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The human pancreatic islet transcriptome: impact of pro-inflammatory cytokines

ABSTRACT: We have used RNA-seq to identify transcripts, including splice variants, expressed in human islets of Langerhans under control condition or following exposure to the pro-inflammatory cytokines interleukin-1β (IL-1β) and interferon-γ (IFN-γ). A total of 29,776 transcripts were identified as expressed in human islets. Expression of around 20% of these transcripts was modified by pro-inflammatory cytokines, including apoptosis- and inflammation-related genes. Chemokines were among the transcripts most modified by cytokines. Interestingly, 35% of the genes expressed in human islets undergo alternative splicing as annotated in RefSeq, and cytokines caused substantial changes in spliced transcripts. Nova1, previously considered a brain-specific regulator of mRNA splicing, is expressed in islets. 25/41 of the candidate genes for type 1 diabetes are expressed in islets, and cytokines modified expression of several of these transcripts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35296 | GEO | 2012/03/09

SECONDARY ACCESSION(S): PRJNA151601

REPOSITORIES: GEO

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The human pancreatic islet transcriptome: impact of pro-inflammatory cytokines

Project description:We have used RNA-seq to identify transcripts, including splice variants, expressed in human islets of Langerhans under control condition or following exposure to the pro-inflammatory cytokines interleukin-1β (IL-1β) and interferon-γ (IFN-γ). A total of 29,776 transcripts were identified as expressed in human islets. Expression of around 20% of these transcripts was modified by pro-inflammatory cytokines, including apoptosis- and inflammation-related genes. Chemokines were among the transcripts most modified by cytokines. Interestingly, 35% of the genes expressed in human islets undergo alternative splicing as annotated in RefSeq, and cytokines caused substantial changes in spliced transcripts. Nova1, previously considered a brain-specific regulator of mRNA splicing, is expressed in islets. 25/41 of the candidate genes for type 1 diabetes are expressed in islets, and cytokines modified expression of several of these transcripts. 5 human islet of Langerhans preparations examined under 2 conditions (control and cytokine treatment)

2012-03-09 | E-GEOD-35296 | biostudies-arrayexpress

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

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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. INS1 cell lines were cultured in medium with or without IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix Rat ST arrays. These experiments were performed on two separate occasions.

2013-12-19 | E-GEOD-53453 | biostudies-arrayexpress

Nova1 is a master regulator of alternative splicing in pancreatic beta cells

Project description:Alternative splicing (AS) is a fundamental mechanism for the regulation of gene expression. It affects more than 90% of human genes but its role in the regulation of pancreatic beta cells, the producers of insulin, remains unknown. Our recently published data indicated that the M-bM-^@M-^\neuron specificM-bM-^@M-^] Nova1 splicing factor is expressed in pancreatic beta cells. We have presently coupled specific knockdown (KD) of Nova1 with RNA-sequencing to determine all splice variants and downstream pathways regulated by this protein in beta cells. Nova1 KD altered the splicing of nearly 5000 transcripts. Pathway analysis indicated that these genes are involved in exocytosis, apoptosis, insulin receptor signalling, splicing and transcription. In line with these findings, Nova1 silencing inhibited insulin secretion and induced apoptosis basally and after cytokine treatment in rodent and human beta cells. These observations identify a novel layer of regulation of beta cell function, namely AS controlled by key splicing regulators such as Nova1. 3 batch of primary rat pancreatic beta cells were examined under 2 conditions: control and with Nova1 splicing factor knock-down

2014-10-01 | E-GEOD-59633 | biostudies-arrayexpress

Nova1 is a master regulator of alternative splicing in pancreatic beta cells

Project description:Alternative splicing (AS) is a fundamental mechanism for the regulation of gene expression. It affects more than 90% of human genes but its role in the regulation of pancreatic beta cells, the producers of insulin, remains unknown. Our recently published data indicated that the “neuron specific” Nova1 splicing factor is expressed in pancreatic beta cells. We have presently coupled specific knockdown (KD) of Nova1 with RNA-sequencing to determine all splice variants and downstream pathways regulated by this protein in beta cells. Nova1 KD altered the splicing of nearly 5000 transcripts. Pathway analysis indicated that these genes are involved in exocytosis, apoptosis, insulin receptor signalling, splicing and transcription. In line with these findings, Nova1 silencing inhibited insulin secretion and induced apoptosis basally and after cytokine treatment in rodent and human beta cells. These observations identify a novel layer of regulation of beta cell function, namely AS controlled by key splicing regulators such as Nova1.

2014-10-01 | GSE59633 | GEO

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.

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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-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.

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

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