Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways

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 coronar...

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Published in:Clinical and experimental hypertension (1993) 2019-07, Vol.41 (5), p.481-491
Main Authors: Yang, Ying, Luo, Hui, Liu, Si, Zhang, Rongyi, Zhu, Xiao, Liu, Murong, Hu, Houxiang, Yang, Yi, Lv, Zhan, Chen, Mao
Format: Article
Language:English
Subjects:
Animals
Blood Platelets - metabolism
Cell Movement - genetics
Cell-Derived Microparticles - genetics
Cells, Cultured
coronary artery disease
Coronary Artery Disease - blood
Down-Regulation
HEK293 Cells
Humans
Macrophages - pathology
Macrophages - physiology
MAP Kinase Signaling System
Mice
microparticles
MicroRNAs - blood
MicroRNAs - genetics
miR-4306
Monocytes
Myocardial Infarction - pathology
NF-kappa B - metabolism
Platelet
vascular endothelial growth factor A
Vascular Endothelial Growth Factor A - metabolism
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Summary: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-κB signaling. In conclusion, our study suggested that intercellular transfer of miR-4306 by platelet microparticles inhibited the HMDMs migration through VEGFA/ERK1/2/NF-κB signaling pathways.
ISSN:1064-1963
1525-6006
DOI:10.1080/10641963.2018.1510941