001     200991
005     20220930130043.0
024 7 _ |a 10.1186/s13287-015-0098-x
|2 doi
024 7 _ |a 2128/8973
|2 Handle
024 7 _ |a WOS:000355979400001
|2 WOS
024 7 _ |a altmetric:4047642
|2 altmetric
024 7 _ |a pmid:25998490
|2 pmid
037 _ _ |a FZJ-2015-03310
041 _ _ |a English
082 _ _ |a 570
100 1 _ |0 P:(DE-HGF)0
|a Rabenstein, M.
|b 0
245 _ _ |a Osteopontin mediates survival, proliferation and migration of neural stem cells through the chemokine receptor CXCR4
260 _ _ |a London
|b BioMed Central
|c 2015
336 7 _ |0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
|a Journal Article
|b journal
|m journal
|s 1436865377_20873
336 7 _ |2 DataCite
|a Output Types/Journal article
336 7 _ |0 0
|2 EndNote
|a Journal Article
336 7 _ |2 BibTeX
|a ARTICLE
336 7 _ |2 ORCID
|a JOURNAL_ARTICLE
336 7 _ |2 DRIVER
|a article
520 _ _ |a 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.
536 _ _ |0 G:(DE-HGF)POF3-572
|a 572 - (Dys-)function and Plasticity (POF3-572)
|c POF3-572
|f POF III
|x 0
700 1 _ |0 P:(DE-HGF)0
|a Hucklenbroich, J.
|b 1
700 1 _ |0 P:(DE-Juel1)144347
|a Willuweit, Antje
|b 2
700 1 _ |0 P:(DE-HGF)0
|a Ladwig, A.
|b 3
700 1 _ |0 P:(DE-Juel1)131720
|a Fink, Gereon Rudolf
|b 4
700 1 _ |0 P:(DE-HGF)0
|a Schroeter, M.
|b 5
700 1 _ |0 P:(DE-Juel1)131777
|a Langen, Karl-Josef
|b 6
700 1 _ |0 P:(DE-HGF)0
|a Rueger, M. A.
|b 7
|e Corresponding author
773 _ _ |0 PERI:(DE-600)2548671-8
|a 10.1186/s13287-015-0098-x
|n 1
|p article 99
|t Stem cell research & therapy
|v 6
|x 1757-6512
|y 2015
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.pdf
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.gif?subformat=icon
|x icon
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.jpg?subformat=icon-1440
|x icon-1440
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.jpg?subformat=icon-180
|x icon-180
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.jpg?subformat=icon-640
|x icon-640
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/200991/files/s13287-015-0098-x.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:juser.fz-juelich.de:200991
|p openaire
|p open_access
|p OpenAPC
|p driver
|p VDB
|p openCost
|p dnbdelivery
910 1 _ |0 I:(DE-588b)5008462-8
|6 P:(DE-HGF)0
|a Forschungszentrum Jülich GmbH
|b 1
|k FZJ
910 1 _ |0 I:(DE-588b)5008462-8
|6 P:(DE-Juel1)144347
|a Forschungszentrum Jülich GmbH
|b 2
|k FZJ
910 1 _ |0 I:(DE-588b)5008462-8
|6 P:(DE-Juel1)131720
|a Forschungszentrum Jülich GmbH
|b 4
|k FZJ
910 1 _ |0 I:(DE-588b)5008462-8
|6 P:(DE-Juel1)131777
|a Forschungszentrum Jülich GmbH
|b 6
|k FZJ
913 0 _ |0 G:(DE-HGF)POF2-333
|1 G:(DE-HGF)POF2-330
|2 G:(DE-HGF)POF2-300
|a DE-HGF
|b Gesundheit
|l Funktion und Dysfunktion des Nervensystems
|v Pathophysiological Mechanisms of Neurological and Psychiatric Diseases
|x 0
913 1 _ |0 G:(DE-HGF)POF3-572
|1 G:(DE-HGF)POF3-570
|2 G:(DE-HGF)POF3-500
|a DE-HGF
|b Key Technologies
|l Decoding the Human Brain
|v (Dys-)function and Plasticity
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
914 1 _ |y 2015
915 _ _ |0 StatID:(DE-HGF)0100
|2 StatID
|a JCR
|b STEM CELL RES THER : 2013
915 _ _ |0 StatID:(DE-HGF)0300
|2 StatID
|a DBCoverage
|b Medline
915 _ _ |0 StatID:(DE-HGF)0199
|2 StatID
|a DBCoverage
|b Thomson Reuters Master Journal List
915 _ _ |0 StatID:(DE-HGF)0111
|2 StatID
|a WoS
|b Science Citation Index Expanded
915 _ _ |0 StatID:(DE-HGF)0150
|2 StatID
|a DBCoverage
|b Web of Science Core Collection
915 _ _ |0 StatID:(DE-HGF)1050
|2 StatID
|a DBCoverage
|b BIOSIS Previews
915 _ _ |0 StatID:(DE-HGF)9900
|2 StatID
|a IF < 5
915 _ _ |0 StatID:(DE-HGF)0510
|2 StatID
|a OpenAccess
915 _ _ |0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
|a Creative Commons Attribution CC BY 4.0
920 _ _ |l yes
920 1 _ |0 I:(DE-Juel1)INM-3-20090406
|k INM-3
|l Kognitive Neurowissenschaften
|x 0
920 1 _ |0 I:(DE-Juel1)INM-4-20090406
|k INM-4
|l Physik der Medizinischen Bildgebung
|x 1
980 1 _ |a FullTexts
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a FullTexts
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-Juel1)INM-3-20090406
980 _ _ |a I:(DE-Juel1)INM-4-20090406
980 _ _ |a APC
981 _ _ |a I:(DE-Juel1)INM-4-20090406


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21