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. Author manuscript; available in PMC: 2016 Aug 3.
Published in final edited form as: Nature. 2016 Feb 3;530(7589):184–189. doi: 10.1038/nature16932

Figure 4. Senescent cells cause glomerulosclerosis, kidney dysfunction and renal RAAS hyperactivity.

Figure 4

a, Images of sclerotic (left) and normal (right) glomeruli from the indicated mice. b, Quantification of sclerotic glomeruli. c, Measurements of blood urea nitrogen levels. d, SA-β-Gal-stained kidney sections. e, Electron micrograph showing a X-Gal crystal-containing renal epithelial cell with brush border membrane (arrowheads). Insets show X-Gal crystal close-ups. f, Percent of cells with X-Gal crystals in renal sections (n = 5 TEM grids for each treatment group). g, Renal expression of Agtr1a analyzed by qRT-PCR (n = 4 mice per group). h, Western blot of kidney lysates probed for Agtr1a (n = 3 mice per treatment group). Ponceau S staining served as loading control. i, Immunostaining of kidney sections for Agtr1a. Yellow circles denotes glomeruli. Scale bars: 50 μm in a; 250 μm in d; 5 μm (main panel) and 200 nm (insets) in e; 100 μm (top) and 50 μm (bottom) in i. Legends in c, f and g are as in b. Error bars indicate s.e.m. Statistical significance was determined by unpaired two-tailed t tests in b, c, f, and g. *, P<0.05; **, P<0.01; ***, P<0.001. For gel source data, see Supplementary Fig. 1. All mice in d–i were C57BL/6 ATTAC. +AP, AP-treated mice, –AP, vehicle-treated mice.