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Integration of transcriptomics and proteomics uncovers novel targets underlying the protective effects of Nrf2 knockout in HEI-OC1 cells

ABSTRACT: Integration of transcriptomics and proteomics uncovers novel targets underlying the protective effects of Nrf2 knockout in HEI-OC1 cells

PROVIDER: PRJNA1119423 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29263062_1.fastq.gz	Fastqsanger.gz
	SRR29263062_2.fastq.gz	Fastqsanger.gz
	SRR29263063_1.fastq.gz	Fastqsanger.gz
	SRR29263063_2.fastq.gz	Fastqsanger.gz
	SRR29263064_1.fastq.gz	Fastqsanger.gz

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Integration of transcriptomics and proteomics uncovers novel targets underlying the protective effects of Nrf2 knockout in HEI-OC1 cells

Project description:Cisplatin, a utilized anticancer drug in clinical practice, induces sensorineural hearing loss (SNHL) in patients. However, the precise mechanism underlying cisplatin-associated ototoxicity remains unknown. HEI-OC1 cells are immortalized cells derived from the organs of Corti mice and nuclear factor erythroid 2-related factor 2 （Nrf2） knockout (KO) significantly enhances cisplatin resistance in these cells. The exploration of transcriptomic data from Nrf2 KO has significant implications for the identification of novel targets to enhance HEI-OC1 cisplatin resistance in Nrf2 KO and for understanding the biological characteristics associated with SNHL. The RNA-seq analysis revealed a significant enrichment of differentially expressed genes (DEGs) in the Nrf2 KO model within key signaling pathways, including the PI3K-Akt, MAPK, as well as Glutathione metabolism signaling pathways. Notably, expression levels of 17 specific genes were confirmed by RT-qPCR (Real-time Quantitative-PCR). The biomarkers identified in this study may be key to understanding the biological mechanism by which Nrf2 KO strongly increases HEI-OC1 cisplatin resistance, and by targeting the PI3K-Akt, MAPK, Glutathione metabolism signaling pathways provide new ideas for the prevention and treatment of cisplatin-induced SNHL.

2024-09-01 | GSE268900 | GEO

Phosphoproteomics on cisplatin or LPS treated on HEI OC1 cells

Project description:HEI-OC1 cells were treated with cisplatin, LPS or PB and lysed with 8 M guanidine hydrochloride. Soluble proteins were digested to peptides with trypsin/LysC mix and desalted. Phosphopeptides were enriched using MagReSyn Ti-IMAC HP beads automtaed by KingFIsher Duo Prime.

2024-12-11 | MSV000096638 | MassIVE

Transcriptomic in silico screens identify niclosamide for protection against cisplatin- and noise-induced hearing loss in zebrafish and mice through Nrf2 activation

Project description:We report the RNA expression of the House Ear Institute-Organ of Corti (HEI-OC1) cells with and without cisplatin exposure to identify differencialyy expressed genes. The results of RNA-seq analysis showed 2732 downregulated, and 1639 upregulated genes above 1-fold change in cisplatin threated cells compared to non-treated controls.

2021-07-16 | GSE180141 | GEO

Project description:HEI-OC1 cells sequencing

| PRJNA1080024 | ENA

Pdx1-Oc1 cooperatively drive the induction of the endocrine pancreatic program

Project description:We report the impact of heterozygous loss of either Pdx1 or Oc1 on the developing pancreas at e15.5

2016-06-09 | GSE77896 | GEO

Effect of MiaPaCa-2 cancer cells on gene expression in HEI-286 Schwann cells and c-Jun KO HEI-286 Schwan cells

Project description:We report the transcriptome analysis of control and c-Jun knock-out HEI-286 human Schwann cells in presence or absence of cancer cells

2024-07-19 | GSE180710 | GEO

Chloracidobacterium thermophilum strain:OC1

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Nrf2 transcript alterations

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Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application.

Project description:IntroductionOne approach to dampen the inflammatory reactions resulting from implantation surgery of cochlear implant hearing aids is to embed dexamethasone into the matrix of the electrode carrier. Possible side effects for sensory cells in the inner ear on the metabolomics have not yet been evaluated.ObjectiveWe examined changes in the metabolome of the HEI-OC1 cell line after dexamethasone incubation as a cell model of sensory cells of the inner ear.Results and conclusionUntargeted GC-MS-profiling of metabolic alterations after dexamethasone treatment showed that dexamethasone had antithetical effects on the metabolic signature of the cells depending on growth conditions. The differentiated state of HEI-OC1 cells is better suited for elucidating metabolic changes induced by external factors. Dexamethasone treatment of differentiated cells led to an increase in intracellular amino acids and enhanced glucose uptake and β-oxidation in the cells. Increased availability of precursors for glycolysis and ATP production by β-oxidation stabilizes the energy supply in the cells, which could be assumed to be beneficial in coping with cellular stress. We found no negative effects of dexamethasone on the metabolic level, and changes may even prepare sensory cells to better overcome cellular stress following implantation surgery.

| S-EPMC8144088 | biostudies-literature

NPC1 Deficiency Contributes to Autophagy-Dependent Ferritinophagy in HEI-OC1 Auditory Cells.

Project description:Niemann-Pick type C disease (NPCD) is a rare genetic syndrome characterized by cholesterol accumulation in multiple organelles. NPCD is mainly caused by gene deficiency of NPC intracellular cholesterol transporter 1 (NPC1). It has been reported that some of the NPCD patients exhibit clinical features of progressive hearing loss at high frequency and iron disorder, but the underlying relationship is unknown. A recent study has reported that ferroptosis contributes to the impairment of cochlear hair cells that are related to sensory hearing. In this study, we generated NPC1-deficient HEI-OC1 cells to show the effect of NPC1 deficiency on cochlear outer hair cells. We found that NPC1 deficiency enhances autophagy-dependent ferritinophagy to release Fe (II). Our work provides important insights into the effect of NPC1 deficiency in auditory cells, indicating that it induces ferroptosis and results in hearing loss.

| S-EPMC9353266 | biostudies-literature

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