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RNA-Sequencing quantitative analysis of transcriptomes changes between veh., and glutamate with or without P.edulis extracts treated mouse hippocampal HT-22 cells

ABSTRACT: RNA-Sequencing quantitative analysis of transcriptomes changes between veh., and glutamate with or without P.edulis extracts treated mouse hippocampal HT-22 cells

PROVIDER: PRJNA764214 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15931277.fastq.gz	Fastqsanger.gz
	SRR15931278.fastq.gz	Fastqsanger.gz
	SRR15931279.fastq.gz	Fastqsanger.gz
	SRR15931280.fastq.gz	Fastqsanger.gz

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RNA-Sequencing quantitative analysis of transcriptomes changes between veh., and glutamate with or without P.edulis extracts treated mouse hippocampal HT-22 cells

Project description:Purpose: RNA-sequencing provides the system-based analysis of cellular pathways. The goals of this stude are to evaluate whether P.edulis attenuate glutamate-induced neurotoxicity via modify the expression of differenterly exprssed genes (DEGs) ant the relatives signaling pathways

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Project description:The effect of glucose-dependent insulinotropic polypeptide (GIP) on cells under oxidative stress induced by glutamate, a neurotransmitter, and the underlying molecular mechanisms were assessed in the present study. We found that in the pre-treatment of HT-22 cells with glutamate in a dose-dependent manner, intracellular ROS were excessively generated, and additional cell damage occurred in the form of lipid peroxidation. The neurotoxicity caused by excessive glutamate was found to be ferroptosis and not apoptosis. Other factors (GPx-4, Nrf2, Nox1 and Hspb1) involved in ferroptosis were also identified. In other words, it was confirmed that GIP increased the activity of sub-signalling molecules in the process of suppressing ferroptosis as an antioxidant and maintained a stable cell cycle even under glutamate-induced neurotoxicity. At the same time, in HT-22 cells exposed to ferroptosis as a result of excessive glutamate accumulation, GIP sustained cell viability by activating the mitogen-activated protein kinase (MAPK) signalling pathway. These results suggest that the overexpression of the GIP gene increases cell viability by regulating mechanisms related to cytotoxicity and reactive oxygen species production in hippocampal neuronal cell lines.

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