Skip to main content
Fig. 2 | Cell & Bioscience

Fig. 2

From: Inhibition of the cardiac fibroblast-enriched histone methyltransferase Dot1L prevents cardiac fibrosis and cardiac dysfunction

Fig. 2

Knockdown or inhibition of Dot1L attenuates TGF-β1-induced ECM deposition in adult rat CFs. A, B Knockdown of Dot1L attenuates ECM deposition in TGF-β1 treated CFs. Dot1L siRNA and control siRNA were transfected into CFs, followed by 5 ng/mL TGF-β1 stimulation for 48 h. The protein expressions of Dot1L, Col 3, FN and MMP9 were analyzed by western blot (A); Representative images of immunofluorescence staining of Dot1L and CTGF (B). C, D EPZ5676 attenuates ECM deposition in TGF-β1-treated CFs. CFs were pretreated with 10 and 20 μmol/L EPZ5676 for 4 h and then co-incubated with 5 ng/mL TGF-β1 for 48 h. H3K79me3, Dot1L, CTGF, Col 1, MMP9 and FN were analyzed by western blot (C); Representative images of immunofluoresence staining of CTGF or Col 1 were shown in 20 μmol/L EPZ5676-treated CFs (D). All data are presented as mean ± SD. ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001 versus Ctrl or Ctrl + siCtrl, #p < 0.05, ##p < 0.01, ###p < 0.001 versus TGF-β1 or TGF-β1 + siCtrl, each acquired from three individual experiments

Back to article page