European journal of clinical investigationApr 28, 2026

miR-150-5p in small particles from amniotic membrane stem cells may protect the heart

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Updated Apr 29, 2026

Abstract

Mice treated with human amniotic membrane mesenchymal stem cells (hAMSCs) 2 days after cardiac ischemia/reperfusion showed improved left ventricular ejection fraction (LVEF) and reduced myocardial necrosis and fibrosis by Day 21.

Minimal engraftment of hAMSCs suggests that their cardioprotective effects may operate through signaling molecules rather than direct integration into heart tissue.
hAMSC treatment significantly upregulated cardiac miR-150 and suppressed HOXA4, which is associated with fibrosis in the heart after ischemia.
Downregulation of MIAT, a long non-coding RNA that sequesters miR-150, was observed following hAMSC treatment, indicating a potential mechanism for cardioprotection.
Silencing miR-150 in hAMSCs severely reduced their cardioprotective effects, highlighting the importance of miR-150 in this process.
Extracellular vesicles from hAMSCs under hypoxic conditions contained miR-150, suggesting its role as a key therapeutic component in promoting heart recovery.
Administration of miR-150-enriched extracellular vesicles replicated the cardioprotective benefits of hAMSCs, indicating their potential as a novel treatment strategy.

Simplified

BACKGROUND: Human amniotic membrane mesenchymal stem cells (hAMSCs) hold strong cardioprotective potential, yet their mechanisms of action remain largely elusive.

METHODS AND RESULTS: C57BL/6 mice were subjected to cardiac ischemia/reperfusion (I/R) and received intravenous (IV) 2 × 10hAMSCs at 2, 7 or 14 days post-reperfusion. Cardiac function and MIAT/miR-150/HOXA4 signalling were assessed. Mice treated 2 days post-I/R markedly improved LVEF and reduced myocardial necrosis and fibrosis by Day 21. Minimal hAMSC engraftment, evidenced by SSEA-4 immunostaining, suggests paracrine rather than direct cellular effects. Guided by GWAS implicating miRNAs in myocardial infarction, we identified miR-150 as a key effector, finding that hAMSC upregulated cardiac miR-150 and suppressed HOXA4, a profibrotic target in ischemic myocardium. In parallel, hAMSC treatment reduced cardiac MIAT, a lncRNA that sequesters miR-150, uncovering a mechanism of cardioprotection via MIAT downregulation post-reperfusion. Notably, CRISPR-Cas9 miR-150-silenced hAMSC exhibited severely impaired cardioprotective effects compared to wild-type cells, confirming the functional role of miR-150. miR-150 was identified as a key extracellular vesicle (EV) cargo released by hAMSC under hypoxic conditions, both in vitro and in hAMSC-injected I/R mice. Strickingly, administration of miR-150-enriched EVs to mice recapitulated the therapeutic benefits of hAMSC, underscoring miR-150-5p as central mediator of hAMSC-iduced cardioprotection. 5

CONCLUSIONS: hAMSCs promote cardioprotection following I/R via the MIAT/miR-150-5p/HOXA4 axis, in which miR-150-5p plays a central role. These findings provide loss-of-function evidence about the therapeutic potential of hAMSC-derived EVs as a novel cell-free exosome-based strategy for the treatment of acute myocardial infarction.

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The authors declare no conflicts of interest.

PubMed

miR-150-5p in small particles from amniotic membrane stem cells may protect the heart

Abstract

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