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ABSTRACT: RNA expression in hepatocytes after GPR31 knockout under 12-HETE treatment

PROVIDER: PRJNA407292 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6037960_1.fastq.gz	Fastqsanger.gz
	SRR6037960_2.fastq.gz	Fastqsanger.gz
	SRR6037961_1.fastq.gz	Fastqsanger.gz
	SRR6037961_2.fastq.gz	Fastqsanger.gz
	SRR6037962_1.fastq.gz	Fastqsanger.gz

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Project description:12-HETE treatment of primary cultured mouse hepatocytes under normoxia and hypoxia conditions

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Effect of pyruvate (PA), lactate (LA), or 12-hydroxyeicosatetraenoic acid (12-HETE) stimulation on type1 conventional dendritic cells (cDC1) from the human ileum

Project description:We here report that GPR31 is specifically expressed in cDC1 in human intestinal mononuclear phagocytes. Since GPR31 has been previously reported to be activated by PA, LA, and 12-HETE, RNA-seq was performed to analyze the transcriptional changes in human ileal cDC1 under the stimulation of PA, LA, or 12-HETE.

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Project description:In type 1 diabetes (T1D), the innate and adaptive immune systems attack and eventually destroy the insulin-secreting islet β cells. During this process, β cells activate inflammatory signaling pathways that augment the dysfunction and destruction imposed by cellular autoimmunity. The 12-lipoxygenase (12-LOX) pathway produces the pro-inflammatory eicosanoid 12-HETE, which induces oxidative and endoplasmic reticulum stress and results in diminished insulin secretion and apoptosis. The G protein-coupled receptor 31 (GPR31) has been identified as a putative receptor for 12-HETE. In this study, we generated conventional GPR31 knockout mice. To interrogate the role of GPR31 in β cells, we treated islets from wildtype and Gpr31b-/- mice with proinflammatory cytokines and subjected the islets to RNA sequencing. Differentially expressed genes in Gpr31b-/- islets included those pertaining to receptor signaling, inflammation, oxidative stress, and macrophage migration — effects that are reminiscent of 12-LOX inhibition. Bone-marrow derived macrophages from Gpr31b-/- mice had reduced macrophage migration compared to wildtype macrophages. To mimic islet and macrophage inflammation as seen in T1D, wildtype and Gpr31b-/- mice were treated with the pro-diabetic toxin streptozotocin. Compared to wildtype, Gpr31b-/- mice had improved glucose tolerance and preserved β-cell mass. These results are consistent with previously published data using 12-LOX knockout mice and suggests that GPR31 mediates the proinflammatory responses of 12-HETE in the β cell.

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Project description:RNA-seq dataset for Alox12-KO and WT primary hepatocytes treated with 12-HETE or vehicle controls

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Project description:Effect of 12-HETE treatment of cardiomyocytes after hypoxia-reoxygenation challenge

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Project description:Gp130 dependent gene expression was analyzed in a previously established hepatocyte-specific gp130-knockout mouse model. Whole transcriptome analysis for isolated hepatocytes was performed to measure tissue specific responses after proinflammatory stimulus with IL-6 across different time points. We observed differences in the hepatocyte-specific transcriptional gp130 dependent response for genes associated with different aspects of the innate immune system. Our findings suggest a complex network of tightly-linked genes involved in the early activation of different parts of the innate immune response including acute phase proteins, complement and coagulation cascade. Total RNA obtained from a total number of 61 samples of isolated hepatocytes of hepatocyte-specific gp130-knockout and gp130flox mice, which were subjected to Il-6 treatment for 0, 1, 3, 6 or 12 hours, respectively.

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