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Prenatal diisononyl phthalate exposure induces the development of pulmonary dysplasia in offspring

GSE315505 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2026/01/06 Platform GPL17021
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 × 3-CM vs 3 × 3-DM vs 3 × 6-CM vs 3 × 6-DMGroups 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.
Summary (written by the submitters)
As a widely used plasticizer, Diisononyl phthalate (DINP) has been considered an emerging environmental pollutant. Epidemiological evidence shows that prenatal DINP exposure is linked to an increased risk of lung diseases in offspring and adults. However, little is known about their relationship at the molecular level. We exposed pregnant mice to DINP (100 mg/kg/day) by intragastric administration throughout gestation.
Read the full summary ↓
On postnatal days (PNDs) 21 and 42 offspring were sacrificed and the lungs were collected. We found that prenatal DINP exposure significantly caused hypoalveolarization on PND 21 in male offspring, which was reversed during postnatal development. Moreover, prenatal DINP exposure significantly caused pulmonary fibrosis on PND 42 in male offspring. However, neither of these changes were observed in female offspring. KEGG enrichment showed that differentially expressed genes (DEGs) in the lungs of male offspring were closely associated with the calcium signaling and IL-17 signaling pathways. Importantly, decreased Htr4 expression might contribute to hypoalveolarization, and the elevated Il-17a expression might be responsible for prenatal DINP exposure-induced pulmonary fibrosis in male offspring. Our results demonstrated that prenatal DINP exposure had a persistent impact on the lung development of the offspring, including early-stage reduced alveolarization and later-stage fibrosis.
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 GSE315505_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 PRJNA1398077 and SRA study SRP659646. Searching any of these in the dataset finder brings you back here.

Study design
3 × 3-CM vs 3 × 3-DM vs 3 × 6-CM vs 3 × 6-DM

Supports a between-group comparison across 12 samples.

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
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