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.

Dublin Core

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  <dc:creator>Doeppner, Thorsten R.</dc:creator>
  <dc:creator>Doehring, Maria</dc:creator>
  <dc:creator>Kaltwasser, Britta</dc:creator>
  <dc:creator>Majid, Arshad</dc:creator>
  <dc:creator>Lin, Fengyan</dc:creator>
  <dc:creator>Bahr, Mathias</dc:creator>
  <dc:creator>Kilic, Ertugrul</dc:creator>
  <dc:creator>Hermann, Dirk M.</dc:creator>
  <dc:date>2017-01-01</dc:date>
  <dc:description>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.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/51479</dc:identifier>
  <dc:identifier>oai:zenodo.org:51479</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>MOLECULAR NEUROBIOLOGY 54(8) 6061-6073</dc:source>
  <dc:title>Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
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