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Engineered miR-122 inhibitors enhance endothelial mitochondrial efficiency and improve vascular function

GSE304654 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2026/01/15 Platform GPL34290
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: 5 × HFD-e-yP-122 I vs 4 × HFD-yP-SC vs 4 × HFD-e-yP-SC vs 3 × HFD-yP-122 IGroups 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)
MicroRNA-122-5p (miR-122) is primarily expressed by the liver and is increasingly released into the bloodstream during obesity. It impacts the function of non-liver tissues, such as vascular endothelial cells, and increases the risk of diabetic vasculopathy. Using a novel gamma-peptide-nucleic acid-based miR-122 inhibitor (γP-122-I), we show that miR-122 regulates blood glucose level and endothelial function in high-fat diet-fed mice.
Read the full summary ↓
Targeting γP-122-I to endothelial cells retains its ability to improve vascular function but reduces metabolic benefits compared to the non-targeted version. Our results show that the endothelial cells take up miR-122 through a neuropilin-1-dependent mechanism. The aortic transcriptomics analysis implicates the role of miR-122 in mitochondrial function. The aortas of high-fat diet-fed mice receiving an inhibitor of miR-122 were more efficient in oxygen consumption despite a decline in the expression of mitochondrial electron transport chain complexes, especially complex I. Our in vitro data show that miR-122 overexpression decreases the abundance of mitochondria with high membrane potential and spare respiratory capacity under hyperglycemic conditions. These findings support the therapeutic potential of the γPNA-based miR-122 inhibition in diabetic vasculopathy.
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 GSE304654_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 PRJNA1302208 and SRA study SRP606923. Searching any of these in the dataset finder brings you back here.

Study design
5 × HFD-e-yP-122 I vs 4 × HFD-yP-SC vs 4 × HFD-e-yP-SC vs 3 × HFD-yP-122 I

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.