Fig 1: Transcriptional profiles of VEGFR-3–specific RelA-deficient mice and floxed controls following inflammation-induced AKI.(A) Lymphatic associated genes’ and (B) NF-κB and Vcam1 genes’ expression analyses from kidney lysate, presented as fold change relative to tamoxifen+saline WT controls. Analysis included data from 4 independent knockout cohorts and 3 WT control cohorts (WT control, N = 11; KO control, N = 7; WT cisplatin, N = 9; KO cisplatin, N = 15 for Flt4, Lyve-1, Ccl21a, Prox-1, and Pdpn; N = 12 for Vcam1; N = 14 for p50, Vegfc, and p52). All transcript levels were normalized to Gapdh. Statistical significance (P < 0.05) was determined using 2-way ANOVA. *P < 0.0332, **P < 0.0021, ***P < 0.0002, ****P < 0.0001. WT, RelAfl/fl; KO, VEGFR-3RelA–/–.