Fig. 6: Antibody-based Tie2 activation and VEGFR2 blockade stabilize EC junctions and suppress EC transcytosis in GBM. | Experimental & Molecular Medicine

Fig. 6: Antibody-based Tie2 activation and VEGFR2 blockade stabilize EC junctions and suppress EC transcytosis in GBM.

From: An agonistic anti-Tie2 antibody suppresses the normal-to-tumor vascular transition in the glioblastoma invasion zone

Fig. 6

Vascular assessment in EGFRVIII GBMs at 2 weeks post-treatment with IgG, 4E2, or DC101. a, b Immunostaining for VE-cadherin in nontumor vessels (a) and GBM vessels (b), with quantification (f, n = 5 per group). c Immunostaining for Caveolin-1, a transcytosis marker, in tumor vessels, with quantification (g, n = 5 per group). d Immunostaining for PLVAP, a transcytosis marker, in tumor vessels, with quantification (h, n = 5 per group). e Transmission electron micrographs showing caveolar vesicle formation (yellow arrowheads) and cell-cell junctions in ECs of normal brain and GBM treated with IgG, 4E2, or DC101. The closed and open arrowheads indicate intact tight junctions and destabilized junctions, respectively. i Quantification of vesicles per EC cross-section (n ≥ 7 per group). j Proportion of intact tight junctions (TJs) (n = 27 per group). Scale bars: 100 µm (a-d), 200 nm (e). **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 vs. IgG. ns not significant; #, P < 0.05; ####, P < 0.0001 vs. DC101.

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