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

Figure 2.

Figure 2

Overexpression of ADAMTS16 accelerates the activation of cardiac fibroblasts (differentiation of cardiac fibroblasts into myofibroblasts with increased α-SMA). (A) Real-time RT–PCR analysis for Acta2 (encoding α-SMA) in mouse cardiac fibroblasts transfected with pcDNA3.1 or a mammalian expression plasmid for human ADAMTS16 and treated with Ang II (48 h) or negative control buffer. (B) Immunostaining analysis of α-SMA for mouse primary cardiac fibroblasts treated as in (A). Scale bar =12.5 μm. (C) Quantification of immunostaining images as in (B). (D) Western blot analysis for α-SMA using protein extracts from mouse cardiac fibroblasts treated as in (A). (E) Quantification of western blotting data as in (D). (F) Collagen lattice contraction analysis of mouse cardiac fibroblasts treated as in (A). (G) Quantification of collagen lattice contraction data as in (F). (H) Migration of cardiac fibroblasts treated as in (A) using scratch wound assays. (I) Quantification of scratch wound data as in (H). Data are shown as mean ± SD. *P < 0.05, **P < 0.01 (A–E, n = 6/group; F-I, n = 4/group). Statistical analysis was carried out by a one-way ANOVA test.