Figures & data
Figure 1. Cabin1 localized in the nuclei of glomerular innate cells of normal rats. Notes: A–E:original magnification: ×400; F: ×1500) (A) Cabin1 mainly localized in the nuclei of glomerular innate cells; (B) WT-1 localized in podocytes nuclei; (C) nuclei; (D) Differential interference contrast (DIC); (E and F) Cabin1 and WT-1 colocalized in podocytes nuclei.
Figure 2. Cabin1 expressed in renal cortex of normal rats. Note: In normal SD rats, western blot showed Cabin1 protein remarkably expressed in renal cortex.
Figure 3. AngII-induced actin cytoskeleton disruption. Notes: Fluorescence microscope ×400. (A) Untreated podocytes, white arrow showed the fine connection of podocyte foot processes; (B) AngII-treated podocytes induced the loss of the cytoplasmic cytoskeleton and the reorganized of actin cytoskeleton at 24 h, white arrow showed the disruption of podocyte foot processes connection; (C) Tacrolimus inhibited the injury of AngII, maintained well-defined actin stress fibers, white arrow showed the maintain of podocyte foot processes connection.
Figure 4. The localization of Cabin1 in AngII injuried podocytes. Notes: Fluorescence microscope ×400). (A and C) In normal podocytes, Cabin1 presented strong staining in cytoplasm yet weak staining in the nuclei; (B, E and H) Immunofluorescence staining of nuclei; (D and F) AngII-induced strong staining of Cabin1 in podocytes nuclei; (G and I) Tacrolimus mildly inhibited the strong staining of Cabin1 in the nuclei.
Figure 5. AngII-induced Cabin1 nuclear protein increased in cultured podocytes. Notes: (A) Western blot showed AngII-induced Cabin1 nuclear protein expression significantly increased at 48 h; (B) Quantification of Cabin1 nuclear and cytoplasmic protein expression. *p < 0.05 versus normal control group. N: normal control.
