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A miR-200b-Filamin A axis drives epicardial contribution to cardiogenesis

GSE311233 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2025/11/29 Platform GPL17021
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples
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)
The epicardium provides essential cellular and molecular cues required for proper cardiogenesis and cardiac repair. Epicardial-derived cells (EPDCs) play a pivotal role in establishing cardiac structure, contributing to coronary vasculature formation, connective tissue organization, and post-ischemic cardiac remodeling. During EPDC emergence, the epicardium must preserve a precise balance between cellular motility and epithelial integrity.
Read the full summary ↓
However, the mechanisms determining why some epicardial cells undergo epithelial-to-mesenchymal transition to become EPDCs while others retain an epithelial state remain unclear. We show that miR-200b is expressed in a specific subset of epicardial cells during embryonic EPDC formation. Gain- and loss-of-function experiments reveal that miR-200b regulates the overall number of EPDCs by modulating the proportion of symmetric and asymmetric cell divisions. RNA pull-down coupled with RNA-seq, together with in vitro and ex vivo functional assays, identified filamin A (FLNA)—a key regulator of spindle positioning during asymmetric division—as a direct miR-200b target in epicardial cells. FLNA loss reduced asymmetric divisions, supporting its role in promoting this division mode. Overall, our study defines a miR-200b–FLNA axis that governs symmetric versus asymmetric division to control epicardial tissue dynamics during cardiogenesis. Additionally, altered miR-200b expression after myocardial infarction in mice and humans suggests a potential role in post-injury cardiac remodeling
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 GSE311233_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 PRJNA1368821 and SRA study SRP648272. Searching any of these in the dataset finder brings you back here.

Samples in this study

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