ArticleGlia2014
p75NTR is highly expressed in vestibular schwannomas and promotes cell survival by activating nuclear transcription factor κB.
Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- 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
- Peripheral nerve defects repaired with autogenous vein grafts filled with platelet-rich plasma and active nerve microtissues and evaluated by novel multimodal ultrasound techniques.Biomaterials research · 2022Article
- A Brief Overview on BDNF-Trk Pathway in the Nervous System: A Potential Biomarker or Possible Target in Treatment of Multiple Sclerosis?Frontiers in neurology · 2022Review
- The biological underpinnings of radiation therapy for vestibular schwannomas: Review of the literature.Laryngoscope investigative otolaryngology · 2021Review
- Neurotrophins as Key Regulators of Cell Metabolism: Implications for Cholesterol Homeostasis.International journal of molecular sciences · 2021Review
- The p75FEBS open bio · 2021Article
- Potential Molecular Biomarkers of Vestibular Schwannoma Growth: Progress and Prospects.Frontiers in oncology · 2021Review
- Effects of Neurod1 Expression on Mouse and Human Schwannoma Cells.The Laryngoscope · 2021Article
- Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration.Acta pharmacologica Sinica · 2020Review
- Thermosensitive heparin-poloxamer hydrogel encapsulated bFGF and NGF to treat spinal cord injury.Journal of cellular and molecular medicine · 2020Article
- A positive feedback loop formed by NGFR and FOXP3 contributes to the resistance of non-small cell lung cancer to icotinib.Translational cancer research · 2020Article
- Article
- Nerve growth factor activates autophagy in Schwann cells to enhance myelin debris clearance and to expedite nerve regeneration.Theranostics · 2020Article
- Mouse Nerve Growth Factor Facilitates the Growth of Interspinal Schwannoma Cells by Activating NGF Receptors.Journal of Korean Neurosurgical Society · 2019Article
- Article
- The p75BMC research notes · 2017Article
- Deletion of the Neurotrophin Receptor p75Journal of diabetes, metabolic disorders & control · 2017Article
- Article
- 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
Vestibular schwannomas (VSs) arise from Schwann cells (SCs) and result from the loss of function of merlin, the protein product of the NF2 tumor suppressor gene. In contrast to non-neoplastic SCs, VS cells survive long-term in the absence of axons. We find that p75(NTR) is overexpressed in VSs compared with normal nerves, both at the transcript and protein level, similar to the response of non-neoplastic SCs following axotomy. Despite elevated p75(NTR) expression, VS cells are resistant to apoptosis due to treatment with proNGF, a high affinity ligand for p75(NTR) . Furthermore, treatment with proNGF protects VS cells from apoptosis due to c-Jun N-terminal kinase (JNK) inhibition indicating that p75(NTR) promotes VS cell survival. Treatment of VS cells with proNGF activated NF-κB while inhibition of JNK with SP600125 or siRNA-mediated knockdown reduced NF-κB activity. Significantly, proNGF also activated NF-κB in cultures treated with JNK inhibitors. Thus, JNK activity appears to be required for basal levels of NF-κB activity but not for proNGF-induced NF-κB activity. To confirm that the increase in NF-κB activity contributes to the prosurvival effect of proNGF, we infected VS cultures with Ad.IκB.SerS32/36A virus, which inhibits NF-κB activation. Compared with control virus, Ad.IκB.SerS32/36A significantly increased apoptosis including in VS cells treated with proNGF. Thus, in contrast to non-neoplastic SCs, p75(NTR) signaling provides a prosurvival response in VS cells by activating NF-κB independent of JNK. Such differences may contribute to the ability of VS cells to survive long-term in the absence of axons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.