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Brain RNA-seq: Esomeprazole/stress interactions.

ABSTRACT: Brain RNA-seq: Esomeprazole/stress interactions.

PROVIDER: PRJNA495330 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7985120.fastq.gz	Fastqsanger.gz
	SRR7985130.fastq.gz	Fastqsanger.gz
	SRR7985140.fastq.gz	Fastqsanger.gz
	SRR7985150.fastq.gz	Fastqsanger.gz
	SRR7985160.fastq.gz	Fastqsanger.gz

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Brain RNA-seq: Esomeprazole/stress interactions.

Project description:Purpose: The goals of this study were to evaluate the effects of acid suppression on the brain transcriptomer in a murine model of stress. In addition, the effects of the proton pump inhibitor (PPI), esomeprazole, on the brain transcriptome were evaluted in the presence or absence of stress. Methods: Male C57BL/6 mice were subjected to three days of stress by hypothermic immobilization or control environment for three hours daily and either esomeprazole 2 mg/kg or saline by intraperitoneal injection daily. Standard RNA-seq methods were employed to assess mRNA expression in the hippocampus and frontal cortex. Results: There was no effect of stress or esomeprazole on the frontal cortex transcriptome. Stress had no impact on the hippocampus transcriptome, but the addition of esomeprazole induced differential expression of 124 genes, many of which are involved in cognitive and behavior pathways. Conclusions: Further studies are needed to evaluate the associations between microbiota, host gene expression, the abundance of CNS neurocognitive modulators, and their impact on cognition and behavior.

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Project description:Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. H + T induce inter-chromosomal RNA-chromatin interactions, particularly among the super enhancers. To test the causal relationship between H + T-induced RNA-chromatin interactions and the expression of EC dysfunction-related genes, we suppress the LINC00607 RNA. This suppression attenuates the expression of SERPINE1, a critical pro-inflammatory and pro-fibrotic gene. Furthermore, the changes of the co-expression gene network between diabetic and healthy donor-derived ECs corroborate the H + T-induced RNA-chromatin interactions. Taken together, caRNA-mediated dysregulation of gene expression modulates EC dysfunction, a crucial mechanism underlying numerous diseases.

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