1 Ocak 2016 Dergi makalesi Açık Erişim

Icli, Basak; Nabzdyk, Christoph S.; Lujan-Hernandez, Jorge; Cahill, Meghan; Auster, Michael E.; Wara, A. K. M.; Sun, Xinghui; Ozdemir, Denizhan; Giatsidis, Giorgio; Orgill, Dennis P.; Feinberg, Mark W.

DataCite XML

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/59271</identifier>
  <creators>
    <creator>
      <creatorName>Icli, Basak</creatorName>
      <givenName>Basak</givenName>
      <familyName>Icli</familyName>
      <affiliation>Harvard Univ, Sch Med, Brigham &amp; Womens Hosp, Dept Med,Cardiovasc Div, 77 Ave Louis Pasteur,NRB 742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Nabzdyk, Christoph S.</creatorName>
      <givenName>Christoph S.</givenName>
      <familyName>Nabzdyk</familyName>
      <affiliation>Harvard Univ, Brigham &amp; Womens Hosp, Sch Med, Dept Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Lujan-Hernandez, Jorge</creatorName>
      <givenName>Jorge</givenName>
      <familyName>Lujan-Hernandez</familyName>
      <affiliation>Harvard Univ, Brigham &amp; Womens Hosp, Sch Med, Dept Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Cahill, Meghan</creatorName>
      <givenName>Meghan</givenName>
      <familyName>Cahill</familyName>
      <affiliation>Harvard Univ, Sch Med, Brigham &amp; Womens Hosp, Dept Med,Cardiovasc Div, 77 Ave Louis Pasteur,NRB 742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Auster, Michael E.</creatorName>
      <givenName>Michael E.</givenName>
      <familyName>Auster</familyName>
      <affiliation>Beth Israel Deaconess Med Ctr, Dept Surg, 330 Brookline Ave, Boston, MA 02215 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Wara, A. K. M.</creatorName>
      <givenName>A. K. M.</givenName>
      <familyName>Wara</familyName>
      <affiliation>Harvard Univ, Sch Med, Brigham &amp; Womens Hosp, Dept Med,Cardiovasc Div, 77 Ave Louis Pasteur,NRB 742F, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Sun, Xinghui</creatorName>
      <givenName>Xinghui</givenName>
      <familyName>Sun</familyName>
      <affiliation>Harvard Univ, Sch Med, 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>
      <affiliation>Harvard Univ, Sch Med, 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 Univ, Brigham &amp; Womens Hosp, Sch Med, Dept Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Orgill, Dennis P.</creatorName>
      <givenName>Dennis P.</givenName>
      <familyName>Orgill</familyName>
      <affiliation>Harvard Univ, Brigham &amp; Womens Hosp, Sch Med, Dept Surg, Boston, MA 02115 USA</affiliation>
    </creator>
    <creator>
      <creatorName>Feinberg, Mark W.</creatorName>
      <givenName>Mark W.</givenName>
      <familyName>Feinberg</familyName>
      <affiliation>Harvard Univ, Sch Med, Brigham &amp; Womens Hosp, Dept Med,Cardiovasc Div, 77 Ave Louis Pasteur,NRB 742F, Boston, MA 02115 USA</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Regulation Of Impaired Angiogenesis In Diabetic Dermal Wound Healing By Microrna-26A</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2016</publicationYear>
  <dates>
    <date dateType="Issued">2016-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/59271</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.yjmcc.2016.01.007</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">Wound healing is a physiological reparative response to injury and a well-orchestrated process that involves hemostasis, cellular migration, proliferation, angiogenesis, extracellular matrix deposition, and wound contraction and re-epithelialization. However, patients with type 2 diabetes mellitus (T2D) are frequently afflicted with impaired wound healing that progresses into chronic wounds or diabetic ulcers, and may lead to complications including limb amputation. Herein, we investigate the potential role of microRNA-26a (miR-26a) in a diabetic model of wound healing. Expression of miR-26a is rapidly induced in response to high glucose in endothelial cells (ECs). Punch skin biopsy wounding of db/db mice revealed increased expression of miR-26a (similar to 3.5-fold) four days post-wounding compared to that of WT mice. Local administration of a miR-26a inhibitor, LNA-anti-miR-26a, induced angiogenesis (up to similar to 80%), increased granulation tissue thickness (by 2.5-fold) and accelerated wound closure (53% after nine days) compared to scrambled anti-miR controls in db/db mice. These effects were independent of altered M1/M2 macrophage ratios. Mechanistically, inhibition of miR-26a increased its target gene SMAD1 in ECs nine days post-wounding of diabetic mice. In addition, high glucose reduced activity of the SMAD1-3'-UTR. Diabetic dermal wounds treated with LNA-anti-miR-26a had increased expression of ID1, a downstream modulator or SMAD1, and decreased expression of the cell cycle inhibitor p27. These findings establish miR-26a as an important regulator on the progression of skin wounds of diabetic mice by specifically regulating the angiogenic response after injury, and demonstrate that neutralization of miR-26a may serve as a novel approach for therapy. (C) 2016 Elsevier Ltd. All rights reserved.</description>
  </descriptions>
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