Adult human dental pulp stem cells promote blood–brain barrier permeability through vascular endothelial growth factor-a expression

Now all we have to do if find an intervention that promotes brain recovery that needs to get thru the blood brain barrier. That a job for 'super stroke leader', but NO leadership is around! 

Adult human dental pulp stem cells promote blood–brain barrier permeability through vascular endothelial growth factor-a expression

1. Joshua N Winderlich1,2
2. Karlea L Kremer1,2
3. Simon A Koblar1,2,3⇑

1. ¹Stroke Research Programme, School of Medicine, University of Adelaide, Adelaide, Australia
2. ²Centre for Stem Cell Research, Robinson Institute, Adelaide, Australia
3. ³Department of Neurology, Queen Elizabeth Hospital, Woodville, Australia

1. Simon A Koblar, School of Medicine, University of Adelaide, Adelaide, SA 5005, Australia. Email: simon.koblar@adelaide.edu.au

Abstract

Stem cell therapy is a promising new treatment option for stroke. Intravascular administration of stem cells is a valid approach as stem cells have been shown to transmigrate the blood–brain barrier. The mechanism that causes this effect has not yet been elucidated. We hypothesized that stem cells would mediate localized discontinuities in the blood–brain barrier, which would allow passage into the brain parenchyma. Here, we demonstrate that adult human dental pulp stem cells express a soluble factor that increases permeability across an in vitro model of the blood–brain barrier. This effect was shown to be the result of vascular endothelial growth factor-a. The effect could be amplified by exposing dental pulp stem cell to stromal-derived factor 1, which stimulates vascular endothelial growth factor-a expression. These findings support the use of dental pulp stem cell in therapy for stroke.(No, it doesn't, getting thru the barrier is not a therapy in itself)

Stromal factors SDF1α, sFRP1, and VEGFD induce dopaminergic neuron differentiation of human pluripotent stem cells

I know this talks about using it for Parkinsons but hell with a little more research we should find out if its useable for stroke.
 http://onlinelibrary.wiley.com/doi/10.1002/jnr.23064/abstract;jsessionid=35622219F6929ED9B952375B676D58C5.d03t02?userIsAuthenticated=false&deniedAccessCustomisedMessage=

Keywords:

• dopaminergic neurons;
• neuronal differentiation;
• stromal cell-derived inducing activity;
• embryonic stem cells

Abstract

Human embryonic stem cell (hESC)-derived dopaminergic (DA) neurons hold potential for treating Parkinson's disease (PD) through cell replacement therapy. Generation of DA neurons from hESCs has been achieved by coculture with the stromal cell line PA6, a source of stromal cell-derived inducing activity (SDIA). However, the factors produced by stromal cells that result in SDIA are largely undefined. We previously reported that medium conditioned by PA6 cells can generate functional DA neurons from NTera2 human embryonal carcinoma stem cells. Here we show that PA6-conditioned medium can induce DA neuronal differentiation in both NTera2 cells and the hESC I6 cell line. To identify the factor(s) responsible for SDIA, we used large-scale microarray analysis of gene expression combined with mass spectrometric analysis of PA6-conditioned medium (CM). The candidate factors, hepatocyte growth factor (HGF), stromal cell-derived factor-1 α (SDF1α), secreted frizzled-related protein 1 (sFRP1), and vascular endothelial growth factor D (VEGFD) were identified, and their concentrations in PA6 CM were established by immunoaffinity capillary electrophoresis. Upon addition of SDF1α, sFRP1, and VEGFD to the culture medium, we observed an increase in the number of cells expressing tyrosine hydroxylase (a marker for DA neurons) and βIII-tubulin (a marker for immature neurons) in both the NTera2 and I6 cell lines. These results indicate that SDF1α, sFRP1, and VEGFD are major components of SDIA and suggest the potential use of these defined factors to elicit DA differentiation of pluripotent human stem cells for therapeutic intervention in PD. © 2012 Wiley Periodicals, Inc.