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Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

ABSTRACT: Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

PROVIDER: PRJNA656998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12446914.fastq.gz	Fastqsanger.gz
	SRR12446915.fastq.gz	Fastqsanger.gz
	SRR12446916.fastq.gz	Fastqsanger.gz
	SRR12446917.fastq.gz	Fastqsanger.gz
	SRR12446918.fastq.gz	Fastqsanger.gz

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Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines [18hrs]

Project description:Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines [18hrs]

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Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

Project description:Exposure to proinflammatory cytokines is believed to contribute to pancreatic β-cells during diabetes development. While some cytokine-mediated changes in islet gene expression are known, the heterogeneity of the response is not well-understood. Following 6 hour treatment with interleukin-1 beta (IL-1β) and interferon-gamma (IFN-γ) alone or together, mouse islets were subjected to single-cell RNA-sequencing (scRNA-seq). Inducible nitric oxide synthase (iNOS) mRNA (Nos2), antiviral genes, and immune-associated genes were induced in a subset of β-cells in response to both cytokines, while IL-1β alone activated only antiviral genes. Subsets of α- and δ-cells expressed Nos2 and exhibited similar gene expression changes as β-cells, including induction of antiviral genes and repression of identity genes. Finally, cytokine-responsiveness was inversely correlated with expression of genes encoding heat shock proteins. Our findings show that all endocrine cell types respond to cytokines, IL-1β induces the expression of protective genes in β-cells, and cellular stress gene expression is associated with an inhibition in cytokine signaling.

2021-04-15 | GSE156175 | GEO

Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines [18hrs]

Project description:Exposure to proinflammatory cytokines is believed to contribute to pancreatic β-cells during diabetes development. While some cytokine-mediated changes in islet gene expression are known, the heterogeneity of the response is not well-understood. Following 18 hour treatment with interleukin-1 beta (IL-1β) and interferon-gamma (IFN-γ) alone or together, mouse islets were subjected to single-cell RNA-sequencing (scRNA-seq). Inducible nitric oxide synthase (iNOS) mRNA (Nos2), antiviral genes, and immune-associated genes were induced in a subset of β-cells in response to both cytokines, while IL-1β alone activated only antiviral genes. Subsets of α- and δ-cells expressed Nos2 and exhibited similar gene expression changes as β-cells, including induction of antiviral genes and repression of identity genes. Finally, cytokine-responsiveness was inversely correlated with expression of genes encoding heat shock proteins. Our findings show that all endocrine cell types respond to cytokines, IL-1β induces the expression of protective genes in β-cells, and cellular stress gene expression is associated with an inhibition in cytokine signaling.

2021-12-20 | GSE183010 | GEO

Single-cell RNA sequencing of mouse islets exposed to proinflammatory cytokines.

Project description:Exposure to proinflammatory cytokines is believed to contribute to pancreatic β-cell damage during diabetes development. Although some cytokine-mediated changes in islet gene expression are known, the heterogeneity of the response is not well-understood. After 6-h treatment with IL-1β and IFN-γ alone or together, mouse islets were subjected to single-cell RNA sequencing. Treatment with both cytokines together led to expression of inducible nitric oxide synthase mRNA (Nos2) and antiviral and immune-associated genes in a subset of β-cells. Interestingly, IL-1β alone activated antiviral genes. Subsets of δ- and α-cells expressed Nos2 and exhibited similar gene expression changes as β-cells, including increased expression of antiviral genes and repression of identity genes. Finally, cytokine responsiveness was inversely correlated with expression of genes encoding heat shock proteins. Our findings show that all islet endocrine cell types respond to cytokines, IL-1β induces the expression of protective genes, and cellular stress gene expression is associated with inhibition of cytokine signaling.

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Human islets exposed to cytokines IL-1β and IFN-γ

Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. Human islets were isolated and exposed (or not) to IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix arrays. These measurements were performed three times.

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RPSA and proinflammatory cytokines after HSV-1 infection

Project description:RPSA and proinflammatory cytokines after HSV-1 infection

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The G Protein-Coupled Receptor GPR31 Promotes Proinflammatory Responses in Pancreatic Islets and Macrophages II

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.

2025-01-06 | GSE285039 | GEO

IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

Project description:IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

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RNA-Seq to identify genes expressed by islets in response to metabolic and inflammatory stress and the role of CN/NFAT signaling in this response

Project description:To identify genes expressed in islets in response to metabolic and inflammatory stress, we performed total RNA-Seq on isolated human islets exposed to IL-1β in the presence of high glucose. Gene ontology (GO) analysis of upregulated transcripts indicated enrichment of genes associated with cytokine signaling and proinflammatory responses. Multiple cytokines and chemokines were induced, and several key regulators of oxidative and ER stress responses were upregulated. The results revealed acute induction of proinflammatory transcripts and upregulation of genes involved in oxidative and ER stress in human islets in response to IL-1β and high glucose. Blockade of CN/NFAT signaling by FK506 pretreatment resulted in suppression of genes required for islet cell differentiation, development, and function.

2022-03-01 | GSE197685 | GEO

Deficiency of RPSA reduces binding of P65 to proinflammatory cytokines promoter regions in HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204891 | GEO

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