Fig 2: Inhibition of Sprouty1 (Spry1) reverses the effect of miR-21 knockout (KO) on angiotensin II (Ang II)-induced ERK/TGF-β/Smad activation in primary cardiac fibroblasts (CFs). (A) Representative and (B–H) quantitative analysis of Western blots. Inhibition of Spry1 reverses the effects of miR-21 KO on Ang II-induced ERK/TGF-β/Smad signaling in primary CFs; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n = 3 per group.

Fig 3: Sprouty1 (Spry1), an miR-21 target, inhibits the activation of ERK1/2 post-myocardial infarction (MI). (A) Relative expression of Spry1 between wild-type (WT) and miR-21 knockout (KO) mice at 2 weeks post-MI; ****P < 0.0001, n = 5 per group. (B–D) Representative (B) and quantitative Western blots (C and D) of Spry1, p-ERK, and ERK in WT and miR-21 KO mice myocardium; miR-21 KO mice that underwent MI induction exhibited increased expression of Spry1 and decreased expression of p-ERK1/2. Inhibition of Spry1 promotes the phosphorylation of ERK1/2. ***P < 0.001, ****P < 0.0001, n = 3 per group.