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Differentially expressed genes in SCC13 NRF3-KO cells and SCC13 cells that re-express endogenous concentrations of recombinant NRF3

ABSTRACT: Differentially expressed genes in SCC13 NRF3-KO cells and SCC13 cells that re-express endogenous concentrations of recombinant NRF3

PROVIDER: PRJNA941808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23724240_1.fastq.gz	Fastqsanger.gz
	SRR23724240_2.fastq.gz	Fastqsanger.gz
	SRR23724241_1.fastq.gz	Fastqsanger.gz
	SRR23724241_2.fastq.gz	Fastqsanger.gz
	SRR23724242_1.fastq.gz	Fastqsanger.gz

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Differentially expressed genes in SCC13 NRF3-KO cells and SCC13 cells that re-express endogenous concentrations of recombinant NRF3

Project description:We identified a tumor-suppressing function of NRF3 in skin cancer. To determine the underlying mechanism of action we wanted to compare the transcriptome of SCC13 NRF3-KO cells and SCC13 cells that re-express endogenous concentrations of recombinant NRF3.

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Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.

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