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Modeling chemotherapy induced neurotoxicity with human induced pluripotent stem cell (iPSC) -derived sensory neurons - RNA-Seq data on transcriptional changes induced by 1µM paclitaxel treatment for 24h

ABSTRACT: Modeling chemotherapy induced neurotoxicity with human induced pluripotent stem cell (iPSC) -derived sensory neurons - RNA-Seq data on transcriptional changes induced by 1µM paclitaxel treatment for 24h

PROVIDER: PRJNA726261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14363054_1.fastq.gz	Fastqsanger.gz
	SRR14363054_2.fastq.gz	Fastqsanger.gz
	SRR14363055_1.fastq.gz	Fastqsanger.gz
	SRR14363055_2.fastq.gz	Fastqsanger.gz
	SRR14363056_1.fastq.gz	Fastqsanger.gz

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Modeling chemotherapy induced neurotoxicity with human induced pluripotent stem cell (iPSC) -derived sensory neurons - RNA-Seq data on transcriptional changes induced by 1µM paclitaxel treatment for 24h

Project description:We report data on transcriptome sequencing analyses of functional iPSC-DSN (maturation >d40) treated with 1 µM paclitaxel for 24h compared to DMSO treatment. RNA-Sequencing analyses revealed 319 significantly differentially (padjusted <0.01) expressed genes out of which 227 were upregulated and 92 downregulated. 84 of the upregulated and 33 of the downregulated changed expression by at least 2 fold. Upregulated genes involve known neuronal injury markers such as the Activation Transcription Factor (ATF3), stress-inducible proteins such as Sestrin-2 (SESN2), apoptosis associated genes such as Caspase 3 (CASP3), the JUN proto-oncogene (JUN) or BCL2-interacting proteins such as BBC3 or Harakiri (HRK). Also, vasoactive substances and pain inducing neuropeptides of the calcitonine gene related peptide family such as CALCB and adrenomedullin (ADM) were found amongst the top 50 differentially regulated genes. Downregulated genes involve pathways of sterol homeostasis, glucose homeostasis and lipogenesis, e.g., 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 (HMGCS1), Insulin Induced Gene 1 (INSIG1) or ELOVL Fatty Acid Elongase 6 (ELOVL6). Gene set enrichment analysis outlined significant deregulation of genes involved in cholesterol biosynthesis pathways, PERK regulated genes and genes involved in amino acid transport across the membrane. In summary, there is a significant overlap of the above mentioned genes and gene sets outlined by unbiased global differential transcriptome analyses with pathways known from the literature of neuropathy and neurodegeneration.

2021-04-30 | GSE173610 | GEO

Longitudinal RNA sequencing of skin and DRG neurons in mice with paclitaxel-induced peripheral neuropathy

Project description:Paclitaxel-induced peripheral neuropathy is a significant problem, which afflicts up to 70% of chemotherapy patients. Therapeutic interventions are currently unavailable due to an incomplete understanding of the underlying mechanisms. We previously discovered a major target in the skin, MMP-13, which underlies the development of paclitaxel-induced peripheral neuropathy in zebrafish and rodents. To better understand gene expression changes in sensory neurons and target tissue prior to and during the progression of neuropathy, we performed longitudinal RNA sequencing of mouse skin and dorsal root ganglion (DRG) neurons. Samples were harvested at time points associated with behavioural responses following injection of mice for 7 days either with vehicle or paclitaxel. The responses were categorized into pain onset (day 4 of paclitaxel injection), maxima (d7), beginning of pain resolution (d11) and recovery phase (d23). This dataset will be useful to understand changes in gene regulation in both neurons and skin, which can aid in the discovery of therapeutic interventions.

2021-10-12 | GSE185084 | GEO

Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

Project description:Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

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Satellite glial contact enhances differentiation and maturation of human induced sensory neurons

Project description:Induced sensory neurons (iSNs) generated from pluripotent stem cells are used to model human peripheral neuropathies, however current differentiation protocols produce sensory neurons with an embryonic phenotype. Peripheral glial cells contact sensory neurons early in development and contribute to formation of the canonical pseudounipolar morphology, but these signals are not encompassed in current iSN differentiation protocols. Here, we show that terminal differentiation of iSNs in co-culture with rodent Dorsal Root Ganglion satellite glia (rSG) advances their differentiation and maturation. Co-cultured iSNs develop pseudounipolar morphology through contact with rSGs. This transition depends on semaphorin-plexin guidance cues and on glial gap junction signaling. In addition to morphological changes, iSNs terminally differentiated in co-culture exhibit enhanced spontaneous action potential firing, more mature gene expression, and increased susceptibility to paclitaxel induced axonal degeneration. Thus, iSNs differentiated in coculture with rSGs provide a better model for understanding human peripheral neuropathies.

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2007-12-21 | GSE4298 | GEO

Fluvoxamine alleviates paclitaxel-induced neurotoxicity.

