Journal
CLINICAL AND EXPERIMENTAL HYPERTENSION
Volume 41, Issue 5, Pages 481-491Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/10641963.2018.1510941
Keywords
Platelet; microparticles; miR-4306; vascular endothelial growth factor A; coronary artery disease
Funding
- China Postdoctoral Science Foundation [Beijing, China] [2016M592678]
- General Financial Grant from education department of Sichuan province [Chengdu, China] [17ZB0168]
- General Finan [2016M592678, 17ZB0168, 2016JY0172]
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Platelets are major sources of microparticles (MPs) in peripheral bloodstream, and platelet-secreted MPs (P-MPs) transfer biological information to neighboring cells. In the present study, we found that the platelet- and P-MPs-derived microRNA-4306 (miR-4306) expression were downregulated in coronary artery disease (CAD) and platelet-derived miR-4306 was an independent poor prognostic factor in CAD. Plasma miRNA-4306 mainly cofractionated with MPs instead of Argonaute2 complexes or HDL. P-MPs could effectively deliver miR-4306 into human monocyte-derived macrophages (HMDMs). MiR-4306 noticeably inhibited the HMDMs migration in vitro and reduced the number of macrophage cells in cardiac tissue in myocardial infarction mice. This functional impact of miR-4306 was mediated directly through VEGFA to inhibit ERK/NF-kappa B signaling. In conclusion, our study suggested that intercellular transfer of miR-4306 by platelet microparticles inhibited the HMDMs migration through VEGFA/ERK1/2/NF-kappa B signaling pathways.
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