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. 2020 Apr 6;24(10):5740–5750. doi: 10.1111/jcmm.15236

FIGURE 6.

FIGURE 6

Mindin knockout reduced pro‐fibrotic protein expression though inhibiting TGF‐β/Smad signal pathway activation in mice after renal ischaemia reperfusion injury. (A) Representative micrographs of collagen I (Col), Smad2 and fibronectin (Fn) immunohistostaining (IHC) and Fn immunofluorescence staining in wild‐type and mindin−/− mice with or without renal IRI. Magnification, 400×. Scale bar, 50 µm. (B and C) Quantitative analysis of IHC with Col and Smad2 in mindin +/+ and mindin−/− mice with or without renal IRI. (D) Western blotting analysis of extracellular matrix‐related proteins fibronectin, E‐Cadherin and Col. GAPDH was used as a loading control. (E) Quantification analysis of these proteins’ levels. (F) Western blotting analysis of TGF‐β, p‐Smad2 and p‐Smad3 and Smad7 proteins. GAPDH was used as a loading control. (G and H) Quantification analysis of the proteins’ expressions. Data are presented as the mean ± SE, n = 5 mice per group. *P < .05 versus sham WT mice, # P < .05 versus WT mice after renal IRI