1 Ocak 2020 Dergi makalesi Açık Erişim

Icli, Basak; Li, Hao; Perez-Cremades, Daniel; Wu, Winona; Ozdemir, Denizhan; Haemmig, Stefan; Guimaraes, Raphael Boesch; Manica, Andre; Marchini, Julio F.; Orgill, Dennis P.; Feinberg, Mark W.

DataCite XML

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/8135</identifier>
  <creators>
    <creator>
      <creatorName>Icli, Basak</creatorName>
      <givenName>Basak</givenName>
      <familyName>Icli</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Med, Cardiovasc Div, 77 Ave Louis Pasteur,NRB-742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Li, Hao</creatorName>
      <givenName>Hao</givenName>
      <familyName>Li</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Med, Cardiovasc Div, 77 Ave Louis Pasteur,NRB-742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Perez-Cremades, Daniel</creatorName>
      <givenName>Daniel</givenName>
      <familyName>Perez-Cremades</familyName>
    </creator>
    <creator>
      <creatorName>Wu, Winona</creatorName>
      <givenName>Winona</givenName>
      <familyName>Wu</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Med, Cardiovasc Div, 77 Ave Louis Pasteur,NRB-742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Ozdemir, Denizhan</creatorName>
      <givenName>Denizhan</givenName>
      <familyName>Ozdemir</familyName>
    </creator>
    <creator>
      <creatorName>Haemmig, Stefan</creatorName>
      <givenName>Stefan</givenName>
      <familyName>Haemmig</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Med, Cardiovasc Div, 77 Ave Louis Pasteur,NRB-742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Guimaraes, Raphael Boesch</creatorName>
      <givenName>Raphael Boesch</givenName>
      <familyName>Guimaraes</familyName>
      <affiliation>Fundacao Univ Cardiol ICFUC, Inst Cardiol Rio Grande, Porto Alegre, RS, Brazil</affiliation>
    </creator>
    <creator>
      <creatorName>Manica, Andre</creatorName>
      <givenName>Andre</givenName>
      <familyName>Manica</familyName>
      <affiliation>Fundacao Univ Cardiol ICFUC, Inst Cardiol Rio Grande, Porto Alegre, RS, Brazil</affiliation>
    </creator>
    <creator>
      <creatorName>Marchini, Julio F.</creatorName>
      <givenName>Julio F.</givenName>
      <familyName>Marchini</familyName>
      <affiliation>Univ Sao Paulo, Med Sch, Heart Inst, Sao Paulo, SP, Brazil</affiliation>
    </creator>
    <creator>
      <creatorName>Orgill, Dennis P.</creatorName>
      <givenName>Dennis P.</givenName>
      <familyName>Orgill</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Surg, Div Plast Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Feinberg, Mark W.</creatorName>
      <givenName>Mark W.</givenName>
      <familyName>Feinberg</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Dept Med, Cardiovasc Div, 77 Ave Louis Pasteur,NRB-742F, Boston, MA 02115 USA</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Mir-4674 Regulates Angiogenesis In Tissue Injury By Targeting P38K Signaling In Endothelial Cells</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2020</publicationYear>
  <dates>
    <date dateType="Issued">2020-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/8135</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1152/ajpcell.00542.2019</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">Neoangiogenesis is critical for tissue repair in response to injury such as myocardial ischemia or dermal wound healing. MicroRNAs are small noncoding RNAs and important regulators of angiogenesis under physiological and pathological disease states. Therefore, identification of microRNAs that may restore impaired angiogenesis in response to tissue injury may provide new targets for therapy. Using a microRNA microarray profiling approach, we identified a human-specific microRNA, miR-4674, that was significantly decreased in patients after myocardial tissue injury and had an endothelial cell (EC)-enriched expression pattern. Functionally, overexpression of miR-4674 markedly attenuated EC proliferation, migration, network tube formation, and spheroid sprouting, whereas blockade of miR-4674 had the opposite effects. Transcriptomic profiling, gene set enrichment analyses, bioinformatics, 3'-untranslated region (3'-UTR) reporter and microribonucleoprotein immunoprecipitation (miRNP-IP) assays, and small interfering RNA dependency studies revealed that miR-4674 regulates VEGF stimulated-p38 mitogen-activated protein kinase (MAPK) signaling and targets interleukin 1 receptor-associated kinase 1 (Irak1) and BICD cargo adaptor 2 (Bicd2) in ECs. Furthermore, Irak1 and Bicd2 were necessary for miR-4674-driven EC proliferation and migration. Finally, neutralization of miR-4674 increased angiogenesis, Irak1 and Bicd2 expression, and p38 phosphorylation in human skin organoids as a model of tissue injury. Collectively, targeting miR-4674 may provide a novel therapeutic target for tissue repair in pathological disease states associated with impaired angiogenesis.</description>
  </descriptions>
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