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      <source-app name="Horizon">Horizon</source-app>
      <rec-number>1</rec-number>
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      <ref-type name="Journal Article">17</ref-type>
      <work-type>ACL : Articles dans des revues avec comité de lecture répertoriées par l'AERES</work-type>
      <contributors>
        <authors>
          <author>
            <style face="normal" font="default" size="100%">Abdallah, F.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Henriet, E.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Suet, A.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Arar, A.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Clemencon, R.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Malinge, J. M.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Lecellier, Gael</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Baril, P.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Pichon, C.</style>
          </author>
        </authors>
      </contributors>
      <titles>
        <title>miR-21-3p/IL-22 axes are major drivers of psoriasis pathogenesis by modulating keratinocytes proliferation-survival balance and inflammatory response</title>
        <secondary-title>Cells</secondary-title>
      </titles>
      <pages>2547 [22 p.]</pages>
      <keywords>
        <keyword>IL-22</keyword>
        <keyword>miR-21-5p</keyword>
        <keyword>miR-21-3p</keyword>
        <keyword>keratinocytes</keyword>
        <keyword>psoriasis</keyword>
        <keyword>proliferation</keyword>
      </keywords>
      <dates>
        <year>2021</year>
      </dates>
      <call-num>fdi:010083303</call-num>
      <language>ENG</language>
      <periodical>
        <full-title>Cells</full-title>
      </periodical>
      <accession-num>ISI:000713178400001</accession-num>
      <number>10</number>
      <electronic-resource-num>10.3390/cells10102547</electronic-resource-num>
      <urls>
        <related-urls>
          <url>https://www.documentation.ird.fr/hor/fdi:010083303</url>
        </related-urls>
        <pdf-urls>
          <url>https://horizon.documentation.ird.fr/exl-doc/pleins_textes/2021-12/010083303.pdf</url>
        </pdf-urls>
      </urls>
      <volume>10</volume>
      <remote-database-provider>Horizon (IRD)</remote-database-provider>
      <abstract>Psoriasis is a chronic inflammatory skin disease that is mediated by complex crosstalk between immune cells and keratinocytes (KCs). Emerging studies have showed a specific psoriatic microRNAs signature, in which miR-21 is one of the most upregulated and dynamic miRNAs. In this study, we focused our investigations on the passenger miR-21-3p strand, which is poorly studied in skin and in psoriasis pathogenesis. Here, we showed the upregulation of miR-21-3p in an IMQ-induced psoriasiform mouse model. This upregulation was correlated with IL-22 expression and functionality, both in vitro and in vivo, and it occurred via STAT3 and NF-kappa B signaling. We identified a network of differentially expressed genes involved in abnormal proliferation control and immune regulatory genes implicated in the molecular pathogenesis of psoriasis in response to miR-21-3p overexpression in KCs. These results were confirmed by functional assays that validated the proliferative potential of miR-21-3p. All these findings highlight the importance of miR-21-3p, an underestimated miRNA, in psoriasis and provide novel molecular targets for therapeutic purposes.&lt;/p&gt;</abstract>
      <custom6>050 ; 020</custom6>
      <custom1>UR250</custom1>
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