GEO series

The Role of Sphingosine 1 Phosphate Receptor 2 Signaling in Chronic Glucocorticoid Exposure Induced Hepatic Steatosis and Hypertriglyceridemia

GSE286363 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/07/23 Platform GPL28330

At a glance

RNA-seq (gene expression) · mouse · 12 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 12 samples: 3 × liver, control no dex, vs 3 × liver, knockdown, no dex vs 3 × liver, control dex, vs 3 × liver, knockdown, dexGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: The sphingosine-1-phosphate receptor 2 S1PR2 mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemiaThe Journal of biological chemistry · 2025

Summary (written by the submitters)

Glucocorticoids (GC) are potent anti-inflammatory agents that are frequently used to treat inflammatory diseases. Chronic glucocorticoid treatment, however, causes unwanted adverse effects such as hypertriglyceridemia and hepatic steatosis. Hepatic sphingosine-1-phosphate receptor 2 knockdown in mice reduced chronic GC treatment induced triglyceride accumulation in the liver and plasma.

Read the full summary ↓

Chronic glucocorticoid treatment increased the recruitment of sterol regulatory element-binding protein 1c (Srebp1c) to the sterol regulatory element of mouse fatty acid synthase (Fasn) gene. This response was attenuated in hepatic S1PR2 knockdown mice. Chronic glucocorticoid treatment also increased the recruitment of carbohydrate response element binding protein (ChREBP) to the carbohydrate response elements (ChOREs) of lipogenic and glycolytic genes such as pyruvate kinase L/R (Pklr) and malic enzyme 1 (Me1) in mice liver. This response was also reduced in hepatic S1PR2 knockdown mice. Reducing hepatic ChREBP expression reduced the expression of Pklr, Me1 and Fasn. However, long-term glucocorticoid induced triglyceride accumulation in the liver and the plasma were not affected whereas the hepatic lactate levels were decreased. Thus, ChREBP plays a major role in chronic glucocorticoid induced glycolysis whereas its role in hypertriglyceridemia and hepatic steatosis was modest. Overall, this study demonstrated that hepatic S1PR2 signaling is involved in chronic glucocorticoid exposure activated Srebp1c and ChREBP, which promote lipogenesis and glycolysis, respectively.

Published in

The sphingosine-1-phosphate receptor 2 S1PR2 mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemia

Chang M, Zhao M, Whang EM et al. · The Journal of biological chemistry 2025 · PMID 40490140 · doi:10.1016/j.jbc.2025.110353

This dataset

Open GSE286363 in finder → Find more mouse RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE286363_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1208981 and SRA study SRP556485. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40490140) ↗

Study design

3 × liver, control no dex, vs 3 × liver, knockdown, no dex vs 3 × liver, control dex, vs 3 × liver, knockdown, dex

Supports a case/control comparison: 6 samples read as cases, 6 as controls.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8724813 liver, control no dex, rep 1 liver, control no dex,
GSM8724814 liver, control no dex, rep 2 liver, control no dex,
GSM8724815 liver, control no dex, rep 3 liver, control no dex,
GSM8724816 liver, knockdown, no dex rep1 liver, knockdown, no dex
GSM8724817 liver, knockdown, no dex rep2 liver, knockdown, no dex
GSM8724818 liver, knockdown, no dex rep3 liver, knockdown, no dex
GSM8724819 liver, control dex, rep1 liver, control dex,
GSM8724820 liver, control dex, rep2 liver, control dex,
GSM8724821 liver, control dex, rep3 liver, control dex,
GSM8724822 liver, knockdown, dex rep1 liver, knockdown, dex
GSM8724823 liver, knockdown, dex rep2 liver, knockdown, dex
GSM8724824 liver, knockdown, dex rep3 liver, knockdown, dex

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