Canonical Wnt Signaling Regulates Organ-Specific Assembly and Differentiation of CNS Vasculature

By Jan M. Stenman, J. Rajagopal, Thomas J. Carroll, M. Ishibashi, J. McMahon, Andrew P. McMahon. Science, 2008

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Tight junctions at the blood brain barrier: physiological architecture and disease-associated dysregulation (2012, positive): “Moreover, in vivo inactivation of Wnt factors (Wnt7a and Wnt7b) [100], Fz4 receptor [101] or injection of a soluble inhibitor of the Wnt/ Frizzled receptor interaction [102] lead to major vascular defects in the CNS (interestingly, not in non-neuronal tissues) and to BBB breakdown, clearly demonstra”
The blood-brain barrier. (2015, background): “…progenitors, a loss of capillary beds, Cite this article as Cold Spring Harb Perspect Biol 2015;7:a020412 9 and the formation of hemorrhagic vascular malformations, which together suggest that Wnt is a migration signal driving vessels into the CNS (Stenman et al. 2008; Daneman et al. 2009).”
In vitro models of the blood–brain barrier: An overview of commonly used brain endothelial cell culture models and guidelines for their use (2016, background): “developmentally relevant in vivo canonical Wnt signaling events between neural progenitor cells and endothelial cells.(118,270,271) Similarly, the cord blood-derived endothelial cells are regulated by addition of Wnt3a or Wnt7a, resulting in increased TEER compared to un-stimulated monocultures.”