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@ARTICLE{Rogall:849944,
author = {Rogall, Rebecca and Rabenstein, Monika and Vay, Sabine and
Bach, Annika and Pikhovych, Anton and Baermann, Johannes and
Hoehn, Mathias and Couillard-Despres, Sébastien and Fink,
Gereon Rudolf and Schroeter, Michael and Rueger, Maria
Adele},
title = {{B}ioluminescence imaging visualizes osteopontin-induced
neurogenesis and neuroblast migration in the mouse brain
after stroke},
journal = {Stem cell research $\&$ therapy},
volume = {9},
issn = {1757-6512},
address = {London},
publisher = {BioMed Central},
reportid = {FZJ-2018-04039},
pages = {183},
year = {2018},
abstract = {BackgroundOsteopontin (OPN), an acidic phosphoglycoprotein,
is upregulated in the brain after cerebral ischemia. We
previously reported that OPN supports migration, survival,
and proliferation of neural stem cells (NSC) in primary cell
culture, as well as their differentiation into neurons. We
here analyzed the effects of OPN on neuroblasts in vivo in
the context of cerebral ischemia.MethodsTransgenic mice
expressing luciferase under the control of the
neuroblast-specific doublecortin (DCX)-promoter, allowing
visualization of neuroblasts in vivo using bioluminescence
imaging (BLI), were injected with OPN
intracerebroventricularly while control mice were injected
with vehicle buffer. To assess the effects of OPN after
ischemia, additional mice were subjected to photothrombosis
and injected with either OPN or vehicle.ResultsOPN enhanced
the migration of neuroblasts both in the healthy brain and
after ischemia, as quantified by BLI in vivo. Moreover, the
number of neural progenitors was increased following OPN
treatment, with the maximum effect on the second day after
OPN injection into the healthy brain, and 14 days after OPN
injection following ischemia. After ischemia, OPN
quantitatively promoted the endogenous, ischemia-induced
neuroblast expansion, and additionally recruited progenitors
from the contralateral hemisphere.ConclusionsOur results
strongly suggest that OPN constitutes a promising substance
for the targeted activation of neurogenesis in ischemic
stroke.},
cin = {INM-3},
ddc = {570},
cid = {I:(DE-Juel1)INM-3-20090406},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29973246},
UT = {WOS:000437301100007},
doi = {10.1186/s13287-018-0927-9},
url = {https://juser.fz-juelich.de/record/849944},
}