Project description:Paclitaxel (Px) is an effective chemotherapeutic agent for the treatment of various cancers. However, it is often associated with neurological side effects, including chemotherapy-associated cognitive impairment (CACI), such as "chemobrain". Previously, we reported that endoplasmic reticulum (ER) stress is involved in Px-induced neurotoxicity, and immunoglobulin heavy chain binding protein (BiP) inducer X (BIX) alleviates Px-induced neurotoxicity. However, BIX has not been used in clinical practice yet. We recently reported that fluvoxamine (Flv) alleviates ER stress via induction of sigma-1 receptor (Sig-1R). The purpose of this study was to investigate whether Flv could alleviate Px-induced neurotoxicity in vitro. SK-N-SH cells were pre-treated for 12 h with or without 10 μg/ml Flv followed by treatment with 1 μM Px with or without co-existence of 10 μg/ml Flv for 24 h. To investigate the involvement of Sig-1R in alleviation effect on Px-induced neurotoxicity,1 μM NE100, an antagonist of Sig-1R, was added for 24 h. Neurotoxicity was assessed using the MTS viability assay and ER stress-mediated neurotoxicity was assessed by evaluating the expression of C/EBP homologous protein (CHOP), cleaved caspase 4, and cleaved caspase 3. Pre-treatment with Flv significantly alleviated the induction of CHOP, cleaved caspase 4, and cleaved caspase 3 in SK-N-SH cells. At the same time, pre-treatment with Flv significantly induced Sig-1R in SK-N-SH cells. In addition, viability was significantly higher in Flv-treated cells than in untreated cells, which was reversed by treatment with NE100. Our results suggest that Flv alleviates Px-induced neurotoxicity in part through the induction of Sig-1R. Our findings should contribute to one of the novel approaches for the alleviation of Px-induced neurotoxicity, including chemobrain.

| S-EPMC5668922 | biostudies-literature

Comparison of Neurotoxic Potential of Abraxane versus Oxaliplatin and Paclitaxel

Project description:Interventions: Patients receiving abraxane chemotherapy for pancreatic cancer, breast cancer, colorectal cancer, non-small cell lung cancer or ovarian cancer will be recruited into the study to document the natural history of Abraxane-induced neurotoxicity through cross-sectional and prospective clinical and neurophysiological assessment. Examples of neurotoxicity seen with abraxane therapy include sensory dysasthesia including numbness and tingling in the hands and feet. Patients will be assessed monthly from the commencement of treatment until cessation, with 3-monthly follow up 6-12 months following cessation of treatment, to a maximum period of 2 years following enrolment. Primary outcome(s): To document the natural history of Abraxane-induced neurotoxicity through cross-sectional and prospective clinical and neurophysiological assessment. The severity of neuropathy will be assessed using the Total Neuropathy Score (TNS). This will be used to evaluate neuropathy in a number of different categories; sensory neuropathic symptoms, examination findings and nerve conduction results.[Assessed at monthly intervals from the commencement of treatment until cessation, with 3-monthly follow up 6-12 months following cessation of treatment.] Study Design: Purpose: Natural history;Duration: Longitudinal;Selection: Defined population;Timing: Prospective

| 2462598 | ecrin-mdr-crc

A quantitative proteomic analysis to reveal effects of N-acetylcystein on H2O2-induced neurotoxicity

Project description:SK-N-MC cell was used to evaluate effects of N-acetylcystein on H2O2-induced neurotoxicity. Proteomic analysis was conducted in three groups: control, H2O2-treatment (disease group), and NAC pretreatment followed by H2O2-treatment (NAC group).

2020-10-13 | PXD018177 | Pride

Evaluation for neurotoxicity of oxaliplatin using Nerve Conduction Velocity

Project description:Interventions: 1.Nerve Conduction Velocity 2.tuning fork Primary outcome(s): 1. Collation between NCV and oxaliplatin induced neurotoxicity 2. Collation between tuning fork and oxaliplatin induced neurotoxicity 3. Analyze the mechanism of oxaliplatin induced neurotoxicity Study Design: Single arm Non-randomized

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Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease

Project description:Prion diseases are fatal transmissible neurodegenerative conditions of humans and animals that arise through neurotoxicity induced by PrP misfolding. The cellular and molecular mechanisms of prion-induced neurotoxicity remain undefined. Understanding these processes will underpin therapeutic and control strategies for human and animal prion diseases, respectively. Prion diseases are difficult to study in their natural hosts and require the use of tractable animal models. Here we used RNA-Seq-based transcriptome analysis of prion-exposed Drosophila to probe the mechanism of prion-induced neurotoxicity. Adult Drosophila transgenic for pan neuronal expression of ovine PrP targeted to the plasma membrane exhibit a neurotoxic phenotype evidenced by decreased locomotor activity after exposure to ovine prions at the larval stage. Pathway analysis and quantitative PCR of genes differentially expressed in prion-infected Drosophila revealed up-regulation of cell cycle activity and DNA damage response, followed by down-regulation of eIF2 and mTOR signalling. Mitochondrial dysfunction was identified as the principal toxicity pathway in prion-exposed PrP transgenic Drosophila. The transcriptomic changes we observed were specific to PrP targeted to the plasma membrane since these prion-induced gene expression changes were not evident in similarly-treated Drosophila transgenic for cytosolic pan neuronal PrP expression, or in non-transgenic control flies. Collectively, our data indicate that aberrant cell cycle activity, repression of protein synthesis and altered mitochondrial function are key events involved in prion-induced neurotoxicity, and correlate with those identified in mammalian hosts undergoing prion disease. These studies highlight the use of PrP transgenic Drosophila as a genetically well-defined tractable host to study mammalian prion biology.

2020-01-31 | GSE144028 | GEO

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