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.
Fig 3: 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 4: Pharmacological or genetic TIE2 activation prevents UUO-induced tubular injury and PDGFB expression.(A) Tubular segments with pathological vacuoles (red arrow) in kidney sections stained with toluidine blue. (B) Quantification of tubular segments with vacuoles from ABTAA-treated (ABT), VeptpiECKO (VeKO), and Tie2iECKO (T2KO) mice. Data are based on n = 4–5 mice/group and >10,000 tubular cross sections. (C) RNA-ISH for Pecam1 (cyan) and Pdgfb (magenta) in 3-day UUO kidneys. Representative image of n = 4 mice. Scale bars: 50 μm. (D and E) Gene expression of Kim1, Pdgfb, Pdgfrb, Tie2, and Angpt1 in UUO kidneys from indicated time points. Data are based on n = 3–7 mice/group. (F) RNA-ISH for Angpt1 (magenta), mesenchymal marker Pdgfrb (cyan), and tubular marker Atp1a1 (blue) in 3-day UUO kidneys. Representative image of n = 3 mice. Scale bars: 50 μm. (G–I) Expression of Pdgfb/PDGFB in 3-day UUO kidneys from ABTAA-treated, VeptpiECKO, and PdgfbiKO (PbKO) mice. Data are based on n = 5–9 mice/group. (J) Patient data retrieved from Nephroseq for renal CDH5 (endothelial marker), ANGPT2, PDGFB, and ANGPT1 expression in CKD and renal dysfunction compared with normal human kidney. Data in graphs (B, D, E, and G–I) 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. Human data (J) represent Log2 expression and statistical differences from Nephroseq (see Methods).
Supplier Page from Abcam for Mouse PDGF BB ELISA Kit