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Fig. 3 | Molecular Medicine

Fig. 3

From: CRTC2 activates the epithelial–mesenchymal transition of diabetic kidney disease through the CREB-Smad2/3 pathway

Fig. 3

CRTC2 modulated EMT in vivo and in vitro. C57BL/6J mice were intraperitoneally injected with STZ (30 mg/Kg) or PBS (control). The STZ mice were fed with high fat diet and control mice were fed with normal diet. A E-cadherin, α-SMA, Vimentun, Snial and β-catenin were detected by immunohistochemistry in the kidney of mice. B E-cadherin and α-SMA were detected by immunohistochemistry in the kidney of db/db mice. C Genes of kidney were detected by real-time PCR (n = 3). D E-cadherin was detected by Western blot (left), and E-cadherin and α-SMA were detected by immunohistochemistry (right) in HK-2 cells with overexpressed CRTC2-Flag plasmid for 48 h. E HK-2 cells were transfected with α-SMA luciferase constructs with or without control vector, as well as CRTC2 overexpression plasmid (CRTC2-Flag) for 48 h. The cells were treated with TGF-β1 (8 ng/ml, 48 h). Luciferase activity was assayed in triplicate. **p < 0.01 compared with Control group. ##p < 0.01 compared with TGF-β1 group

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