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Doeppner, Thorsten R.; Doehring, Maria; Kaltwasser, Britta; Majid, Arshad; Lin, Fengyan; Bahr, Mathias; Kilic, Ertugrul; Hermann, Dirk M.
{ "@context": "https://schema.org/", "@id": 51479, "@type": "ScholarlyArticle", "creator": [ { "@type": "Person", "name": "Doeppner, Thorsten R." }, { "@type": "Person", "affiliation": "Oberhavel Kliniken, Dept Internal Med, Oranienburg, Germany", "name": "Doehring, Maria" }, { "@type": "Person", "affiliation": "Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany", "name": "Kaltwasser, Britta" }, { "@type": "Person", "affiliation": "Univ Sheffield, Sheffield Inst Translat Neurosci, Sheffield, S Yorkshire, England", "name": "Majid, Arshad" }, { "@type": "Person", "affiliation": "Jilin Univ, Affiliated Hosp 1, Ctr Canc, Changchun, Jilin, Peoples R China", "name": "Lin, Fengyan" }, { "@type": "Person", "affiliation": "Univ Gottingen, Dept Neurol, Sch Med, Gottingen, Germany", "name": "Bahr, Mathias" }, { "@type": "Person", "affiliation": "Istanbul Medipol Univ, Regenerat & Restorat Med Res Ctr, Istanbul, Turkey", "name": "Kilic, Ertugrul" }, { "@type": "Person", "affiliation": "Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany", "name": "Hermann, Dirk M." } ], "datePublished": "2017-01-01", "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.", "headline": "Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation", "identifier": 51479, "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", "license": "http://www.opendefinition.org/licenses/cc-by", "name": "Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation", "url": "https://aperta.ulakbim.gov.tr/record/51479" }
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