<?xml version="1.0"?>
<Articles JournalTitle="Iranian Journal of Public Health">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Iranian Journal of Public Health</JournalTitle>
      <Issn>2251-6085</Issn>
      <Volume>52</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2023</Year>
        <Month>03</Month>
        <Day>02</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Serum Exosome-Derived MiR-7 Exacerbates Chronic Obstructive  Pulmonary Disease by Regulating Macrophage Differentiation</title>
    <FirstPage>563</FirstPage>
    <LastPage>574</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Yiming</FirstName>
        <LastName>Jiang</LastName>
        <affiliation locale="en_US">Department of Emergency, The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, 213003, China</affiliation>
      </Author>
      <Author>
        <FirstName>Jinhai</FirstName>
        <LastName>Wang</LastName>
        <affiliation locale="en_US">Department of Emergency, The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, 213003, China</affiliation>
      </Author>
      <Author>
        <FirstName>He</FirstName>
        <LastName>Zhang</LastName>
        <affiliation locale="en_US">Department of Emergency, The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, 213003, China</affiliation>
      </Author>
      <Author>
        <FirstName>Yeping</FirstName>
        <LastName>Min</LastName>
        <affiliation locale="en_US">Department of Emergency, The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, 213003, China</affiliation>
      </Author>
      <Author>
        <FirstName>Tijun</FirstName>
        <LastName>Gu</LastName>
        <affiliation locale="en_US">Department of Emergency, The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, 213003, China</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2022</Year>
        <Month>08</Month>
        <Day>19</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2022</Year>
        <Month>12</Month>
        <Day>18</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Background: Polarization of macrophages and miR-7 have been reported to greatly influence the progress of chronic obstructive pulmonary disease (COPD). However, the interaction is unclear. We aimed to investigate the role of miR-7 in the serum exosome of COPD, thus further revealing the underlying mechanism of COPD.
&#xD;

Methods: The study was conducted in 2022 in The Affiliated Changzhou No.2 People&#x2019;s Hospital of Nanjing Medical University, Changzhou, China. COPD mouse model was established. Macrophages were sorted by flow cytometry assay. ELISA kits were used to detect the levels of TNF-&#x3B1; and IL-6. Exosomes were identified by confocal microscopy and PKH67 staining. RT-qPCR and western blot assay were performed to determine the mRNA and protein expressions. H&amp;E staining assay was used to assess the tissue injury. CCK-8 assay was applied to evaluate cell viability. Luciferase reporter assay was used to confirm the binding between PIM1 and miR-7.&#xA0;
&#xD;

Results: The exosomes derived from the COPD mice serum exerted high level of miR-7, which induced M1 differentiation of macrophages and increased the secretion of proinflammatory factors in vivo and in vitro. The effects of exosomes from COPD mice could be inhibited by miR-7 inhibitor. Bioinformatic prediction, luciferase reporter assay, and western blot assay showed an interaction between miR-7 and PIM1. Further examination showed that miR-7 regulated macrophage activation and differentiation to M1 via PIM1 in vitro.
&#xD;

Conclusions: miR-7 from serum exosomes might exacerbate COPD by stimulating macrophage differentiation to M1, supplying a potential therapeutic target for COPD treatment.
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&#xA0;</abstract>
    <web_url>https://ijph.tums.ac.ir/index.php/ijph/article/view/29596</web_url>
    <pdf_url>https://ijph.tums.ac.ir/index.php/ijph/article/download/29596/7883</pdf_url>
  </Article>
</Articles>
