Epsin bioactive coating reduced in-stent intimal hyperplasia by promoting early phase reendothelialization and inhibiting smooth muscle cell proliferation
Fig 2
The effect of knocking down Epsin on EC proliferation and migration.
(A) and (B) Ki67 incorporation assays of EC. Representative immunofluorescence of Ki67 (green) and DAPI (blue). percentages of Ki67 incorporated EC. (C) and (D) Scratch‐wound assays showed the effect of VEGF on the migration of EC infected with siEpsin1 + siEpsin2. (E) and (F): expression levels of Epsin1, Epsin2, VEGFR2 and Erk were determined by Western blotting using the appropriate antibodies. GAPDH served as a loading control. GAPDH served as a loading control. t-test, n = 3, in each group. * : P ＜ 0.05 vs. sinormal control (NC); #: P ＜ 0.05 vs. siEpsin1 + siEpsin2; &: P ＜ 0.05 vs. siNC+VEGF.