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Fig. 3 | Fluids and Barriers of the CNS

Fig. 3

From: The role of plasmalemma vesicle-associated protein in pathological breakdown of blood–brain and blood–retinal barriers: potential novel therapeutic target for cerebral edema and diabetic macular edema

Fig. 3

(Adapted from [68])

PLVAP regulates vascular development and function. a Absence of Wnt and Norrin ligands for the Lpr5/Frzd receptor complex results in inactive canonical β-catenin signaling in non-barrier endothelium and in early embryonic stages in barrier endothelium. As a consequence, cytosolic β-catenin is targeted for proteolytic degradation through phosphorylation by the “β-catenin destruction complex”, which consists of the APC/axin/GSK3b-complex. Low levels of β-catenin allow upregulation of PLVAP expression in endothelial cells. However, it is unknown how PLVAP expression is upregulated during vascular development. PLVAP expression in the developing vasculature is essential during angiogenesis. PLVAP may directly promote angiogenesis or give mechanical support to capillaries, which prevents the formation of leaky vessels after the drastic remodeling steps of angiogenesis. b The canonical β-catenin signaling pathway is active in late embryonic stages in barrier endothelium. In the presence of Wnt or Norrin ligands, the “β-catenin destruction complex” is inhibited which results in the accumulation of β-catenin in cells. Nuclear β-catenin induces the transcription of β-catenin-target genes, which results in the downregulation of PLVAP expression. Low levels of PLVAP expression induce maturation of the BRB and BBB. EC endothelial cell

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