Axonal cytoskeleton changes in experimental optic neuritis

Zhu, Bing; Moore, George R.; Zwimpfer, Thomas J.; Kastrukoff, Lorne F.; Dyer, Jason K.; Steeves, J. D.; Paty, Donald W.; Cynader, Max S.

doi:10.1016/s0006-8993(99)01191-9

Cited by 38 publications

(23 citation statements)

References 56 publications

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“…Recently, it has become clear that acute axonal damage is a feature of demyelinating pathology in the human CNS in addition to destruction of myelin and oligodendrocytes and delayed axonal damage (Chang et al, 2002;Kuhlmann et al, 2002;Trapp et al, 1998). Further, it has been suggested that some forms of myelin and oligodendrocyte pathology may be preceded by axonal pathology (Grigoriadis et al, 2004;Zhu et al, 1999).…”

Section: Demyelination Ng2mentioning

confidence: 99%

Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse

Nielsen

Ladeby

Drøjdahl

et al. 2006

Glia

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Proliferation of the adult NG2-expressing oligodendrocyte precursor cells has traditionally been viewed as a remyelination response ensuing from destruction of myelin and oligodendrocytes, and not to the axonal pathology that is also a characteristic of demyelinating disease. To better understand the response of the NG2+ cells to the different components of demyelinating pathology, we investigated the response of adult NG2+ cells to axonal degeneration in the absence of primary myelin or oligodendrocyte pathology. Axonal degeneration was induced in the hippocampal dentate gyrus of adult mice by transection of the entorhino-dentate perforant path projection. The acutely induced degeneration of axons and terminals resulted in a prompt response of NG2+ cells, consisting of morphological transformation, cellular proliferation, and upregulation of NG2 expression days 2-3 after surgery. This was followed by a reduction of cellular NG2 expression to subnormal levels from day 5 to 7 and reappearance of normal appearing NG2+ cells from day 10. Mice that had received repeated injections of bromodeoxyuridine from 24 to 72 h after surgery contained significant numbers of bromodeoxyuridine-incorporating oligodendrocytes in the areas with axonal degeneration at day 7. The results suggest that axonal degeneration induces a unique sequence of changes of NG2+ cells and that a subpopulation of the newly generated NG2+ cells differentiate into oligodendrocytes.

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Section: Demyelination Ng2mentioning

confidence: 99%

Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse

Nielsen

Ladeby

Drøjdahl

et al. 2006

Glia

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show abstract

“…They were fresh frozen in liquid nitrogen, and 10-m frozen sections were prepared. Luxol fast blue staining, toluidine blue staining, and immunostaining were performed following the established protocols (30). ED1, OX-42, OX-19, and W3/13 Abs were obtained from Serotec (Oxford, U.K.).…”

Section: Morphological Techniquesmentioning

confidence: 99%

Intrathecal Fas Ligand Infusion Strengthens Immunoprivilege of Central Nervous System and Suppresses Experimental Autoimmune Encephalomyelitis

Zhu

Luo

Chen

et al. 2002

The Journal of Immunology

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Fas ligand (FasL) is an essential molecule strongly expressed in some immunoprivileged sites, but is expressed at very low levels in normal CNS. In this study, acute experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats with guinea pig myelin basic protein. Intrathecal infusion of recombinant FasL before EAE onset dose dependently suppressed acute EAE and alleviated pathological inflammation in lumbosacral spinal cord. This treatment greatly increased apoptosis in CNS inflammatory cells, but did not inhibit systemic immune response to myelin basic protein. Systemic administration of a similar dose of rFasL was ineffective. In vitro, encephalitogenic T cells were highly sensitive to rFasL-induced cell death, and activated macrophages were also susceptible. In addition, in vitro rFasL treatment potentiated the immunosuppressive property of rat cerebrospinal fluid. We conclude that intrathecal infusion of rFasL eliminated the initial wave of infiltrating T cells and macrophages, and therefore blocked the later recruitment of inflammatory cells into CNS. Although Fas receptor expression was observed on spinal cord neurons, astrocytes, and oligodendrocytes, no damage to these cells or to the myelin structure was detected after rFasL infusion.

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“…One such modality is diffusion MRI: there is evidence that axial diffusion is relatively specific to axonal degeneration (Song et al, 2003), while increased radial diffusion is mainly driven by demyelination (Budde et al, 2009;Zhu et al, 1999). The use of advanced tractography methods suggests that a connectional framework may lead to improved sensitivity and specificity to the disease and its related clinical impairment (Ciccarelli et al, 2005;Lin et al, 2005;Dineen et al, 2009).…”

mentioning

confidence: 99%

Classifying minimally disabled multiple sclerosis patients from resting state functional connectivity

et al. 2012

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Axonal cytoskeleton changes in experimental optic neuritis

Cited by 38 publications

References 56 publications

Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse

Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse

Intrathecal Fas Ligand Infusion Strengthens Immunoprivilege of Central Nervous System and Suppresses Experimental Autoimmune Encephalomyelitis

Classifying minimally disabled multiple sclerosis patients from resting state functional connectivity

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Axonal cytoskeleton changes in experimental optic neuritis

Cited by 38 publications

References 56 publications

Axonal degeneration stimulates the formation of NG2+ cells and oligodendrocytes in the mouse

Axonal degeneration stimulates the formation of NG2+ cells and oligodendrocytes in the mouse

Intrathecal Fas Ligand Infusion Strengthens Immunoprivilege of Central Nervous System and Suppresses Experimental Autoimmune Encephalomyelitis

Classifying minimally disabled multiple sclerosis patients from resting state functional connectivity

Contact Info

Product

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Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse

Axonal degeneration stimulates the formation of NG2⁺ cells and oligodendrocytes in the mouse