ArticleExperimental and therapeutic medicine2013
Protective role of Wallerian degeneration slow (Wld(s)) gene against retinal ganglion cell body damage in a Wallerian degeneration model.
Article in Experimental and therapeutic medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 9 citations in OpenAlex.
- Effects of targeted muscle reinnervation on spinal cord motor neurons in rats following tibial nerve transection.Neural regeneration research · 2022Article
- Emergence of SARM1 as a Potential Therapeutic Target for Wallerian-type Diseases.Cell chemical biology · 2020Review
- Mechanisms of distal axonal degeneration in peripheral neuropathies.Neuroscience letters · 2015Review
- DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury.Neurobiology of disease · 2014Article
- Wallerian degeneration: an emerging axon death pathway linking injury and disease.Nature reviews. Neuroscience · 2014Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve distal axon injury-induced Wallerian degeneration is significantly delayed in Wallerian degeneration slow (Wld(s)) mutant mice, although the associated mechanisms are not completely clear and the role of Wld(s) in retinal ganglion cell (RGC) body damage is not fully understood. In the present study, a Wallerian degeneration model was established in wild-type (WT) and Wld(s) mutant mice by creating mechanical injury in the optic nerves. Wallerian degeneration and RGC body collapse were observed to be significantly delayed in the Wld(s) mice. Electroretinograms (ERG) and visual evoked potentials (VEPs) in Wld(s) mice were also significantly improved at the earlier stages (one week) following injury. The retina immunohistochemistry results showed that Wld(s) mice had more ordered cells and improved inner granular cell layer arrangement compared with the WT mice. Optic nerve Luxol Fast Blue (LFB) staining showed greater axon demyelination in WT mice than in Wld(s) mice. A large number of apoptotic cells were also observed in the WT mice. The present results suggest that the Wld(s) gene may also protect the RGC body following nerve injury.
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