Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 10

Similar Datasets

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

Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

Project description:Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

| PRJNA641207 | ENA

Gene expression changes induced by paclitaxel in MCF7 breast cancer cells

Project description:Time-dependent changes in gene expression induced by paclitaxel in the breast adenocarcinoma cell line MCF7. Keywords: genetic modification

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

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

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

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

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

| 2619755 | ecrin-mdr-crc

OATP1B2 deficiency protects against paclitaxel-induced neurotoxicity.

Project description:Paclitaxel is among the most widely used anticancer drugs and is known to cause a dose-limiting peripheral neurotoxicity, the initiating mechanisms of which remain unknown. Here, we identified the murine solute carrier organic anion-transporting polypeptide B2 (OATP1B2) as a mediator of paclitaxel-induced neurotoxicity. Additionally, using established tests to assess acute and chronic paclitaxel-induced neurotoxicity, we found that genetic or pharmacologic knockout of OATP1B2 protected mice from mechanically induced allodynia, thermal hyperalgesia, and changes in digital maximal action potential amplitudes. The function of this transport system was inhibited by the tyrosine kinase inhibitor nilotinib through a noncompetitive mechanism, without compromising the anticancer properties of paclitaxel. Collectively, our findings reveal a pathway that explains the fundamental basis of paclitaxel-induced neurotoxicity, with potential implications for its therapeutic management.

| S-EPMC5785270 | biostudies-literature

Microglia activation during CAR T cell induced neurotoxicity is dependent on TGF-β-activated kinase-1

Project description:Treatment with chimeric antigen receptor (CAR) T-cell therapy targeting CD19 (CAR19) can cause neurotoxicity in patients. The role of microglia in CAR19-induced neurotoxicity was unclear. We observed morphological microglia alterations, increased production of GM-CSF, MCP-1 and TNF by microglia and neurocognitive deficits in B-cell lymphoma-bearing mice upon CAR19 transfer. Gene expression analysis was performed to determine the microglial activation and downstream signalling in response to CAR19 transfer.

2024-01-22 | GSE193696 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data