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Fig. 4 | Fluids and Barriers of the CNS

Fig. 4

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. 4

PLVAP induces vascular leakage through promoting VEGF-dependent caveolae formation. a The BBB and inner BRB are hallmarked by high trans-endothelial electrical resistance (TEER), which is the result of an elaborated junctional network, limited presence of caveolae and absence of fenestrae. In physiological conditions, the availability of VEGFR1 homodimers predominantly localized at the luminal side of the BBB and BRB induces important vascular protective functions [120]. In contrast, VEGFR2 homodimers at the abluminal side [120], which are probably present at a very low concentration under physiological conditions, as VEGFR2 is usually not detectable by immunohistochemistry in brain and retinal vessels [74, 75], mediate vascular leakage (not shown). b In pathological conditions such as diabetic retinopathy, tissue VEGF-A levels are high. In addition, VEGFR2 and VEGFR3 are highly expressed in retinal vessels of diabetic patients. Together, this results in VEGFR2/PI3K/p38MAPK-dependent PLVAP expression and formation of caveolae, which promotes leakage of plasma proteins and edema formation. EC endothelial cell, PC pericyte

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