a) PCR showing genotyping of WT (Flox +/+Cre ERT2−) and Srsf1 /Cre −/− ERT2 (Flox +/+Cre ERT2+) mice. Band in the upper image indicates the product from SRSF1 flox/flox, and lower image indicates product from SMA-Cre ERT2. ( b) Representative western blots showing SRSF1 levels in the vessel and liver from inducible smooth muscle cell-specific Srsf1 knockout ( Srsf1 /Cre −/− ERT2) mice. ( c, d) Representative photomicrographs of haematoxylin and eosin staining (scale bars, 50 μm) ( c) and averaged data ( d) of the neointimal area, neointima/media ratio, media area and circumference of external elastic lamina (EEL) of carotid arteries from Srsf1 /Cre −/− ERT2 and WT control mice 14 and 28 days after wire injury (N, neointima; M, media); n=9 per group. ( e, f) Representative photomicrographs of immunohistochemical staining (scale bar, 25 μm) ( e) and averaged data ( f) showing the percentages of PCNA-positive cells in carotid arteries from Srsf1 /Cre −/− ERT2 and WT control mice 14 and 28 days after wire injury. Arrows indicate PCNA-positive cells (dark brown); n=9 per group. ( g, h) Representative pictures ( g) and averaged data ( h) of re-endothelialization. Re-endothelialization was quantified in Evans blue-stained carotid arteries at 3 and 7 days after vascular injury. Blue staining indicates endothelial denudation. Scale bar, 1 mm; n=9 per group. ** P<0.01, NS, not significant; Student’s t-test ( d, f, h). Data are mean±s.e.m. of five independent experiments ( d, f, h).