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...
Main Authors: | , , , , , , , , , |
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2019-07-01
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Series: | Clinical and Experimental Hypertension |
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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. |
first_indexed | 2024-03-11T23:43:40Z |
format | Article |
id | doaj.art-166af5bc18444d7eb172371888a667bc |
institution | Directory Open Access Journal |
issn | 1064-1963 1525-6006 |
language | English |
last_indexed | 2024-03-11T23:43:40Z |
publishDate | 2019-07-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Clinical and Experimental Hypertension |
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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