Journal Article

FZJ-2018-04039

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Bioluminescence imaging visualizes osteopontin-induced neurogenesis and neuroblast migration in the mouse brain after stroke

Rogall, R. ; Rabenstein, M. ; Vay, S. ; Bach, A. ; Pikhovych, A. ; Baermann, J. ; Hoehn, M. ; Couillard-Despres, S. ; Fink, G. R.FZJ* ; Schroeter, M.FZJ* ; Rueger, M. A. (Corresponding author)FZJ*

2018
BioMed Central London

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Please use a persistent id in citations: http://hdl.handle.net/2128/19270  doi:10.1186/s13287-018-0927-9

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.

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Contributing Institute(s):

1. Kognitive Neurowissenschaften (INM-3)

Research Program(s):

1. 572 - (Dys-)function and Plasticity (POF3-572) (POF3-572)

Appears in the scientific report 2018

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Database coverage:
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