Single-dose VEGF-C treatment does not improve tMCAO outcomes. (A) VEGFR-3 and VEGFR-2 immunoprecipitation (IP) of brain protein extracts followed by western blot detection of phosphorylated tyrosine (pTYR) from mice injected with saline or VEGF-C protein (1 μg) at 1 and 24 h after administration (n = 3/group). (B and C) Quantification of tyrosine phosphorylation levels of VEGFR-3 (B) and VEGFR-2 (C) normalized to immunoprecipitated VEGFR-3 and VEGFR-2 proteins, respectively. *P < 0.05, **P < 0.01. (D) VEGFR-3 and VEGFR-2 IP of brain protein extracts followed by western blot detection of phosphorylated tyrosine from mice injected with either saline or VEGF-C156S protein (1 μg) at 1 and 24 h after administration (n = 5/group). (E and F) Quantification of tyrosine phosphorylation levels of VEGFR-3 (E) and VEGFR-2 (F) normalized to immunoprecipitated VEGFR-3 and VEGFR-2 proteins, respectively. *P < 0.05, **P < 0.01. (G) Experimental setting: mice underwent tMCAO and, after reperfusion, received an ICM injection of either recombinant VEGF-C (VEGF-C156S) or vehicle control (0.25% BSA). (H) Anti-LYVE-1–immunolabeled MLVs in the COS at 7 d-pso, and quantification of MLV coverage and diameter (n = 5 mice/group; Unpaired t test). (I) Neuroscore scale and corner test quantifications at 3 d- and 7 d-pso (n = 7, 5 mice/group; one-way ANOVA test). (J) Representative MRI anatomical T2 weighted scans showing the infarct lesion. Quantification of the lesion volume at 3 d- and 7 d-pso (n = 7–5 mice/group; Kruskal–Wallis test). Scale bar: 170 µm (H). MRI scale bar: 400 µm. Source data are available for this figure: SourceData F9.