Fig. 7
From: Podocyte GSK3 is an evolutionarily conserved critical regulator of kidney function
Hippo signalling is disrupted in GSK3 deficient podocytes in vivo. a, b Western blot (a) and quantification (b) of glomeruli isolated from mpodGSK3DKO and littermate control mice showing increased expression of Ajuba, n = 2 mice per group. c, d Immunohistochemistry showing increased Ajuba (top panels) and YAP/TAZ nuclear translocation (arrowed, bottom panels) in the podocytes of podGSK3DKO (c) and mpodGSK3DKO (d) mice. Representative immunohistochemistry and quantification shown (>5 glomeruli per mouse analysed, 3 mice per group, ANOVA ***p < 0.001. Scale bar = 25 μm). e Immunohistochemistry showing an increase in the number of cells positive for the YAP/TAZ TEAD target Cyclin A2. Three mice from each group analysed, t test *p < 0.5. f Immunofluorescence staining showing increased expression of c-myc in podGSK3DKO and mpodGSK3DKO mice. Three mice analysed per group, t test ***p < 0.001. Scale bar = 50 μm. g Representative immunohistochemistry using an anti-Ajuba antibody in a glomerulus from a rat given high dose lithium for 6 months and in a biopsy from a patient on long-term lithium therapy. Ajuba expression is increased with lithium treatment relative to control tissue. Scale bar = 25 μm. Data are presented as the mean ± SEM
