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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},
}