CCL11 differentially affects post-stroke brain injury and neuroregeneration in mice depending on age

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dc.authorid0000-0001-6494-8923
dc.authorid0000-0002-1222-9211
dc.contributor.authorLieschke, Simone
dc.contributor.authorZechmeister, Bozena
dc.contributor.authorHaupt, Matteo
dc.contributor.authorZheng, Xuan
dc.contributor.authorJin, Fengyan
dc.contributor.authorHein, Katharina
dc.contributor.authorWeber, Martin S.
dc.contributor.authorHermann, Dirk M.
dc.contributor.authorBähr, Mathias
dc.contributor.authorKılıç, Ertuğrul
dc.contributor.authorDoeppner, Thorsten R.
dc.date.accessioned2020-03-05T09:12:29Z
dc.date.available2020-03-05T09:12:29Z
dc.date.issued2020
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalı
dc.description.abstractCCL11 has recently been shown to differentially affect cell survival under various pathological conditions including stroke. Indeed, CCL11 promotes neuroregeneration in neonatal stroke mice. The impact of CCL11 on the adult ischemic brain, however, remains elusive. We therefore studied the effect of ectopic CCL11 on both adolescent (six-week) and adult (six-month) C57BL6 mice exposed to stroke. Intraperitoneal application of CCL11 significantly aggravated acute brain injury in adult mice but not in adolescent mice. Likewise, post-stroke neurological recovery after four weeks was significantly impaired in adult mice whilst CCL11 was present. On the contrary, CCL11 stimulated gliogenesis and neurogenesis in adolescent mice. Flow cytometry analysis of blood and brain samples revealed a modification of inflammation by CCL11 at subacute stages of the disease. In adolescent mice, CCL11 enhances microglial cell, B and T lymphocyte migration towards the brain, whereas only the number of B lymphocytes is increased in the adult brain. Finally, the CCL11 inhibitor SB297006 significantly reversed the aforementioned effects. Our study, for the first time, demonstrates CCL11 to be a key player in mediating secondary cell injury under stroke conditions. Interfering with this pathway, as shown for SB297006, might thus be an interesting approach for future stroke treatment paradigms.
dc.identifier.citationLieschke, S., Zechmeister, B., Haupt, M., Zheng, X., Jin, F., Hein, K. ... Doeppner, T. R. (2020). CCL11 differentially affects post-stroke brain injury and neuroregeneration in mice depending on age. Cells, 9(1). https://doi.org/10.3390/cells9010066
dc.identifier.doi10.3390/cells9010066
dc.identifier.issn2073-4409
dc.identifier.issue1
dc.identifier.urihttps://doi.org/10.3390/cells9010066
dc.identifier.urihttps://hdl.handle.net/20.500.12511/4998
dc.identifier.volume9
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMDPI
dc.relation.ispartofCellsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsAttribution 4.0 International*
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subjectCerebral İschemia
dc.subjectCCL11
dc.subjectEotaxin-1
dc.subjectNeuroprotection
dc.subjectInflammation
dc.subjectStroke
dc.subjectNeuroregeneration
dc.titleCCL11 differentially affects post-stroke brain injury and neuroregeneration in mice depending on age
dc.typeArticle

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