Post-stroke intracatheter delivery of VEGF-C exacerbates stroke damage without inducing additional expansion of cpLVs. (A) Experimental design for administering control or VEGF-C156S through the artery after reperfusion of tMCAO (day 0) and euthanasia at days 3 and 7 for decalcification steps (created using https://BioRender.com). (B) Coronal sections of CP areas were stained with Lyve-1 fluorescent antibody after either control or VEGF-C156S treatment of tMCAO mice at day 7. Representative confocal images of lymphatic vessels near the CP. Quantitation of each image (n = 3 mice per group; mean ± SEM, unpaired Student’s t test). Scale bars = 100 µm. (C) T2-weighted MRI scanned images of brain sections between tMCAO and tMCAO with VEGF-C156S treatment at days 3 and 7. Representative images of MRI brain scans. White dashed lines mark brain infarcts, which are quantified into a graph (n = 3 mice per group, n = 4 mice for tMCAO with VEGF-C156S at day 3; mean ± SEM, *P ≤ 0.05, **P ≤ 0.0, two-way ANOVA with mixed effects). (D) Coronal brain sections were stained with CD45 fluorescent antibody (Alexa 647) at day 3 after tMCAO/VEGF-C treatment. Subfornical vessels near the third ventricle were analyzed for perivascular leukocyte cell number. (n = 4 mice for tMCAO, n = 3 mice for tMCAO with VEGF-C156S; mean ± SEM, **P ≤ 0.01, unpaired Student’s t test). Scale bars = 20 µm. BV = blood vessel. Source data are available for this figure: SourceData F6.