ArticleScientific reports2025
Plasma extracellular vesicle-associated miR-512-3p modulates angiogenesis in pediatric Moyamoya disease by targeting ARHGEF3.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Obesity-driven extracellular vesicle signaling in cancer: mechanistic insights and clinical implications.Oncogenesis · 2026Review
- Molecular and multimodal biomarkers in Moyamoya disease: from pathogenic mechanisms to clinical translation.European journal of medical research · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Moyamoya disease (MMD) is a chronic cerebrovascular disorder and a leading cause of pediatric stroke. Extracellular vesicles (EVs) carrying microRNAs (miRNAs) play a pivotal role in intercellular communication within cerebrovascular diseases. This study aimed to identify specific miRNAs within plasma-derived EVs from MMD patients and investigate their functional implications. Study subjects included healthy controls (N = 13) and MMD patients (N = 23). EVs were isolated from plasma samples and characterized by transmission electron microscopy, nanoparticle tracking analysis, ExoView, RT-qPCR, and immunoblotting. miRNA profiles were assessed through NanoString analysis. Functional effects of miR-512-3p inhibition were evaluated in MMD endothelial colony-forming cells (ECFCs) by analyzing guanosine triphosphatase (GTPase) activity, tubule formation, and cell viability. MMD-derived EVs exhibited an upregulation of miR-512-3p compared to controls. Bioinformatics analysis identified RHO guanine nucleotide exchange factor 3 (ARHGEF3) as a potential target of miR-512-3p. Inhibition of miR-512-3p in MMD ECFCs resulted in increased expression of ARHGEF3 and its downstream effector RHOA, leading to enhanced GTPase activity and improved tubule formation, indicative of restored angiogenic function. Elevated levels of miR-512-3p within plasma-derived EVs may serve as a novel biomarker for MMD diagnosis. The modulation of ARHGEF3 and subsequent RHOA signaling by targeting miR-512-3p contributes to the dysregulated angiogenesis in MMD.
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