<?xml version="1.0"?>
<Articles JournalTitle="Acta Medica Iranica">
  <Article>
    <Journal>
      <PublisherName>Tehran University of Medical Sciences</PublisherName>
      <JournalTitle>Acta Medica Iranica</JournalTitle>
      <Issn>0044-6025</Issn>
      <Volume>52</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="epublish">
        <Year>2014</Year>
        <Month>03</Month>
        <Day>15</Day>
      </PubDate>
    </Journal>
    <title locale="en_US">Effect of Eicosapentaenoic Acid on the Expression of ABCG1 Gene in the Human Monocyte THP-1 Cells</title>
    <FirstPage>176</FirstPage>
    <LastPage>181</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mostafa</FirstName>
        <LastName>Moradi Sarabi</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Mahmood</FirstName>
        <LastName>Doosti</LastName>
        <affiliation locale="en_US">Department of Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Nahid</FirstName>
        <LastName>Einollahi</LastName>
        <affiliation locale="en_US">Department of Clinical Laboratory Sciences, Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Soroush Shahryar</FirstName>
        <LastName>Hesami</LastName>
        <affiliation locale="en_US">Department of Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.</affiliation>
      </Author>
      <Author>
        <FirstName>Nasrin</FirstName>
        <LastName>Dashti</LastName>
        <affiliation locale="en_US">Department of Clinical Laboratory Sciences, Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.</affiliation>
      </Author>
    </AuthorList>
    <History>
      <PubDate PubStatus="received">
        <Year>2015</Year>
        <Month>10</Month>
        <Day>11</Day>
      </PubDate>
    </History>
    <abstract locale="en_US">Cardiovascular disease (CVD) is the leading cause of death and disability in developed countries. Atherosclerosis is the major cause of CVD, accounting for about half of the attributed deaths. Cholesterol homeostasis is one of the most important factors in atherosclerosis. ATP-Binding cassette transporters cholesterol. Omega (&#x3C9;) 3 fatty acids are important ligands for regulation of ABC transporters such as ABCG1. Concern has been raised that the low absolute intakes of EPA and high ratios of &#x3C9;-6 polyunsaturated fatty acids (&#x3C9;-6 PUFA) to EPA may predispose some individuals to CVD. Eicosapentaenoic acid (EPA) is the most abundant &#x3C9;3 fatty acid in the diet. The objective of this study was to evaluate the effect of different concentrations of EPA on the expression of ABCG1 gene in the human monocyte THP-1 cells. In this study, THP-1 cells were cultured in RPMI 1640 medium, THP-1 monocytes were then differentiated to macrophages with PMA (phorbol myristic acid) and stimulated with 50, 75 and 100 &#x3BC;M of EPA for 24 h at 37&#xB0;C. We examined the effects of EPA treatment on the expression of ABCG1 gene using Quantitative Real time RT-PCR (qRT-PCR). Our results, indicate that ABCG1 mRNA expression was significantly reduced by 50, 75 and 100 &#x3BC;M EPA fatty acid treatments as compared to the control cells (&#x440; = 0.009, &#x440; &lt; 0.001 and &#x440; = 0.002, respectively). These results suggest that polyunsaturated fatty acids (PUFAs) such as EPA have an effect on the cholesterol homeostasis in macrophages, and they can change the expression of ABCG1 gene. It seems that EPA has different effects on gene expression and lipid metabolism.</abstract>
    <web_url>https://acta.tums.ac.ir/index.php/acta/article/view/4685</web_url>
    <pdf_url>https://acta.tums.ac.ir/index.php/acta/article/download/4685/4320</pdf_url>
  </Article>
</Articles>
