Fig 1: Post-injury treatment with ABTAA slows progression of fibrosis.(A) Schematic diagram of administration of ABTAA for evaluation in 10-day UUO kidneys. (B–F) Immunohistochemistry of renal cortex for capillary density (endomucin [EMCN] and podocalyxin [PODXL]) and tubulointerstitial fibrosis (aSMA and vimentin) in 10-day UUO kidneys from ABTAA-treated mice (ABT) and Tie2iECKO (T2KO) mice. Data are based on n = 6–7 mice/group and quantification of >220 images/marker. Scale bars: 50 μm. (E) Protein concentration for PDGFB in 10-day UUO kidneys from ABTAA-treated mice. Data are based on n = 5 mice/group. Data in graphs represent mean ± SD, and each symbol represents 1 mouse (females, magenta; males, cyan). *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001, determined by 1-way ANOVA and Tukey’s post hoc test.
Fig 2: Pharmacological or genetic TIE2 activation, or inhibition of PDGFB signaling, protects the kidney transcriptome following UUO injury.Bulk RNA-Seq of 3-day UUO kidneys. (A) Heatmaps of genes relevant for ECM modifications, tubular injury, endothelium, and inflammation in ABTAA/IgG-treated (n = 7–8), VeptpiECKO/VeptpWT (n = 6–8), and PdgfbiKO/PdgfbWT (n = 4) mice. aP < 0.05 versus respective CL; b,cP < 0.05 UUO versus UUO. (B and C) Venn diagrams of downregulated and upregulated DEGs and Metascape analysis of linked GO for DEGs.
Supplier Page from Abcam for Mouse PDGF BB ELISA Kit