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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [In_vivo]

ABSTRACT: Single cell transcriptomic profiling (sc RNA-seq) of diatery arachidonic acid (AA) induced gene expression pogram associated with regeneration in intestinal organoids.

ORGANISM(S): Mus musculus

PROVIDER: GSE210724 | GEO | 2023/03/01

REPOSITORIES: GEO

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [Organoid]

Project description:Single cell transcriptomic profiling (sc RNA-seq) of arachidonic acid (AA) induced gene expression pogram associated with regeneration in intestinal organoids.

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [intestinal organoids]

Project description:We evaluated the effects of arachidonic acid (AA) on intestinal stem cell regeneration by RNA-seq and found that AA treatment led to strong upregulation of genes that are associated with stem cell reprogramming across the time points. AA elicits a conserved stem cell regeneration program in mouse intestinal organoids.

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [intestinal organoids]

Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [intestinal organoids]

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [In_vivo]

Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [In_vivo]

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [Organoid]

Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [Organoid]

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-01 | GSE210730 | GEO

Arachidonic acid promotes intestinal regeneration by activating Wnt signaling

Project description:We identify arachidonic acid (AA), as a direct proliferation promoter of intestinal epithelial cells, facilitating small intestinal regeneration. In the transcriptomes, it shows that AA treatment upregulated proliferation-related genes including Wnt signaling target genes, while downregulated differentiation-related genes including enterocyte, goblet cell, Paneth cell, enteroendocrine cell, and tuft cell markers. Additionally, AA could also upregulate stem cell-associated genes which have been highly expressed three days after 12Gy IR injury (e.g. Clu, Lamc2, Anxa1, Areg, and Ly6d). The study shows that AA treatment can be considered a potential therapy for irradiation injury repair and tissue regeneration.

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Arachidonic acid targets pneumococcal fatty acid homeostasis

Project description:Free fatty acids play an important role during infection by modulating immune responses, but also by directly functioning as antimicrobials. Particularly, the host’s long chain polyunsaturated fatty acids, not commonly found in bacterial pathogens, have significant antibacterial potential. Of these arachidonic acid (AA) is in high abundance, and in this study we show that upon infection with the Streptococcus pneumoniae the AA concentration in the blood increases. Hence, we investigated the transcriptmoic effects of AA on this extremely problematic bacterial pathogen.

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ENO1 promotes liver carcinogenesis through YAP1-dependent arachidonic acid metabolism

Project description:Enolase 1 (ENO1) is a glycolytic enzyme that plays essential roles in various pathological activities including cancer development. However, the mechanisms underlying ENO1-contributed tumorigenesis are not well explained. Here, we uncover that ENO1, as an RNA-binding protein, binds to the cytosine-uracil-guanine-rich elements of YAP1 messenger RNA to promote its translation. ENO1 and YAP1 positively regulate alternative arachidonic acid (AA) metabolism by inverse regulation of PLCB1 and HPGD (15-hydroxyprostaglandin dehydrogenase). The YAP1/PLCB1/HPGD axis-mediated activation of AA metabolism and subsequent accumulation of prostaglandin E2 (PGE2) are responsible for ENO1-mediated cancer progression, which can be retarded by aspirin. Finally, aberrant activation of ENO1/YAP1/PLCB1 and decreased HPGD expression in clinical hepatocellular carcinoma samples indicate a potential correlation between ENO1-regulated AA metabolism and cancer development. These findings underline a new function of ENO1 in regulating AA metabolism and tumorigenesis, suggesting a therapeutic potential for aspirin in patients with liver cancer with aberrant expression of ENO1 or YAP1.

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