Fig. 3
Fig. 3. Vegfr tyrosine kinase inhibitors, DMH4 and AV-951, block CNS angiogenesis but not barriergenesis. (A) Representative confocal images (dorsal views; anterior left) of untreated, DMSO-treated, or inhibitor-treated glut1b:mCherry, plvap:EGFP embryos. Embryos were treated at 24 hpf then imaged at 54 hpf. Note that the inhibitor-treated embryos lack CtAs but express glut1b:mCherry in the PHBCs indicating that barriergenesis occurs in the absence of CNS angiogenesis. In addition, 1 ??M DMH4 was as effective as 5 ??M DMH4 at blocking CNS angiogenesis. AV-951 (1 ??M) showed similar effects as 5 ??M DMH4. Scale bars are 100 ??m (top left) and 50 ??m (top right). (B) Quantification of the number of CtAs at 2 dpf for untreated, DMSO-treated, or inhibitor-treated embryos (n ?= ?3). (C) Quantification of the normalized RFI of glut1b:mCherry in untreated, DMSO-treated, or inhibitor-treated embryos at 2 dpf (n ?= ?3). Data for (B) and (C) are presented as means ?± ?SEM (???p ?< ?0.001; ns ?= ?not significant).
Reprinted from Developmental Biology, 494, Fetsko, A.R., Sebo, D.J., Taylor, M.R., Brain endothelial cells acquire blood-brain barrier properties in the absence of Vegf-dependent CNS angiogenesis, 46-59, Copyright (2022) with permission from Elsevier. Full text @ Dev. Biol.