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. 2022 Feb 22;298(4):101759. doi: 10.1016/j.jbc.2022.101759

Figure 1.

Figure 1

Wild-type and mutant AGGF1-C1 and C2, but not AGGF1-C3, increase the expression of VSMC phenotypic switching markers α-SMA, SM22, and MYH11 in VSMCs.A, Western blot analysis for α-SMA, SM22, and MYH11. MOVAS cells were treated with 20 μl control PBS or 20 μl of 5 μg/ml wild-type AGGF1 (AGGF1-WT) or mutant AGGF1 (AGGF1-C1, AGGF1-C2 and AGGF1-C3) for 24 h, lysed, and used for Western blot analysis. B, quantification of Western blot images as in (A) (mean ± SD, one-way ANOVA with Dunnett test for multiple comparison; ∗p < 0.05, ∗∗p < 0.01, n = 3/group). C, luciferase assays showing that AGGF1-WT, AGGF1-C1 and AGGF1-C2 increased transcriptional activation of VSMC contractile marker genes encoding MYH11, a-SMA and SM22 in the presence of SRF (serum response factor), but the effects were not observed for AGGF1-C3. MOVAS cells were cotransfected with an expression plasmid for SRF together with a MYH11, ACTA2, or TAGLN promoter luciferase reporter gene with or without an expression plasmid for wild type or mutant AGGF1. Cells were lysed and used for luciferase assays 48 h after transfection. NC, empty vector. Data are shown as mean ± SD (one-way ANOVA with Dunnett test for multiple comparison; ∗p < 0.05, n = 3/group). NS, not significant. AGGF1, angiogenic factor with G patch and FHA domains 1; VSMCs, vascular smooth muscle cells.