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. 2017 Aug 11;8:16016. doi: 10.1038/ncomms16016

Figure 7. SRSF1 promotes VSMC proliferation via KLF5–p21 signal.

Figure 7

(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.