Fig. 3: SENP1 deficiency in VSMCs augments the SRF-ELK complex during vascular remodeling.
From: SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling

Carotid arteries from WT and Senp1SMCKO mice on day 0–28 post-injury. A Western blots for proteins and protein 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 Immunofluorescence staining on day 28 post-injury. C Fractional number of p-ELK+ cells within the neointimal areas or ECs were quantified (n = 10 left carotid arteries per group). D, E Immunofluorescence staining in carotid arteries on day 28 post-injury. D Representative images. E Fractional number of SRF+ cells within the neointimal areas or ECs were quantified (n = 10 left carotid arteries per group). F Western blots for SRF and myocardin. 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. G qRT-PCR for mRNAs in carotid arteries. Relative mRNA levels are presented by taking non-injured WT as 1.0 (n = 3). H Western blots for phospho-SRF. Protein fold changes are presented by taking non-injured WT carotid arteries as 1.0 (n = 1). I SRF SUMOylation in day 7 post-injury carotid arteries. Co-immunoprecipitation assays with anti-SRF or IgG followed by western blot with SUMO1 or SUMO2/3 as indicated. Protein fold changes are presented by taking non-injured WT carotid arteries as 1.0 (n = 2). J SRF-SUMO1, SRF-ELK and SRF-myocardin complexes by co-immunoprecipitation assays in VSMCs. Protein fold changes are presented by taking untreated VSMC as 1.0 (n = 1). K Effects of AZD6244. VSMCs were treated with PGDF-BB in the absence or presence of AZD6244 (0.5 μmol/L) for 60 min. Co-immunoprecipitation assays were performed and protein fold changes are presented by taking untreated VSMC from WT as 1.0 (n = 1). Data are mean ± SEM, compared with WT mice (two-tailed Student’s t test) (C, E) and compared with un-injured or untreated groups (one-way ANOVA with Bonferroni post hoc analysis) (G). ns no significance. Scale bars, 50 μm (B, D). Source data are provided as a Source Data file.