Figure 1
Regulation of PLPP3 expression by AngII and NF-κB in caHSMC. (A) caHSMC were treated with vehicle (n = 3), Mβ-CD Cholesterol (10 μg/ul, n = 3) LPA (1 μM, n = 3)), AngII (1 μM, n = 3), or transforming growth factor beta (TGFβ, 1 μM, n = 3) for 72 h and gene expression analyzed by qRT-PCR using 18 s as internal control. Results are presented as relative gene expression (mean ± SEM), *P < 0.05, One-way ANOVA. (B) caHSMCs were treated with vehicle (n = 3) or AngII (1 μM,) for 12 (n = 3), 24 (n = 3), 48 (n = 3) or 72 h (n = 6). Results are presented as relative gene expression (mean ± SEM). *P < 0.05, One-way ANOVA, #P < 0.05 Kruskal–Wallis One-way ANOVA on Ranks. (C) caHSMCs were treated with vehicle (n = 4) or AngII (1 μM, n = 6) for 72 h. Results are presented as relative gene expression (mean ± SEM), *P < 0.05, unpaired two-tailed student t-test. (D) caHSMCs were treated with vehicle, AngII (1 μM), AngII + Irbesartan (1 μM), or AngII + PD-123,319 (1 μM) for 72 h, n = 3 for all treatment conditions. Results are presented as relative PLPP3 gene expression. (E) caHSMCs were treated with vehicle (n = 4), angiotensin II (1 μM, n = 8) or angiotensin II + parthenolide (1 μM, n = 3) for 72 h. Results are presented as relative gene expression (mean ± SEM) *P < 0.05, One-way ANOVA.
