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PARP 1 inhibition mediates a switch from cell death to transient senescence improving repair from acute oxidative injury

GSE260758 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2024/03/07 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 16 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
16 samples: 4 × Kidney, Ischemia Reperfusion, PJ34, vs 4 × Kidney, Ischemia Reperfusion, Vehicle, vs 4 × Kidney, Normal, PJ34, vs 4 × Kidney, Normal, Vehicle,Groups 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
Converting cell death into senescence by PARP1 inhibition improves recovery from acute oxidative injuryNature aging · 2024
Summary (written by the submitters)
Excessive amounts of Reactive Oxygen Species (ROS) lead to macromolecular damage and high levels of cell death and pathological sequelae. Switching cell death to a tissue regenerativestate can potentially improve short – and long-term consequences of ROS-associated acute tissueinjury. However, the mechanisms regulating oxidative stress-induced cell fate decision and their manipulation for improving repair remain poorly understood.
Read the full summary ↓
Here, we show that cells exposed tohigh oxidative stress enter a PARP1-mediated regulated cell death, and that blocking PARP1activation promotes conversion of cell death into senescence (CODIS). We demonstrate that CODIS depends on reducing mitochondrial Ca2+ overload as a consequence of retaining thehexokinase HKII onto mitochondria. In a mouse model of kidney ischemia/reperfusion damage,PARP1 inhibition lowers necrosis and increases acute and transient senescence at the injury site,leading to improved recovery from damage. For the first time, we provide evidence that strategiesconverting cell death into acute senescence can therapeutically reduce the detriment of accidental tissue damage. _x000B_
Published in
Converting cell death into senescence by PARP1 inhibition improves recovery from acute oxidative injury
Nehme J, Mesilmany L, Varela-Eirin M et al. · Nature aging 2024 · PMID 38724734 · doi:10.1038/s43587-024-00627-x
This dataset
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.

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 GSE260758_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA945397 and SRA study SRP427609. Searching any of these in the dataset finder brings you back here.

Study design
4 × Kidney, Ischemia Reperfusion, PJ34, vs 4 × Kidney, Ischemia Reperfusion, Vehicle, vs 4 × Kidney, Normal, PJ34, vs 4 × Kidney, Normal, Vehicle,

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 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
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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.