Fig. 7: Interaction between UHRF1 and DNMT1 mediates KLF15 hypermethylation and fibroblasts activation. | Cell Death Discovery

Fig. 7: Interaction between UHRF1 and DNMT1 mediates KLF15 hypermethylation and fibroblasts activation.

From: Inhibition of epigenetic regulator UHRF1 attenuates renal fibrosis and retains transcription factor Krüppel-like factor 15 expression

Fig. 7

A Western blots showed the DNMT1 expression in NRK-49F cells transfected with UHRF1 siRNA or control siRNA with or without TGF-β1 treatment. B DNMT1 enzyme activity of NRK-49F cells transfected with UHRF1 siRNA or control siRNA with or without TGF-β1 treatment. C Co-IP analysis showed anti-UHRF1 antibody pulled down endogenous DNMT1. D PLA assay showed the interaction between UHRF1 and DNMT1 in NRK-49F cells with or without TGF-β1 treatment, presented by red fluorenscent signals (×400). Scale bar: 20 μm. E MeDIP-qPCR analysis showed inhibition of the interaction between UHRF1 and DNMT1 with NSC232003 prevented TGF-β1-induced KLF15 hypermethylation in NRK-49F cells. F Western blots demonstrated blocking effect of NSC232003 on TGF-β1-induced fibroblasts activation in NRK-49F cells. G NRK-49F cells infected with CRISPR-Cas9 lentivirus targeting KLF15 or scramble lentivirus were treated with TGF-β1 and NSC232003. Fibroblasts activation was assessed by immunoblots of α-SMA and Fibronectin. n = 3–6 samples per group. Data were shown as mean ± SEM. Data were analyzed using unpaired Student’s t test (D, G) or One-way ANOVA followed by Tukey (A, B, E, F). *P < 0.05, **P < 0.01.

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