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@ARTICLE{Rabenstein:200991,
author = {Rabenstein, M. and Hucklenbroich, J. and Willuweit, Antje
and Ladwig, A. and Fink, Gereon Rudolf and Schroeter, M. and
Langen, Karl-Josef and Rueger, M. A.},
title = {{O}steopontin mediates survival, proliferation and
migration of neural stem cells through the chemokine
receptor {CXCR}4},
journal = {Stem cell research $\&$ therapy},
volume = {6},
number = {1},
issn = {1757-6512},
address = {London},
publisher = {BioMed Central},
reportid = {FZJ-2015-03310},
pages = {article 99},
year = {2015},
abstract = {IntroductionOsteopontin (OPN) is a phosphoglycoprotein with
important roles in tissue homeostasis, wound healing, immune
regulation, and stress responses. It is expressed
constitutively in the brain and upregulated during
neuroinflammatory responses; for example, after focal
cerebral ischemia. To date, its effects on neural stem cells
(NSC) remain to be elucidated and are, accordingly, the
subject of this study.MethodPrimary fetal rat NSC were
cultured as homogenous monolayers and treated with different
concentrations of OPN. Fundamental properties of NSC were
assessed following OPN exposure, including proliferative
activity, survival under oxidative stress, migration, and
differentiation potential. To elucidate a putative action of
OPN via the CXC chemokine receptor type 4 (CXCR4), the
latter was blocked with AMD3100. To investigate effects of
OPN on endogenous NSC in vivo, recombinant OPN was injected
into the brain of healthy adult rats as well as rats
subjected to focal cerebral ischemia. Effects of OPN on NSC
proliferation and neurogenesis in the subventricular zone
were studied immunohistochemically.ResultsOPN
dose-dependently increased the number of NSC in vitro. As
hypothesized, this effect was mediated through CXCR4. The
increase in NSC number was due to both enhanced cell
proliferation and increased survival, and was confirmed in
vivo. Additionally, OPN dose-dependently stimulated the
migration of NSC via CXCR4. Moreover, in the presence of
OPN, differentiation of NSC led to a significant increase in
neurogenesis both in vitro as well as in vivo after cerebral
ischemia.ConclusionData show positive effects of OPN on
survival, proliferation, migration, and neuronal
differentiation of NSC. At least in part these effects were
mediated via CXCR4. Results suggest that OPN is a promising
substance for the targeted activation of NSC in future
experimental therapies for neurological disorders such as
stroke.},
cin = {INM-3 / INM-4},
ddc = {570},
cid = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-4-20090406},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000355979400001},
pubmed = {pmid:25998490},
doi = {10.1186/s13287-015-0098-x},
url = {https://juser.fz-juelich.de/record/200991},
}