1 Ocak 2019 Dergi makalesi Açık Erişim

Icli, Basak; Wu, Winona; Ozdemir, Denizhan; Li, Hao; Cheng, Henry S.; Haemmig, Stefan; Liu, Xin; Giatsidis, Giorgio; Avci, Seyma Nazli; Lee, Nathan; Guimaraes, Raphael Boesch; Manica, Andre; Marchini, Julio F.; Rynning, Stein Erik; Risnes, Ivar; Hollan, Ivana; Croce, Kevin; Yang, Xianbin; Orgill, Dennis P.; Feinberg, Mark W.

DataCite XML

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/112080</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>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>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>Cheng, Henry S.</creatorName>
      <givenName>Henry S.</givenName>
      <familyName>Cheng</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>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>Liu, Xin</creatorName>
      <givenName>Xin</givenName>
      <familyName>Liu</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>Giatsidis, Giorgio</creatorName>
      <givenName>Giorgio</givenName>
      <familyName>Giatsidis</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Div Plast Surg, Dept Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Avci, Seyma Nazli</creatorName>
      <givenName>Seyma Nazli</givenName>
      <familyName>Avci</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>Lee, Nathan</creatorName>
      <givenName>Nathan</givenName>
      <familyName>Lee</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 Sul, 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 Sul, 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, Inst Heart, Sao Paulo, Brazil</affiliation>
    </creator>
    <creator>
      <creatorName>Rynning, Stein Erik</creatorName>
      <givenName>Stein Erik</givenName>
      <familyName>Rynning</familyName>
      <affiliation>LHL Hosp Gardermoen, Dept Cardiac Surg, Jessheim, Norway</affiliation>
    </creator>
    <creator>
      <creatorName>Risnes, Ivar</creatorName>
      <givenName>Ivar</givenName>
      <familyName>Risnes</familyName>
      <affiliation>LHL Hosp Gardermoen, Dept Cardiac Surg, Jessheim, Norway</affiliation>
    </creator>
    <creator>
      <creatorName>Hollan, Ivana</creatorName>
      <givenName>Ivana</givenName>
      <familyName>Hollan</familyName>
      <affiliation>Lillehammer Hosp Rheumat Dis, Dept Rheumatol, Lillehammer, Norway</affiliation>
    </creator>
    <creator>
      <creatorName>Croce, Kevin</creatorName>
      <givenName>Kevin</givenName>
      <familyName>Croce</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>Yang, Xianbin</creatorName>
      <givenName>Xianbin</givenName>
      <familyName>Yang</familyName>
      <affiliation>AM Biotechnol LLC, Houston, TX USA</affiliation>
    </creator>
    <creator>
      <creatorName>Orgill, Dennis P.</creatorName>
      <givenName>Dennis P.</givenName>
      <familyName>Orgill</familyName>
      <affiliation>Harvard Med Sch, Brigham &amp; Womens Hosp, Div Plast Surg, Dept 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>Microrna-615-5P Regulates Angiogenesis And Tissue Repair By Targeting Akt/Enos (Protein Kinase B/Endothelial Nitric Oxide Synthase) Signaling In Endothelial Cells</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2019</publicationYear>
  <dates>
    <date dateType="Issued">2019-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/112080</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1161/ATVBAHA.119.312726</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">Objective- In response to tissue injury, the appropriate progression of events in angiogenesis is controlled by a careful balance between pro and antiangiogenic factors. We aimed to identify and characterize microRNAs that regulate angiogenesis in response to tissue injury. Approach and Results- We show that in response to tissue injury, microRNA-615-5p (miR-615-5p) is rapidly induced and serves as an antiangiogenic microRNA by targeting endothelial cell VEGF (vascular endothelial growth factor)-AKT (protein kinase B)/eNOS (endothelial nitric oxide synthase) signaling in vitro and in vivo. MiR-615-5p expression is increased in wounds of diabetic db/db mice, in plasma of human subjects with acute coronary syndromes, and in plasma and skin of human subjects with diabetes mellitus. Ectopic expression of miR-615-5p markedly inhibited endothelial cell proliferation, migration, network tube formation in Matrigel, and the release of nitric oxide, whereas miR-615-5p neutralization had the opposite effects. Mechanistic studies using transcriptomic profiling, bioinformatics, 3 ' untranslated region reporter and microribonucleoprotein immunoprecipitation assays, and small interfering RNA dependency studies demonstrate that miR-615-5p inhibits the VEGF-AKT/eNOS signaling pathway in endothelial cells by targeting IGF2 (insulin-like growth factor 2) and RASSF2 (Ras-associating domain family member 2). Local delivery of miR-615-5p inhibitors, markedly increased angiogenesis, granulation tissue thickness, and wound closure rates in db/db mice, whereas miR-615-5p mimics impaired these effects. Systemic miR-615-5p neutralization improved skeletal muscle perfusion and angiogenesis after hindlimb ischemia in db/db mice. Finally, modulation of miR-615-5p expression dynamically regulated VEGF-induced AKT signaling and angiogenesis in human skin organoids as a model of tissue injury. Conclusions- These findings establish miR-615-5p as an inhibitor of VEGF-AKT/eNOS-mediated endothelial cell angiogenic responses and that manipulating miR-615-5p expression could provide a new target for angiogenic therapy in response to tissue injury.</description>
  </descriptions>
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