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. 2019 Jul 11;116(5):956–969. doi: 10.1093/cvr/cvz187

Figure 5.

Figure 5

The RRFR peptide inhibits the interaction between ADAMTS16 and LAP-TGF-β and induces the activation of TGF-β. (A) Co-IP analysis for the interaction between Adamts16 and LAP-TGF-β in mouse cardiac fibroblasts treated with different concentrations of the RRFR peptide. An anti-FLAG antibody was used for immunoprecipitation and an anti-ADAMTS16 antibody was used for immunoblotting (IB). (B) Western blot analysis showing the effect of the RRFR peptide on the level of LAP-TGF-β in mouse cardiac fibroblasts. Data are shown as mean ± SD. **P < 0.01 (n = 6). Statistical analysis was carried out by a one-way ANOVA test. (C) ELISA showing the effect of the RRFR peptide on the level of active TGF-β in the supernatant of mouse cardiac fibroblasts. Data are shown as mean ± SD. **P < 0.01 (n = 5). Statistical analysis was carried out by a two-way ANOVA analysis. NS, not significant. (D) Luciferase assays for TGF-β-mediated transcriptional activation in HeLa cells transfected with the TGF-β-responsive 3TPE luciferase reporter gene and treated with Adamts16 siRNA or negative control siRNA (siNC) for 18 h. Cells were then incubated with the RRFR peptide or IIFI peptide for 18 h, and used for luciferase assays. Data are shown as mean ± SD. **P < 0.01 (n = 5). Statistical analysis was carried out by a two-way ANOVA analysis. NS, not significant.