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Next generation sequencing of mRNA in control human schwannoma cells (HEI-193) and human schwannoma cells exposed to electromagnetic field (EMF)

ABSTRACT: Next generation sequencing of mRNA in control human schwannoma cells (HEI-193) and human schwannoma cells exposed to electromagnetic field (EMF)

PROVIDER: PRJNA729717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14521923_1.fastq.gz	Fastqsanger.gz
	SRR14521923_2.fastq.gz	Fastqsanger.gz
	SRR14521925_1.fastq.gz	Fastqsanger.gz
	SRR14521925_2.fastq.gz	Fastqsanger.gz
	SRR14521926_1.fastq.gz	Fastqsanger.gz

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Next generation sequencing of mRNA in control human schwannoma cells (HEI-193) and human schwannoma cells exposed to electromagnetic field (EMF)

Project description:Hearing loss (HL) is the most common sensory disorder in the world population. One common cause of hearing loss is the presence of vestibular schwannoma (VS) a benign tumor of the VIII cranial nerve, arising from Schwann cells (SCs) transformation. In the last decade, an increasing incidence of VSs may be ascribed to the exposure to electromagnetic field (EMF), which may be considered a pathogenic cause of VS development and HL. In this paper, we explore the possible molecular mechanisms underlying the biologic changes of human SCs and/or their oncogenic transformation following EMF exposure. We investigated, by NGS technology RNA-Seq transcriptomic analysis, the genomic profile and the differential display of HL-related genes following chronic EMF. We found that cell proliferation in parallel with intracellular signaling and metabolic pathways, mostly related to translation and mitochondrial activity were modified by chronic EMF exposure. Importantly, the expression of some HL-related genes, such as NEFL, TPRN, OTOGL, GJB2 and REST appeared regulated chronic EMF.

2021-07-28 | GSE174389 | GEO

Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by NF2-restoring or TEW7197 treatment.

Project description:Neurofibromatosis type 2 (NF2) syndrome is a very rare human genetic disease and until now, it’s proper treatment has not been suggested. In our recent study, it has been reported that the loss of NF2 activates MAPK signaling through reduction of RKIP in a mesothelioma model. Here, we show that loss of NF2 induces reduction of the TGF-β receptor 2 (TβR2) expression and an overwhelming expression of TGF-β receptor 1 is activated by physical stimuli such as pressure or heavy materials. Activated TR1 induced the phosphorylation and degradation of RKIP. RKIP reduction consequently results in MAPK activation as well as Snail-mediated p53 suppression and occurrence of EMT in NF2-deficient cells by physical stimuli. Thus, TβR1 kinase inhibitors restore cell differentiation and induce growth suppression in NF2 deficient Schwannoma cell line and MEF. Moreover, TEW7197, a specific TβR1 kinase inhibitor, reduces tumor formation in the NF2-model mouse (Postn-Cre;NF2f/f). Gene expression profiling reveals that TEW7197-treatment induces the expression of lipid metabolism-related gene set such as NF2-restored cells in HEI-193 (NF2-deficient Schwannoma). Our results indicate that reduction or deletion of TβR2 or NF2 induces the TβR1-mediated oncogenic pathway, and therefore inhibition of the unbalanced TGF-β signaling is a putative strategy for NF2-related cancers (NF2 syndrome and mesothelioma) and TβR2 mutated advanced cancers. To know the global effect of TEW7197, we performed the microarray with HEI-193.

2018-06-06 | GSE115359 | GEO

Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by Nf18001 or TEW7197 treatment.

Project description:Loss of NF2 (merlin) has been suggested as a genetic cause of neurofibromatosis type 2 and malignant peripheral nerve sheath tumor (MPNST). Previously, we demonstrated that NF2 sustained TGF- receptor 2 (TR2) expression and reduction or loss of NF2 activated non-canonical TGF- signaling, which reduced RKIP expression via TR1 kinase activity. Here, we show that a selective RKIP inducer (novel chemical, Nf18001) inhibits tumor growth and promotes schwannoma cell differentiation into mature Schwann cells under NF2-deficient conditions. In addition, Nf18001 is not cytotoxic to cells expressing NF2 and is not disturb canonical TGF- signaling. Moreover, the novel chemical induces expression of SOX10, a marker of differentiated Schwann cells, and promotes nuclear export and degradation of SOX2, a stem cell factor. Treatment with Nf18001 inhibited tumor growth in an allograft model with mouse schwannoma cells. These results strongly suggest that selective RKIP inducers could be useful for the treatment of neurofibromatosis type 2 as well as NF2-deficient MPNST. To know the global effect of Nf18001, we performed the microarray with HEI-193.

2021-10-22 | GSE186107 | GEO

Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by Nf18001 or TEW7197 treatment.

Project description:Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by Nf18001 or TEW7197 treatment.

| PRJNA772686 | ENA

Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by NF2-restoring or TEW7197 treatment.

Project description:Gene expression changes in HEI-193 (NF2-deficient Schwannoma) cells by NF2-restoring or TEW7197 treatment.

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Effect of electromagnetic fields on the chondrogenic differentiation under microgravity conditions

Project description:A combination therapy of electromagnetic fields (EMF) and simulated microgravity (SMG) has not been examined in regenerative medicine of cartilage. In the present study, a bioreactor system using extremely low-frequency EMF and SMG was applied during the chondrogenic differentiation of human mesenchymal stem cells (hMSCs). It was hypothesized that a beneficial effect of EMF regarding chondrogenesis (COL2A) could be combined with an avoiding effect of SMG regarding hypertrophy (COLXA1) of cartilage. Pellet cultures of hMSCs formed cartilaginous tissue under the addition of growth factors (FGF; TGF-Î²3). Pure SMG reduced COLXA1 expression but also COL2A expression of hMSCs. Pure EMF showed no gene expression changes of hMSCs during chondrogenic differentiation. Combining EMF/SMG resulted in a re-increase of COL2A but did not reach control levels. The COL2A to COLXA1 ratio of combined EMF/SMG was not significantly different from control levels. The combination therapy of EMF/SMG did not significantly improve the chondrogenic potential of hMSCs. chondrogenic differentiation, electromagnetic stimulation-control, 1 timepoint with/without stimulation

2015-12-31 | E-GEOD-57298 | biostudies-arrayexpress

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray1]

Project description:Electromagnetic fields (EMF) are physical energy generated by electrically charged objects that can influence numerous biologic processes, including control of cell fate and plasticity. In this study, we show that magnetic gold nanoparticles in the presence of EMF can facilitate efficient direct lineage reprogramming to induced dopamine neurons both in vitro and in vivo. Remarkably, electromagnetic stimulation leads to the specific activation of the histone acetyl transferase Brd2, resulting in H3K27 acetylation and robust activation of neuronal-specific gene expression. In vivo reprogramming in conjunction with EMF stimulation efficiently alleviated symptoms in a mouse model of Parkinson’s disease (PD) in a noninvasive and controllable manner. These studies provide a proof of principle that EMF-based approaches may represent a viable and safe therapeutic strategy facilitating in vivo lineage conversion for neurodegenerative disorders.

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray2]

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Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [ChIP-Seq]

2018-04-10 | GSE86049 | GEO

Study of extremely low frequency electromagnetic field (ELF-EMF) responses of human HaCaT keratinocytes: Control vs. ELF-EMF

Project description:Use DNA microarray technology to discover transciprtional insights of HaCaT for continuous exposure to ELF-EMF

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