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Series GSE189282 Query DataSets for GSE189282
Status Public on Jul 27, 2022
Title Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling [bulkRNA-seq_Hepatocyte]
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary 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.
Overall design Primary hepatocyte were isolated from wild type mouse, then cultured and stimulated with cAMP or glucagon, in the presence or absence of IL-13. Then RNA of each sample was extracted and subjected to RNA-seq to evaluted metabolism related genes including gluconeogenic enzyme.
Contributor(s) Fujimoto M, Motohiko O, Atsushi I, Tanaka T
Citation(s) 36109558
Submission date Nov 21, 2021
Last update date Sep 27, 2022
Contact name Masanori Fujimoto
Organization name Chiba University
Department Graduate School of Medicine
Lab 1. Department of Molecular Diagnosis, 2. Department of Endocrinology, Hematology and Gerontology
Street address Inohana 1-8-1
City Chiba-city
State/province Chiba-prefecture
ZIP/Postal code 260-8677
Country Japan
Platforms (1)
GPL18480 Illumina HiSeq 1500 (Mus musculus)
Samples (15)
GSM5696998 cAMP1
GSM5696999 cAMP2
GSM5697000 cAMP3
This SubSeries is part of SuperSeries:
GSE189287 Liver ILC2s suppress gluconeogenesis and limit blood glucose elevation through IL-13 signaling
BioProject PRJNA782347
SRA SRP347114

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SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE189282_FPKMCuffDiff.xlsx 11.1 Mb (ftp)(http) XLSX
GSE189282_RAW.tar 966.4 Mb (http)(custom) TAR (of BEDGRAPH)
GSE189282_TagCountCuffDiff.xlsx 10.9 Mb (ftp)(http) XLSX
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Raw data are available in SRA
Processed data are available on Series record
Processed data provided as supplementary file

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