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Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ChIP-Seq]

ABSTRACT: Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ChIP-Seq]

PROVIDER: PRJNA782345 | ENA |

REPOSITORIES: ENA

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Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling

Project description:Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling

| PRJNA782343 | ENA

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_Hepatocyte]

Project description:Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_Hepatocyte]

| PRJNA782349 | ENA

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [bulkRNA-seq_Hepatocyte]

Project description:Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [bulkRNA-seq_Hepatocyte]

| PRJNA782347 | ENA

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_ILC2]

Project description:Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_ILC2]

| PRJNA782350 | ENA

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ATAC-Seq]

Project description:Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ATAC-Seq]

| PRJNA782346 | ENA

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_Hepatocyte]

Project description:The liver stores glycogen and releases blood glucose and is therefore essential for glucose metabolism. Group 2 innate lymphoid cells (ILC2s) in adipose and pancreatic tissues are involved in glucose homeostasis, but the metabolic contribution of liver ILC2s remains unclear. Herein, we show that interleukin (IL)-33 treatment induced IL-13 production in liver ILC2s, which consequently reduced blood glucose levels. IL-13 also directly suppressed gluconeogenesis in primary hepatocytes. Single-cell RNA sequencing (scRNA-seq) and cell-cell interaction analysis in liver ILC2s and hepatocytes demonstrated that IL-33 administration suppressed gluconeogenesis in a specific Hnf4a/G6pchigh-hepatocyte cluster involving expression of Stat3, which significantly interacted with liver ILC2s via IL-13/IL-13 receptor signaling. To address the regulatory mechanism underlying IL-13 production in liver ILC2s, we performed GATA3 transcriptional complex analysis, and GATA3-ChIP-seq, ATAC-seq, and scRNA-seq trajectory analyses, focusing on GATA3-interacting proteins that were functionally specific in ILC2s. AP-1 family members were found to suppress the induction of IL-13 in liver ILC2s. Thus, our study revealed a novel role for liver ILC2s in glucose homeostasis.

2022-07-27 | GSE189286 | GEO

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ChIP-Seq]

2022-07-27 | GSE189284 | GEO

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [ATAC-Seq]

2022-07-27 | GSE189283 | GEO

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [bulkRNA-seq_Hepatocyte]

2022-07-27 | GSE189282 | GEO

Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [scRNA-seq_ILC2]

2022-07-27 | GSE189285 | GEO