GEO series

Perilipin 5 deletion protects against nonalcoholic fatty liver disease and hepatocellular carcinoma by modulating lipid metabolism and inflammatory responses

GSE242852 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2024/03/11 Platform GPL19057

At a glance

RNA-seq (gene expression) · mouse · 18 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: 18 samples: 18 samples, each with a distinct title — no replicated groupsGroups 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: Perilipin 5 deletion protects against nonalcoholic fatty liver disease and hepatocellular carcinoma by modulating lipid metabolism and inflammatory responsesCell death discovery · 2024

Summary (written by the submitters)

The molecular mechanisms underlying nonalcoholic fatty liver disease (NAFLD) transition to hepatocellular carcinoma (HCC) are incompletely understood. During NAFLD development, Perilipin 5 (PLIN5) can regulate lipid metabolism by suppressing lipolysis and preventing lipotoxicity. Other reports suggest that lack of PLIN5 decreases hepatic injury, indicating a protective role in NAFLD pathology.

Read the full summary ↓

To better understand the role of PLIN5 in liver disease, we established mouse models of NAFLD and NAFLD-induced HCC, in which wild type and Plin5 null mice were exposed to a single dose of acetone or 7,12-dimethylbenz[a]anthracene (DMBA) in acetone, followed by a 30-week high-fat diet supplemented with glucose/fructose. In the NAFLD model, RNA-seq revealed significant changes in genes related to lipid metabolism and immune response. At the protein level, signaling pathways such as AMP-activated protein kinase (AMPK), signal transducer and activator of transcription 3 (STAT3), Janus kinase (JNK) and protein kinase B (AKT) were blunted in Plin5 deficient (Plin5-/-) mice compared to wild type mice (WT). In the NAFLD-HCC model, only WT mice developed hepatic tumors, while Plin5-/- mice were resistant to tumorigenesis. Furthermore, only 32 differentially expressed genes were identified that were associated with NAFLD progession in Plin5 null mice. Markers of mitochondrial function and immune response such as the peroxisome proliferator‐activated receptor-γ, coactivator 1‐α (PGC-1a) and pSTAT3 were decreased. Lipidomics analysis revealed differential levels of some sphingomyelins between WT and Plin5-/- mice. Interestingly, these changes were not detected in the HCC model, indicating a possible shift in the metabolism of sphingomelins during carcinogenesis.

Published in

Perilipin 5 deletion protects against nonalcoholic fatty liver disease and hepatocellular carcinoma by modulating lipid metabolism and inflammatory responses

Mass-Sanchez PB, Krizanac M, Štancl P et al. · Cell death discovery 2024 · PMID 38388533 · doi:10.1038/s41420-024-01860-4

This dataset

Open GSE242852 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 GSE242852_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 PRJNA1015167 and SRA study SRP459658. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38388533) ↗

Study design

18 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 18 sample titles: 18 distinct titles with little repetition. 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

GSM7771985 Liver, WT, acetone, control, rep1 [01_PM]
GSM7771986 Liver, WT, acetone, control, rep2 [02_PM]
GSM7771987 Liver, WT, acetone, control, rep3 [03_PM]
GSM7771988 Liver, WT, acetone, western, rep1 [04_PM]
GSM7771989 Liver, WT, acetone, western, rep2 [05_PM]
GSM7771990 Liver, WT, acetone, western, rep3 [06_PM]
GSM7771991 Liver, PLIN5, acetone, western, rep1 [10_PM]
GSM7771992 Liver, PLIN5, acetone, western, rep2 [11_PM]
GSM7771993 Liver, PLIN5, acetone, western,rep 3 [12_PM]
GSM7771994 Liver, WT, DMBA, control, rep1 [19_PM]
GSM7771995 Liver, WT, DMBA, control, rep2 [20_PM]
GSM7771996 Liver, WT, DMBA, control, rep3 [21_PM]
GSM7771997 Liver, WT, DMBA, western, rep1 [22_PM]
GSM7771998 Liver, WT, DMBA, western, rep2 [23_PM]
GSM7771999 Liver, WT, DMBA, western, rep3 [24_PM]
GSM7772000 Liver, PLIN5, DMBA, western, rep1 [28_PM]
GSM7772001 Liver, PLIN5, DMBA, western, rep2 [29_PM]
GSM7772002 Liver, PLIN5, DMBA, western, rep3 [30_PM]

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