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Circulating myocardial microRNAs from infarcted hearts are carried in exosomes and mobilise bone marrow progenitor cells

Min Cheng (), Junjie Yang, Xiaoqi Zhao, Eric Zhang, Qiutang Zeng, Yang Yu, Liu Yang, Bangwei Wu, Guiwen Yi, Xiaobo Mao, Kai Huang, Nianguo Dong, Min Xie, Nita A. Limdi, Sumanth D. Prabhu, Jianyi Zhang and Gangjian Qin ()
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Min Cheng: Huazhong University of Science and Technology
Junjie Yang: University of Alabama at Birmingham, School of Medicine and School of Engineering
Xiaoqi Zhao: Huazhong University of Science and Technology
Eric Zhang: University of Alabama at Birmingham, School of Medicine and School of Engineering
Qiutang Zeng: Huazhong University of Science and Technology
Yang Yu: University of Alabama at Birmingham, School of Medicine and School of Engineering
Liu Yang: Huazhong University of Science and Technology
Bangwei Wu: Fudan University
Guiwen Yi: Huazhong University of Science and Technology
Xiaobo Mao: Huazhong University of Science and Technology
Kai Huang: Huazhong University of Science and Technology
Nianguo Dong: Huazhong University of Science and Technology
Min Xie: University of Alabama at Birmingham, School of Medicine
Nita A. Limdi: University of Alabama at Birmingham, School of Medicine
Sumanth D. Prabhu: University of Alabama at Birmingham, School of Medicine
Jianyi Zhang: University of Alabama at Birmingham, School of Medicine and School of Engineering
Gangjian Qin: University of Alabama at Birmingham, School of Medicine and School of Engineering

Nature Communications, 2019, vol. 10, issue 1, 1-9

Abstract: Abstract Myocardial microRNAs (myo-miRs) are released into the circulation after acute myocardial infarction (AMI). How they impact remote organs is however largely unknown. Here we show that circulating myo-miRs are carried in exosomes and mediate functional crosstalk between the ischemic heart and the bone marrow (BM). In mice, we find that AMI is accompanied by an increase in circulating levels of myo-miRs, with miR-1, 208, and 499 predominantly in circulating exosomes and miR-133 in the non-exosomal component. Myo-miRs are imported selectively to peripheral organs and preferentially to the BM. Exosomes mediate the transfer of myo-miRs to BM mononuclear cells (MNCs), where myo-miRs downregulate CXCR4 expression. Injection of exosomes isolated from AMI mice into wild-type mice downregulates CXCR4 expression in BM-MNCs and increases the number of circulating progenitor cells. Thus, we propose that myo-miRs carried in circulating exosomes allow a systemic response to cardiac injury that may be leveraged for cardiac repair.

Date: 2019
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08895-7

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DOI: 10.1038/s41467-019-08895-7

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