Fig. 2: SENP1 deficiency in VSMCs results in a loss of contractile phenotype in injury-induced neointima.

WT and Senp1^SMCKO mice at age of 10–12 weeks were subjected to wire injury on left carotid arteries, and tissues were harvested for analyses on day 3–28 post-injury as indicated. Non-injured mice were used as controls (time 0). A Western blots for proteins of VSMC contractile and synthetic markers on day 0–28 post-injury. Each tissue sample was pooled from three individual aortas and protein bands were quantified by densitometry and fold changes are presented by taking non-injured WT carotid arteries as 1.0. Additional two experiments were performed with different biological repeats presented in Supplemental Fig. 12. B, C Carotid arteries on day 28 post-injury were subjected to immunofluorescence co-staining of various contractile and synthetic markers as indicated with DAPI counterstaining for nuclei (blue) (B). Fractional areas of the neointima occupied by each marker were quantified (n = 10 left carotid arteries per group) (C). D, E VSMCs isolated from non-injured WT and Senp1^SMCKO mice treated with PDGF-BB (10 ng/ml) for indicated times. D VSMC contractile and synthetic markers were detected by Western blot (0, 6, 12 and 24 h time points) and (E) immunofluorescence staining (0 and 24 h time point). Protein bands were quantified by densitometry and fold changes are presented by taking untreated VSMC from WT as 1.0 (n = 2). Data are mean ± SEM. Unpaired, two-tailed Student’s t test (C). Scale bars, 50 μm (B). 10 μm (E). Source data are provided as a Source Data file.