Article
- 1,25-Dihydroxyvitamin D3 enhances neural stem cell proliferation and oligodendrocyte differentiation.Experimental and molecular pathology · 2015Article
- Cerebrospinal fluid ceramides from patients with multiple sclerosis impair neuronal bioenergetics.Brain : a journal of neurology · 2014Article
- Astrogliosis during acute and chronic cuprizone demyelination and implications for remyelination.ASN neuro · 2012Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
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.
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Registered trials
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