Primary Culture of Human Vestibular Schwannomas

Schularick, Nathan M.; Clark, J. Jason; Hansen, Marlan R.

doi:10.3791/51093

Cited by 11 publications

(5 citation statements)

References 17 publications

(25 reference statements)

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“…Primary human VS cultures: Human VS tumors were collected for primary cell culture as previously described. [33][34][35] After VS cells were cultured without passaging for 10 days, adenovirus (Ad) CMVempty vector (EV) at 5 × 10 9 pfu/mL, AdCMVNeuro D1 at 2 × 10 9 pfu/mL, or AdCMVNeuroD1 at 5 × 10 9 pfu/mL (ViraQuest, Inc. Coralville, IA) were applied to the culture medium for 72 hours as before. 34,36,37 Edu staining was performed using Click-it EdU Alexa Fluor 633 Image Kit (Fisher Scientifc C10340, Carlsbad, CA) as before.…”

Section: Methodsmentioning

confidence: 99%

Effects of Neurod1 Expression on Mouse and Human Schwannoma Cells

Kersigo¹,

Gu²,

Xu³

et al. 2020

The Laryngoscope

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Objectives The objective was to explore the effect of the proneuronal transcription factor neurogenic differentiation 1 (Neurod1, ND1) on Schwann cells (SC) and schwannoma cell proliferation. Methods Using a variety of transgenic mouse lines, we investigated how expression of Neurod1 effects medulloblastoma (MB) growth, schwannoma tumor progression, vestibular function, and SC cell proliferation. Primary human vestibular schwannoma (VS) cell cultures were transduced with adenoviral vectors expressing Neurod1. Cell proliferation was assessed by 5‐ethynyl‐2'‐deoxyuridine (EdU) uptake. Study Design Basic science investigation. Results Expression of Neurod1 reduced the growth of slow‐growing but not fast‐growing MB models. Gene transfer of Neurod1 in human schwannoma cultures significantly reduced cell proliferation in dose‐dependent way. Deletion of the neurofibromatosis type 2 (Nf2) tumor‐suppressor gene via Cre expression in SCs led to increased intraganglionic SC proliferation and mildly reduced vestibular sensory‐evoked potentials (VsEP) responses compared to age‐matched wild‐type littermates. The effect of Neurod1‐induced expression on intraganglionic SC proliferation in animals lacking Nf2 was mild and highly variable. Sciatic nerve axotomy significantly increased SC proliferation in wild‐type and Nf2‐null animals, and expression of Neurod1 reduced the proliferative capacity of both wild‐type and Nf2‐null SCs following nerve injury. Conclusion Expression of Neurod1 reduces slow‐growing MB progression and reduces human SC proliferation in primary VS cultures. In a genetic mouse model of schwannomas, we find some effects of Neurod1 expression; however, the high variability indicates that more tightly regulated Neurod1 expression levels that mimic our in vitro data are needed to fully validate Neurod1 effects on schwannoma progression. Level of Evidence NA Laryngoscope, 131:E259–E270, 2021

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Section: Methodsmentioning

confidence: 99%

Effects of Neurod1 Expression on Mouse and Human Schwannoma Cells

Kersigo¹,

Gu²,

Xu³

et al. 2020

The Laryngoscope

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“…The reliability of our NF2 defective cellular model was supported by the HEI-193 phenotype, which is in accordance with the cell characteristics already published by Hung et al [ 15 , 16 ]. Indeed, these cells are a good paradigm of SCs phenotype, bearing the characteristic spindle-shaped morphology and expression of known SC markers [ 21 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Profile Reveals Deregulation of Hearing-Loss Related Genes in Vestibular Schwannoma Cells Following Electromagnetic Field Exposure

Colciago

Audano

Bonalume

et al. 2021

Cells

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Hearing loss (HL) is the most common sensory disorder in the world population. One common cause of HL is the presence of vestibular schwannoma (VS), a benign tumor of the VIII cranial nerve, arising from Schwann cell (SC) transformation. In the last decade, the increasing incidence of VS has been correlated to electromagnetic field (EMF) exposure, which might be considered a pathogenic cause of VS development and HL. Here, we explore the molecular mechanisms underlying the biologic changes of human SCs and/or their oncogenic transformation following EMF exposure. Through NGS technology and RNA-Seq transcriptomic analysis, we investigated the genomic profile and the differential display of HL-related genes after chronic EMF. We found that chronic EMF exposure modified the cell proliferation, in parallel with intracellular signaling and metabolic pathways changes, mostly related to translation and mitochondrial activities. Importantly, the expression of HL-related genes such as NEFL, TPRN, OTOGL, GJB2, and REST appeared to be deregulated in chronic EMF exposure. In conclusion, we suggest that, at a preclinical stage, EMF exposure might promote the transformation of VS cells and contribute to HL.

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“…While the prolific evaluation of clinical outcomes following IR for VSs continues, there is a paucity of research on the radiobiology of VSs. This is likely due, at least in part, to the low numbers of tumors that have been resected following IR and the challenges of growing large numbers of primary VS cells in culture (17,18). Here we had a unique opportunity to analyze IR-induced cellular damage in a series of four paired VS specimens that progressed or recurred after microsurgical excision, were treated with IR, progressed again and ultimately required salvage re-resection.…”

Section: Discussionmentioning

confidence: 99%