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MyD88 Signaling in Trophoblasts is Necessary for Maternal High Fat Diet-Associated Developmental Programming of Obesity

GSE237410 Mus musculus (mouse) RNA-seq (gene expression) 24 samples Submitted 2026/06/25 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 24 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
24 samples: 8 conditions, mostly in triplicateGroups 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)
Maternal obesity contributes to persistent programming of offspring obesity. A causal role for placental inflammatory mechanisms in developmental programming remains to be established. We examined the role of the toll-like receptor (TLR) pathway in mediating maternal obesity associated programming by trophoblast deletion of the TLR adapter protein, MyD88.
Read the full summary ↓
Female MyD88fl/fl:Cyp19 Cre+ (MyD88-CKO) at 5 wks of age were provided control (17% fat calories, CON) or high-fat diets (HFD, 45% fat calories) for 12 wk and mated with MyD88fl/fl:Cyp19 Cre-(flox-control) males. Placenta were studied at dpc 17.5. In a subset, offspring were randomized to CON or HFD for 16 weeks. Placental weight and gene expression changes associated with HFD showed MyD88-dependence for pro-inflammatory and lipid metabolism related responses. Male MyD88 flox offspring from HFD-dams fed postnatal HFD (HH) showed an increase in body weight, liver steatosis and gene expression. These changes were absent in MyD88 CKO HH offspring, demonstrating a causal link between placental MyD88 mediated changes and long-term changes. Overall, these findings provide the first unequivocal evidence that placental changes due to maternal HFD are causally related to offspring obesity risk.
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 GSE237410_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 PRJNA994908 and SRA study SRP449591. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in triplicate
F_Con_CKO ×3 F_Con_FL ×3 F_HF_CKO ×3 F_HF_FL ×3 M_Con_CKO ×3 M_Con_FL ×3 M_HF_CKO ×3 M_HF_FL ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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.