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<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>50</Volume>
      <Issue>7</Issue>
      <PubDate PubStatus="epublish">
        <Year>2021</Year>
        <Month>07</Month>
        <Day>01</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Association of CCL5 rs2107538, and CCL2 rs3760396 Gene Polymorphisms with the Risk of Cardiovascular Disease</title>
    <FirstPage>1436</FirstPage>
    <LastPage>1444</LastPage>
    <AuthorList>
      <Author>
        <FirstName>Naser</FirstName>
        <LastName>Mohtavinejad</LastName>
        <affiliation locale="en_US">Department of Radiopharmacy, School of Pharmacy, University of Baqiyatallah, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Alireza</FirstName>
        <LastName>Nakhaee</LastName>
        <affiliation locale="en_US">Department of Clinical Biochemistry, School of Medicine, University of Zahedan, Zahedan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Honey</FirstName>
        <LastName>Harati</LastName>
        <affiliation locale="en_US">Department of Cardiology, School of Medicine, University of Zahedan, Zahedan, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Nazila</FirstName>
        <LastName>Gholipour</LastName>
        <affiliation locale="en_US">Department of Radiopharmacy, School of Pharmacy, University of Baqiyatallah, Tehran, Iran</affiliation>
      </Author>
      <Author>
        <FirstName>Yavar</FirstName>
        <LastName>Mahmoodzade</LastName>
        <affiliation locale="en_US">Department of Clinical Biochemistry, School of Medicine, University of Ardabil, Ardabil, Iran</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>09</Month>
        <Day>08</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2020</Year>
        <Month>05</Month>
        <Day>12</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Background: Chemokines are proinflammatory cytokines that play key roles in development of cardiovascular diseases (CVD). Chemokine-induced recruitment of peripheral leucocytes to tissues is a crucial step in the CVD progression. CC chemokines ligand 5, 2 (CCL5 and CCL2), have been characterized as emerging inflammatory biomarkers of atherosclerotic CVD. The aim of this study was to find out whether genetic polymorphisms of CCL5 -403 G&gt;A (rs2107538) and CCL2 &#x2013;927 G&gt;C, (rs3760396) were associated with the risk of CVD.
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Methods: In this case-control study, 500 Iranian individuals including 250 CVD patients and 250 healthy subjects as the control group participated in 2017. Genotyping of CCL5 -403 G&gt;A and CCL2 &#x2013;927 G&gt;C polymorphisms were executed using Tetra-ARMS PCR method.
&#xD;

Results: At genotypic level both CCL5 -403 G&gt;A and CCL2 &#x2013;927 G&gt;C polymorphisms were not associated with the risk of CVD (P&gt;0.05), even after adjustment by age, sex, race, and history of hypertension, DM and smoking. However, the CCL2 &#x2013;927 C allele was associated with an increased risk of CVD (OR=1.42, P=0.050) with a higher prevalence in CVD patient than in controls (17% vs. 12%). Moreover, the haplotype analysis revealed that CCL5/CCL2 haplotype (G/C) was a risk factor for CVD (OR=2.13, P=0.001), and that carriers of this haplotype were at 2.13-fold higher risk of CVD than subjects with G/G haplotype.
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Conclusion: CCL2 &#x2013;927 C variant and CCL5/CCL2 haplotype (G/C) were associated with susceptibility to CVD, and were risk factors for CVD in our population but more studies with large sample size are recommended.</abstract>
    <web_url>https://ijph.tums.ac.ir/index.php/ijph/article/view/18321</web_url>
    <pdf_url>https://ijph.tums.ac.ir/index.php/ijph/article/download/18321/7289</pdf_url>
  </Article>
</Articles>
