1 Ocak 2017 Dergi makalesi Açık Erişim

Doeppner, Thorsten R.; Doehring, Maria; Kaltwasser, Britta; Majid, Arshad; Lin, Fengyan; Bahr, Mathias; Kilic, Ertugrul; Hermann, Dirk M.

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/51479</identifier>
  <creators>
    <creator>
      <creatorName>Doeppner, Thorsten R.</creatorName>
      <givenName>Thorsten R.</givenName>
      <familyName>Doeppner</familyName>
    </creator>
    <creator>
      <creatorName>Doehring, Maria</creatorName>
      <givenName>Maria</givenName>
      <familyName>Doehring</familyName>
      <affiliation>Oberhavel Kliniken, Dept Internal Med, Oranienburg, Germany</affiliation>
    </creator>
    <creator>
      <creatorName>Kaltwasser, Britta</creatorName>
      <givenName>Britta</givenName>
      <familyName>Kaltwasser</familyName>
      <affiliation>Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany</affiliation>
    </creator>
    <creator>
      <creatorName>Majid, Arshad</creatorName>
      <givenName>Arshad</givenName>
      <familyName>Majid</familyName>
      <affiliation>Univ Sheffield, Sheffield Inst Translat Neurosci, Sheffield, S Yorkshire, England</affiliation>
    </creator>
    <creator>
      <creatorName>Lin, Fengyan</creatorName>
      <givenName>Fengyan</givenName>
      <familyName>Lin</familyName>
      <affiliation>Jilin Univ, Affiliated Hosp 1, Ctr Canc, Changchun, Jilin, Peoples R China</affiliation>
    </creator>
    <creator>
      <creatorName>Bahr, Mathias</creatorName>
      <givenName>Mathias</givenName>
      <familyName>Bahr</familyName>
      <affiliation>Univ Gottingen, Dept Neurol, Sch Med, Gottingen, Germany</affiliation>
    </creator>
    <creator>
      <creatorName>Kilic, Ertugrul</creatorName>
      <givenName>Ertugrul</givenName>
      <familyName>Kilic</familyName>
      <affiliation>Istanbul Medipol Univ, Regenerat &amp; Restorat Med Res Ctr, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Hermann, Dirk M.</creatorName>
      <givenName>Dirk M.</givenName>
      <familyName>Hermann</familyName>
      <affiliation>Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection Via Hsp70-Mediated Proteasome Inhibition And Facilitates Neural Progenitor Cell Transplantation</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2017</publicationYear>
  <dates>
    <date dateType="Issued">2017-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/51479</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1007/s12035-016-0137-3</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">In view of the failure of pharmacological therapies, alternative strategies promoting post-stroke brain repair are needed. Post-conditioning is a potentially promising therapeutic strategy, which induces acute neuroprotection against ischemic injury. To elucidate longer lasting actions of ischemic post-conditioning, mice were exposed to a 60-min stroke and post-conditioning by an additional 10-min stroke that was induced 10 min after reperfusion onset. Animals were sacrificed 24 h or 28 days post-stroke. Post-conditioning reduced infarct volume and neurological deficits 24 h poststroke, enhancing blood-brain barrier integrity, reducing brain leukocyte infiltration, and reducing oxidative stress. On the molecular level, post-conditioning yielded increased Hsp70 expression, whereas nuclear factor (NF)-kappa B and proteasome activities were decreased. Reduced infarct volume and proteasome inhibition were reversed by Hsp70 knockdown, suggesting a critical role of the Hsp70 proteasome pathway in ischemic post-conditioning. The survival-promoting effects of ischemic post-conditioning, however, were not sustainable as neuroprotection and neurological recovery were lost 28 days post-stroke. Although angioneurogenesis was not increased by post-conditioning, the favorable extracellular milieu facilitated intracerebral transplantation of neural progenitor cells 6 h post-stroke, resulting in persisted neuroprotection and neurological recovery. Thus, post-conditioning might support brain repair processes, but in view of its transient, neuroprotection is unlikely useful as stroke therapy in its current form.</description>
  </descriptions>
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