ArticleNeurobiology of disease2015
Merlin status regulates p75(NTR) expression and apoptotic signaling in Schwann cells following nerve injury.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Unveiling the Proteomic Landscape of Extracellular Vesicles: Implications for Neurodegeneration and Neuroprotection.Journal of neurochemistry · 2026Review
- Reduction of sporadic and neurofibromatosis type 2-associated vestibular schwannoma growth in vitro and in vivo after treatment with the c-Jun N-terminal kinase inhibitor AS602801.Journal of neurosurgery · 2023Article
- Application and underlying mechanism of acupuncture for the nerve repair after peripheral nerve injury: remodeling of nerve system.Frontiers in cellular neuroscience · 2023Review
- Gene replacement therapy in a schwannoma mouse model of neurofibromatosis type 2.Molecular therapy. Methods & clinical development · 2022Article
- The biological underpinnings of radiation therapy for vestibular schwannomas: Review of the literature.Laryngoscope investigative otolaryngology · 2021Review
- Cell Shape and Matrix Stiffness Impact Schwann Cell Plasticity via YAP/TAZ and Rho GTPases.International journal of molecular sciences · 2021Article
- Effects of Neurod1 Expression on Mouse and Human Schwannoma Cells.The Laryngoscope · 2021Article
- Saikosaponin-d impedes hippocampal neurogenesis and causes cognitive deficits by inhibiting the survival of neural stem/progenitor cells via neurotrophin receptor signaling in mice.Clinical and translational medicine · 2020Article
- Proteomics analysis of Schwann cell-derived exosomes: a novel therapeutic strategy for central nervous system injury.Molecular and cellular biochemistry · 2019Article
- Nf2 Mutation in Schwann Cells Delays Functional Neural Recovery Following Injury.Neuroscience · 2018Article
- Photopolymerized Microfeatures Guide Adult Spiral Ganglion and Dorsal Root Ganglion Neurite Growth.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2018Article
- Structural and Ultrastructural Changes to Type I Spiral Ganglion Neurons and Schwann Cells in the Deafened Guinea Pig Cochlea.Journal of the Association for Research in Otolaryngology : JARO · 2017Article
- Review
- STAT3 Controls the Long-Term Survival and Phenotype of Repair Schwann Cells during Nerve Regeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Schwannomas provide insight into the role of p75(NTR) and merlin in Schwann cells following nerve injury and during regeneration.Neural regeneration research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
After nerve injury, Schwann cells (SCs) dedifferentiate, proliferate, and support axon regrowth. If axons fail to regenerate, denervated SCs eventually undergo apoptosis due, in part, to increased expression of the low-affinity neurotrophin receptor, p75(NTR). Merlin is the protein product of the NF2 tumor suppressor gene implicated in SC tumorigenesis. Here we explore the contribution of merlin to SC responses to nerve injury. We find that merlin becomes phosphorylated (growth permissive) in SCs following acute axotomy and following gradual neural degeneration in a deafness model, temporally correlated with increased p75(NTR) expression. p75(NTR) levels are elevated in P0SchΔ39-121 transgenic mice that harbor an Nf2 mutation in SCs relative to wild-type mice before axotomy and remain elevated for a longer period of time following injury. Replacement of wild-type, but not phospho-mimetic (S518D), merlin isoforms suppresses p75(NTR) expression in primary human schwannoma cultures which otherwise lack functional merlin. Despite elevated levels of p75(NTR), SC apoptosis following axotomy is blunted in P0SchΔ39-121 mice relative to wild-type mice suggesting that loss of functional merlin contributes to SC resistance to apoptosis. Further, cultured SCs from mice with a tamoxifen-inducible knock-out of Nf2 confirm that SCs lacking functional merlin are less sensitive to p75(NTR)-mediated cell death. Taken together these results point to a model whereby loss of axonal contact following nerve injury results in merlin phosphorylation leading to increased p75(NTR) expression. Further, they demonstrate that merlin facilitates p75(NTR)-mediated apoptosis in SCs helping to explain how neoplastic SCs that lack functional merlin survive long-term in the absence of axonal contact.
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