# Plasma extracellular vesicle modulate immune cell transcriptional responses following acute myocardial infarction

## TL;DR

The study shows that plasma extracellular vesicles containing miRNA-320b activate immune cells after heart attacks, potentially offering new ways to improve recovery.

## Contribution

The paper identifies miRNA-320b in extracellular vesicles as a novel driver of immune cell activation following acute myocardial infarction.

## Key findings

- Plasma EVs from MI patients are enriched in miRNA-320b, which promotes monocyte adhesion and pro-inflammatory gene expression.
- Endothelial cells increase miRNA-320b in EVs during inflammation, linking it to immune cell priming.
- EV-miR-320b targets are enriched in neutrophils and monocytes from MI patients, suggesting a role in immune modulation.

## Abstract

Plasma extracellular vesicles (EVs) increase during acute myocardial infarction (MI), correlate with myocardial injury, and mobilize immune cells from the spleen to the circulation. These cells are transcriptionally activated even before tissue recruitment, yet the mechanisms driving this priming are unclear. We show that plasma EVs isolated at hospital presentation with MI are enriched in miRNA-320b. Endothelial cells upregulate miRNA-320b in EVs following inflammatory stimulation. Target gene pathway analysis revealed enrichment in adhesion and cytokine signaling. Endothelial EVs promoted monocyte adhesion and induced IL6 and TNF mRNA expression in macrophages while dampening cytokine secretion. RNA-sequencing of MI patient neutrophils and monocytes confirmed significant enrichment of miRNA-320b targets. Peripheral blood mononuclear cells treated with MI plasma EVs showed similar gene regulation. These findings suggest that EV-mediated transfer of miRNA-320b primes immune cells for adhesion and cytokine signaling. Understanding this signaling axis may enable therapeutic immunomodulation of immune cells to improve repair following MI.

•Plasma extracellular vesicle (EV)-miR‑320b elevates in patients with myocardial infarction•Endothelial inflammatory activation promotes miR‑320b enrichment in secreted EV•miR‑320b‑EV enhance monocyte adhesion and pro‑inflammatory gene expression•EV‑miR‑320b represents a potential target for monocyte immunomodulation post-infarction

Plasma extracellular vesicle (EV)-miR‑320b elevates in patients with myocardial infarction

Endothelial inflammatory activation promotes miR‑320b enrichment in secreted EV

miR‑320b‑EV enhance monocyte adhesion and pro‑inflammatory gene expression

EV‑miR‑320b represents a potential target for monocyte immunomodulation post-infarction

Immunity; Transcriptomics