NI-35/250/nogo-a: A neurite growth inhibitor restricting structural plasticity and regeneration of nerve fibers in the adult vertebrate CNS

Bandtlow, Christine E.; Schwab, Martin E.

doi:10.1002/(sici)1098-1136(20000115)29:2<175::aid-glia11>3.0.co;2-f

Cited by 113 publications

(51 citation statements)

References 63 publications

(78 reference statements)

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“…Even though progenitor proliferation occurs in the periinfarct region, however, it remains purely speculative at present that these cells have the capacity to myelinate any newly formed axons. Indeed, the presence of myelinating oligodendrocytes may hinder rather than promote tissue reorganization essential for recovery of function, since regeneration and structural plasticity in the adult brain are inhibited by myelin-associated neurite growth inhibitors (Bandtlow and Schwab, 2000). The effect of oligodendrocyte proliferation on periinfarct recovery remains unknown.…”

Section: Oligodendrocytes and Recovery After Ischemiamentioning

confidence: 99%

Oligodendrocytes and Ischemic Brain Injury

Dewar

Underhill

Goldberg

2003

J Cereb Blood Flow Metab

262

129

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Summary:Oligodendrocytes, myelin-forming glial cells of the central nervous system, are vulnerable to damage in a variety of neurologic diseases. Much is known of primary myelin injury, which occurs in settings of genetic dysmyelination or demyelinating disease. There is growing awareness that oligodendrocytes are also targets of injury in acute ischemia. Recognition of oligodendrocyte damage in animal models of ischemia requires attention to their distinct histologic features or use of specific immunocytochemical markers. Like neurons, oligodendrocytes are highly sensitive to injury by oxidative stress, excitatory amino acids, trophic factor deprivation, and activation of apoptotic pathways. Understanding mechanisms of oligodendrocyte death may suggest new therapeutic strategies to preserve or restore white matter function and structure after ischemic insults.

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Section: Oligodendrocytes and Recovery After Ischemiamentioning

confidence: 99%

Oligodendrocytes and Ischemic Brain Injury

Dewar

Underhill

Goldberg

2003

J Cereb Blood Flow Metab

262

129

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“…Myelin proteins that inhibit axonal regeneration include Nogo (Caroni and Schwab, 1988;Schwab, 1990, 1993;Bandtlow and Schwab, 2000), myelin-associated glycoprotein (MAG) (McKerracher et al, 1994;Mukhopadhyay et al, 1994;DeBellard et al, 1996;Schafer et al, 1996), and oligodendrocyte-myelin glycoprotein (OMgp) (Wang et al, 2002b). Each of these proteins appears to inhibit regeneration by the same mechanism.…”

Section: Introductionmentioning

confidence: 99%

Axonal Regeneration and Lack of Astrocytic Gliosis in EphA4-Deficient Mice

et al. 2004

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Spinal cord injury usually results in permanent paralysis because of lack of regrowth of damaged neurons. Here we demonstrate that adult mice lacking EphA4 (Ϫ/Ϫ), a molecule essential for correct guidance of spinal cord axons during development, exhibit axonal regeneration and functional recovery after spinal cord hemisection. Anterograde and retrograde tracing showed that axons from multiple pathways, including corticospinal and rubrospinal tracts, crossed the lesion site. EphA4Ϫ/Ϫ mice recovered stride length, the ability to walk on and climb a grid, and the ability to grasp with the affected hindpaw within 1-3 months of injury. EphA4 expression was upregulated on astrocytes at the lesion site in wild-type mice, whereas astrocytic gliosis and the glial scar were greatly reduced in lesioned EphA4Ϫ/Ϫ spinal cords. EphA4Ϫ/Ϫ astrocytes failed to respond to the inflammatory cytokines, interferon-␥ or leukemia inhibitory factor, in vitro. Neurons grown on wild-type astrocytes extended shorter neurites than on EphA4Ϫ/Ϫ astrocytes, but longer neurites when the astrocyte EphA4 was blocked by monomeric EphrinA5-Fc. Thus, EphA4 regulates two important features of spinal cord injury, axonal inhibition, and astrocytic gliosis.

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“…Neurite outgrowth inhibitor, also known as Reticulon-4, is a protein that in humans is encoded by the RTN4 gene that has been identified as an inhibitor of neurite outgrowth specific to the central nervous system and obtained the name as "Nogo" [2,3] . Using either alternate splicing or different promoter region there are three isoforms of Nogo produced from RTN4 gene (Figure 1) [4][5][6] . The distribution of the three Nogo isoforms is different.…”

Section: Reticulonsmentioning

confidence: 99%