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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Main Authors: Ying Yang, Hui Luo, Si Liu, Rongyi Zhang, Xiao Zhu, Murong Liu, Houxiang Hu, Yi Yang, Zhan Lv, Mao Chen
Format: Article
Language:English
Published: Taylor & Francis Group 2019-07-01
Series:Clinical and Experimental Hypertension
Subjects:
Online Access:http://dx.doi.org/10.1080/10641963.2018.1510941
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author Ying Yang
Hui Luo
Si Liu
Rongyi Zhang
Xiao Zhu
Murong Liu
Houxiang Hu
Yi Yang
Zhan Lv
Mao Chen
author_facet Ying Yang
Hui Luo
Si Liu
Rongyi Zhang
Xiao Zhu
Murong Liu
Houxiang Hu
Yi Yang
Zhan Lv
Mao Chen
author_sort Ying Yang
collection DOAJ
description 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.
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spelling doaj.art-166af5bc18444d7eb172371888a667bc2023-09-19T15:19:27ZengTaylor & Francis GroupClinical and Experimental Hypertension1064-19631525-60062019-07-0141548149110.1080/10641963.2018.15109411510941Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathwaysYing Yang0Hui Luo1Si Liu2Rongyi Zhang3Xiao Zhu4Murong Liu5Houxiang Hu6Yi Yang7Zhan Lv8Mao Chen9Affiliated Hospital of North Sichuan Medical CollegeNanchong Central HospitalAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeAffiliated Hospital of North Sichuan Medical CollegeWest China Hospital, Sichuan UniversityPlatelets 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.http://dx.doi.org/10.1080/10641963.2018.1510941plateletmicroparticlesmir-4306vascular endothelial growth factor acoronary artery disease
spellingShingle Ying Yang
Hui Luo
Si Liu
Rongyi Zhang
Xiao Zhu
Murong Liu
Houxiang Hu
Yi Yang
Zhan Lv
Mao Chen
Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
Clinical and Experimental Hypertension
platelet
microparticles
mir-4306
vascular endothelial growth factor a
coronary artery disease
title Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
title_full Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
title_fullStr Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
title_full_unstemmed Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
title_short Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through VEGFA/ERK1/2/NF-κB signaling pathways
title_sort platelet microparticles containing mir 4306 inhibits human monocyte derived macrophages migration through vegfa erk1 2 nf κb signaling pathways
topic platelet
microparticles
mir-4306
vascular endothelial growth factor a
coronary artery disease
url http://dx.doi.org/10.1080/10641963.2018.1510941
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