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. 2020 Jan;190(1):176–189. doi: 10.1016/j.ajpath.2019.09.013

Figure 2.

Figure 2

Genetic deletion of Tlr2 reduces tubular damage, inflammation, and fibrosis in Glis2 knockout kidneys. A: Representative bright-field microscopy images of periodic acid–Schiff (PAS)–stained kidney sections at low (top row) and high (bottom row) magnification for Glis2, Tlr2 double-knockout (Glis2−/−;Tlr2−/−) versus Glis2 knockout (Glis2−/−) mice. B–D: Comparison of kidney damage in kidney sections from the two genotypes, as assessed by PAS staining–based injury score (B), percentage of cystic area (calculated on the basis of digital image; C), and serum urea concentrations (D). E and F: Analysis of kidney fibrosis in both genotypes on the basis of Masson's trichrome staining. E: Kidney sections at low (top row) and high (bottom row) magnification. F: Quantification of trichrome staining by digital image analysis. G: Ratio of collagen/total protein content for kidneys of both genotypes. H–K: Analysis of inflammation in both genotypes. H and I: Representative immunofluorescence confocal images of kidney sections immunostained for the fibroblast marker fibroblast specific protein 1 (FSP1) (H) and the macrophage marker CD68 (I). J and K: Quantification of staining in H and I, respectively, based on digital image analysis. L–N: Comparison of markers of inflammation in the kidney, at the RNA level (quantitative real-time PCR). P values were calculated by two-tailed t-test. Numbers of mice per group are reported in each panel. Data are expressed as means ± SD (B–D, F, G, and J–N). *P < 0.05, **P < 0.01, and ***P < 0.001. Scale bars: 1 mm (A and E, top row); 200 μm (A and E, bottom row); 20 μm (H and I). TNF-α, tumor necrosis factor-α.