GEO series

Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice

GSE279588 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2024/10/16 Platform GPL24247

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 × C-A vs 4 × C-C vs 4 × S-A vs 4 × S-CGroups 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: Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in miceJournal of the Royal Society, Interface · 2021

Summary (written by the submitters)

Hypertension induces significant aortic remodelling, often adaptive but sometimes not. To identify immuno-mechanical mechanisms responsible for differential remodelling, we studied thoracic aortas from 129S6/SvEvTac and C57BL/6 J mice before and after continuous 14-day angiotensin II infusion, which elevated blood pressure similarly in both strains.

Read the full summary ↓

Histological and biomechanical assessments of excised vessels were similar at baseline, suggesting a common homeostatic set-point for mean wall stress. Histology further revealed near mechano-adaptive remodelling of the hypertensive 129S6/SvEvTac aortas, but a grossly maladaptive remodelling of C57BL/6 J aortas. Bulk RNA sequencing suggested that increased smooth muscle contractile processes promoted mechano-adaptation of 129S6/SvEvTac aortas while immune processes prevented adaptation of C57BL/6 J aortas. Functional studies confirmed an increased vasoconstrictive capacity of the former while immunohistochemistry demonstrated marked increases in inflammatory cells in the latter. We then used multiple computational biomechanical models to test the hypothesis that excessive adventitial wall stress correlates with inflammatory cell infiltration. These models consistently predicted that increased vasoconstriction against an increased pressure coupled with modest deposition of new matrix thickens the wall appropriately, restoring wall stress towards homeostatic consistent with adaptive remodelling. By contrast, insufficient vasoconstriction permits high wall stresses and exuberant inflammation-driven matrix deposition, especially in the adventitia, reflecting compromised homeostasis and gross maladaptation.

Published in

Excessive adventitial stress drives inflammation-mediated fibrosis in hypertensive aortic remodelling in mice

Spronck B, Latorre M, Wang M et al. · Journal of the Royal Society, Interface 2021 · PMID 34314650 · doi:10.1098/rsif.2021.0336

This dataset

Open GSE279588 in finder → Find more mouse RNA-seq datasets →

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.

Series matrix ↓

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 GSE279588_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA1173561 and SRA study SRP538912. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 34314650) ↗

Study design

4 × C-A vs 4 × C-C vs 4 × S-A vs 4 × S-C

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

GSM8576526 C-A1 C-A
GSM8576527 C-A2 C-A
GSM8576528 C-A3 C-A
GSM8576529 C-A5 C-A
GSM8576530 C-C1 C-C
GSM8576531 C-C2 C-C
GSM8576532 C-C3 C-C
GSM8576533 C-C5 C-C
GSM8576534 S-A1 S-A
GSM8576535 S-A2 S-A
GSM8576536 S-A4 S-A
GSM8576537 S-A5 S-A
GSM8576538 S-C1 S-C
GSM8576539 S-C2 S-C
GSM8576540 S-C3 S-C
GSM8576541 S-C4 S-C

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