a) Venn diagram of modulated genes in HASMCs overexpressing Δ133p53 and treated with Ang II, showing 247 genes that fit the criteria of >0.5 FPKM (fragments per kilobase of exon per million fragments mapped) and an adjusted P-value of <0.05 (Wald tests implemented in the DESeq R package), commonly modulated in both conditions. ( b, c) The mRNA levels ( b) and protein abundance ( c) of KLF5 in HASMCs with Δ133p53 overexpression or Δ133p53 knockdown; n=7–8 per group. ( d, e) KLF5 expression in HASMCs with SRSF1 overexpression or SRSF1 knockdown at mRNA level ( d) and protein level ( e); n=6 per group. ( f) Cell-cycle distributions in HASMCs infected with Ad- SRSF1 in the absence or presence of KLF5 siRNA stimulated with Ang II (200 nM) for 24 h; n=9 per group. ( g) KLF5 siRNAs ( KLF5 si1 and KLF5 si2) knock down KLF5 protein in HASMCs; n=8 per group. ( h) Expression of p21 in HASMCs infected with Ad- SRSF1 or Ad- Δ133p53; n=5 per group. ( i) p21 levels in HASMCs with SRSF1 knockdown or Δ133p53 knockdown; n=7 per group. ( j) PCNA and p21 levels in HASMCs infected with KLF5 siRNAs in the absence or presence of Ad- SRSF1; n=7 per group. ( k) KLF5 and p21 levels in HASMCs infected with Δ133p53 siRNAs ( Δ133 si1 and Δ133 si2) in the presence or absence of Ad- SRSF1; n=7 per group. ( l, m) KLF5 and p21 levels in cultured HASMCs infected with SRSF1 siRNAs ( l) or Δ133p53 siRNAs ( m) after Ang II stimulation (200 nM, 24 h); n=5–7 per group. ( n) KLF5 and p21 levels in the arteries from Srsf1 −/− or WT control mice; n=7 per group. ( o) KLF5 and p21 levels in rat carotid arteries transfected with Ad- SRSF1 1 week after balloon injury; n=10 per group. Scr indicates scrambled siRNA control; BI, balloon injury. * P<0.05, ** P<0.01, one-way ANOVA ( b– f, h– m, o) or Student’s t-test ( n). Data are mean±s.e.m. of four ( b, d) or five ( c, e– o) independent experiments.