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. 2023 Nov 28;79:101841. doi: 10.1016/j.molmet.2023.101841

Figure 2.

Figure 2

Treatment with FXR agonists or FXR overexpression suppress fibronectin, α-SMA and Snail and recover E-cadherin induced by ox-LDL. After pretreatment with different concentrations of GW4064 (A), chenodeoxycholic acid (CDCA) (B), or vehicle control DMSO for 30 min, NRK-52E cells were incubated with 50 μg/mL ox-LDL for 24 h. The protein levels of fibronectin, α-SMA, Snail and E-cadherin were examined by Western blot analysis. (C) Overexpression of FXR in NRK-52E cells is confirmed by Western blotting with anti-Flag antibody. NRK-52E cells were transiently transfected with either the expression vector of Flag-tagged FXR (pFXR) or empty vector (pcDNA3). Ox-LDL incudes fibronectin and suppresses E-cadherin in NRK-52E cells and treatment with forced expression of FXR suppresses fibronectin and increases E-cadherin expression. (D–E) The quantitative data of fibronectin level is presented. Values normalized to GAPDH and reported as mean ± S.E.M, ∗p < 0.05. Immunofluorescence staining (F–H) shows that ox-LDL suppresses epithelial marker E-cadherin and induces fibronectin and α-SMA expression in NRK-52E cells. Then, treatment with GW4064 suppresses fibronectin and α-SMA expression and recovers E-cadherin.